Switram kc020 hyd

A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH”IN THE MANAGEMENT OF SWITRAM (VITILIGO)

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INTRODUCTION

The aim of medicine is to safeguard and rescue men from the consequences of their

vices. Since its inception Ayurveda emphasizes on maintenance of positive health and

alleviation of the diseases pestering humankind, among which skin diseases are one.

Switra is a dermatological disorder having its references cited in the Vedas. The

term is derived from “Sweth Varne” meaning white colour. It is basically a disease

related to hypopigmentation. Switra is also known as “Sweta Kustam” or “Kilasam”.

Switra emerges as a sequel to irregular dietary habits, life style changes, and

genetic predisposition. Constant use of chemicals, cosmetics, plastic, rubbers, and

pollution may accelerate the attack of the disease. The disease involves the skin and does

not cause pain, ulceration or any secretions. Switra inflates an inferiority complex in the

persons affected.

Skin is the vital organ involved in this disease. Skin being the largest organ of the

body and on the surface is continually exposed to injury. The colour of the skin plays an

important role as high cosmetic value is attributed to it. Colouring, tattooing, adorning

with jewellery are all part of skin appeal.

The general state of the health is reflected in the appearance and condition of the

skin and the earliest signs of many systemic diseases may be observed by inspecting it.

As the skin is on the surface and it is on display patient with skin diseases are always in

public eye. The greatest handicap of all is to be unwelcome and isolation by the

community.

The functions of the skin are impaired in skin diseases making those more

affected, more vulnerable and less able to reconstitute themselves after damage. 20-30%

of skin diseases require serious attention. (Davidson) The disease Switra is one among

them, as it causes immense mental agony and social embarrassment.


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Based on the clinical features of switra, it can be correlated to vitiligo of the

modern medicine. Vitiligo on the face is ranked 17th by WHO in world’s most Disabling

diseases. Vitiligo is also an ancient malady having references cited in Bible and other

contemporary Texts. It is defined as a common acquired discolouration of the skin

characterized by well circumscribed, ivory or chalky white macules which are flush on to

the surface. Sometimes systemic, Cutaneous, ocular associations may be present. The

hair over the patch may be white or normal.

Vitiligo occurs world wide with an overall prevalence of 1%. The higher

incidence of the condition has been recorded in India from Asia, followed by Mexico and

Japan. The incidence is 6% in Calcutta, 4% in Vellore, 8% in Amaravati, 2.9% in Goa,

8.8% in Delhi. The difference of its incidence may be due to higher reporting of vitiligo

in a population where an apparent colour contrast and stigma attached to the condition

may force them to seek early consultation. Both males and females are equally affected

with no predilection of sex. The age of first onset is below 20 years and the lower limbs

are generally the site of first onset.

The imperatives of its epidemiology both in rural India and in global are

reckoning and have been highlighted. In spite of the latest advancements made in modern

medicine the etiology of vitiligo remains unknown. It is expected to be of autoimmune

origin as it is associated to some of the autoimmune disorders. Occasionally it may be

possible to identify the triggering factors.

An effective panacea for the disease could not be found till date. Generally topical

corticosteriod therapy, topical PUVA, Oral Psoralen Photo chemotherapy or oral PUVA,

Surgical techniques like skingrafting, other techniques like tatooing, camouflage creams

are employed to manage vitiligo. But all the above mentioned methods are associated

with high risk factors, are expensive, and unsuitable for people living in different

climatic conditions and the success rate is not commendable.


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Ayurveda offers absolution to many diseases among which switra is one.

Innumerable yogas have been described to combat the disease.

One such comprehensive formula is “Dhatri- Khadira Kwath” from Bhaishajya

Ratnavali, contemporary text of 19 A.D.

A total of 30 patients were taken for this study and all the patients received the

treatment for 45 days. The medicine was administered in kwath form, followed by honey

as anupana. The main aim was to assess the efficacy of the formula in causing

pigmentation in the white patches of switra. And three Clinical parameters – colour of the

patch, number of patches and size of the patches were taken into consideration to assess

the result.

Present study is divided into five parts. The first part deals with review of

literature of the disease, second part deals with drug review, third part deals with clinical

study – observations and results, fourth part deals with discussion, conclusion, summary

and fifth part deals with references, bibliography and annexure.

Thus a humble step has been made to probe into various aspects of switra and its

management with the trial drug.


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HISTORICAL REVIEW

Switra is an ancient malady and a historical background will facilitate continuity with

current research .Many earliest references of switra dating back to Vedic kala are found

and the contribution of our ancestors in combating the disease is known.

For convenience sake time period is divided into:

1. PRACHEENA KALA (5000 BC- 7 A.D )

2. MADHYAMA KALA ( 8 A.D –15 A.D )

3. ADHUNIKA KALA (16 A.D ONWARDS )

PRACHEENA KALA (5000 BC- 7 A.D):

VEDIC PERIOD: includes description of the disease in Rig, Yajur, Sama &Atharvavedas.

RIG VEDA:

a) Old looking unmarried princess Ghosa, the daughter of Kaksivana was cured of

kusta roga and was made young and beautiful, and was married .1

b) Sujava was cured of kusta and rejuvenated and was married to a good looking

girl .2

c) Diseases like kilasa and Palithya were described .3

d) Application of Bringraj, Harida , Neelika , Indravaruni in kusta ,palitya rogas

.Here Sayanu interprets kusta as Svetha kustam.4

YAJUR VEDA:

There is a reference of moon being affected by the disease.5


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ATHARVA VEDA:

a) There is a refernce in Atharva Veda that white coloured patches appear in a

disease called Sweta kusta, and when it penetrates into deeper dhatus it is called

Kilasa

kusta .6

In this context “ASIKINI “and “RAJINI” are the drugs used which are very

important in the disease.

SAMA VEDA : No references found in this veda

.Aitheraya Aranyaka: Sage Bharadwaja mentioned twak, mamsa .rakta are derived from

mother and in a stage all the three are affected

During Uanishad period Asvatayana mentioned maharogas .Narayana interprets Kusta

as one among them.7

In Mahabharata (400 B.C) mentioning of many twag doshas are found but no special

reference of Switra is found.

Puranas (500 B.C) were influenced by the medical concepts and description of many

diseases are found in them.

Padmapurana mentions kusta and Switra as diseases caused due to the imbalance of the

tridoshas.8

Markandeya purana mentioned two girls suffered with this disease and were eventually

cured 9It is regarded by this purana that all twag rogas are due to past life sins.

Vayu purana regarded kusta and kilasa to have evolved due to faulty practice of yoga10.


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Vishnu purana mentioned a wide variety of skin diseases in sharirika rogas 11.In

anatomical chapters a detailed description of embryological development of organs is

found and seven layers of skin have been described in this context.

Itihasa purana mentioned switra among several diseases caused due to derangement of

the doshas .Sins or the papakarmas are considered to play a major role in causing the skin

diseases in particular .12.

Brahma vaivartha purana mentioned many skin diseases under the heading GALITHA

VYADHIS 13among which switra is one.

Agni purana mentioned kusta as a broad term to describe all the skin diseases including

switra.

In Yagnavalkya smriti skin or the twacha has been described having six layers and all

the diseases arise from these layers .14

Manu smriti (200B.C-200 A.D) has clearly mentioned that a stealer of clothes suffers

from switram .It is aquainted as hereditary disease and people suffering with this disease

are not eligible for marriage .15

OTHER LITERATURE DURING VEDIC PERIOD:

Other than the Indian literature, earliest references of the condition can be traced back to

the period of Aushooryan (2200 B.C) in the classic TARIKH –E-TIL-IRAN.16

Pharaonic medicine in the ebers papyrus (1500B.C) described two types of diseases

affecting the colour of the skin. a) With tremors probably leprosy b) with colour change

probably Vitiligo .The latter was said to treatable .17

In Arabic medicine the terms “BOHAK “BAHAK” ‘BARAS’ are the terms mentioned to

denote a similar condition like Vitiligo.18

In Bible the term “ZORAAT”denotes Vitiligo.19


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In Japanese literature (1200BC) SHIRABITO is the term used for the condition like like

switra .20

SAMHITA KALA:

Charaka samhita: In this treatise switra is described in the kusta roga chapter .A

detailed description of the disease is found in this text.A special etiology is mentioned for

switram, types and treatment has been vividly described .21

Sushruta samhita: Has also described switra in a detailed fashion.In nidana Stan 5th

chapter description of the disease is found .22

Bhela samhita; Bhela included switra in eleven kshudra kustas and mentioned it as

asadya roga .23

Harita samhita :did not give a detailed description of the disease but mentioned a stealer

of clothes and money is prone to get this disease .And arista lakshanas of kusta rogas are

mentioned and said to be applicable to switra also.24

Kashyapa samhita: included switra in eleven types of kshudra kustas .Five types are

mentioned but no names and clinical features are found .it is said to be a asadya vyadhi.25

SANGRAHA KALA;

Astang Sangraha: switra as a bahya vikruti and in sutra Stan mentions that using a

poisonous jalouka for rakta mokshanam shall cause the disease 26.

Astang Hrudayam: describes switra as a separate disease .Etiology, types, clinical

features, prognosis and treatment are clearly mentioned .Vagbatta has considered switra

to a medical emergency as delayed medical intervention may lead to complete

depigmentation.27


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MADHYAMA KALA (8 A.D. - 15 A.D):

Vangasena: a text book of 10 A.D describes about the etiological factors responsible for

the disease. Specially seven dietary factors are mentioned which cause kusta rogas.The

etiology of kusta and switra are considered same .28

Madhava Nidan: a special text on etiology of different diseases describes switra in

49thchapter .complete description of the disease is found vividly in this book.29

Sharangdhara samhita :( 11-12 A.D) has mentioned the etiology of kusta and switra to

be same and mentioned three types of the disease based on the involvement of the

dhatus .30

BhavaPrakash: written by Bhavmisra has given a detailed description about the disease

the etiology, types ,clinical features ,prognosis and treatment have been in the text.31

BUDDHIST LITERATURE:

Tripitika literature is the oldest source to have a glimpse of Indian medicine in

Buddhist tradition. It is mentioned that kusta, kilasa, ganda, sosa, apasmara, are five

prevalent abadhas.

Vinaya pitam mentioned the disease kilasa i.e spotted deer 32.

Sardulakarnavadana: In this book Ayurveda is mentioned along with four vedas.

Kushta and kilasa are mentioned seperately33.

Lalithavistara: One among the nine important texts deals with the advent of Lord

Buddha and his teachings. In this context those diseases caused by vata, pitta, sleshma

and sannipata diasease of kushta and kilasa34

Saddharmapundarika: Diseases like kusta and kilasa are mentioned seperately35

JAIN TRADITION: 16 diseases are enumerated among which leprosy is one.

Kalyanakaraka: By Vugraditycharya. 20 chapters are present. From 8 th chapter onwards

diseases are mentioned. Kusta is one among mahamayas.


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OTHER NON-MEDICAL SOURCES:

Panini (7th B.C): Sutras were annotated by patanjali in 2nd B.C. Kusta and Kilasa are

mentioned separately.

Kautilya’s Arthasastra: (321-297 B.C) In a chapter on secret means, a number of

diseases has been mentioned among which kusta is one. In this disease this physician’s

certificate is honoured.36

Bana Bhatta (606-648 A.D): In Harsacharitra and Kadambari mentioned the concept of

health and described Switra separately.37

Amarakosha (600 A.D): Has mentioned switra separately and terms like “Padasphota”,

“Twak pushpi” are mentioned in this context.38

ADHUNIKA KALA (16 A.D ONWARDS):

Yogaratnakar: mentioned switra as kilasa and described it in kusta chapter.

Bhaishajya Ratnavali: switra is described in kusta roga adhikar. Treatment of switra is

described with various formulations .39

RESEARCH WORKS DONE IN VARIOUS INSTITUTIONS :

1. Dr.Sheela ratna M.V, Switra roga and its management Mysore 1979.

2. Dr.Patil A.K, Survey of Switra in Jamnagar and Vicinity in reference to its nidana

and Chikitsa .Jamnagar 1984.

3. Dr.Upadhyaya R.K, Therapuetic assessment of some Ayurvedic drugs in

treatment of Vitiligo.Varnasi 1985.

4. Dr.Shankaran.K, Managament of Switra with special reference to Bakuchi

Trivendrum 1986.


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5. Dr.Lahiri P.K, Clinical studies and management of Switra kusta (leucoderma)

with Ayurvedic drugs, Calcutta 1987.

6. Dr.PrithviRaj, Concept of switra and its management in Ayurveda, varnasi1988.

7. Dr.ThakoreS.R, Switra mein Kakodumbara ka Prayogika Adhyayan.

Ahmedabad1989.

8. Dr.Srikanth Babu, Evolution of Kakodumbaradi yoga in management of Switra.

Mysore 1992.

9. Dr.Sharada C.L, Clinical study of Switra (leucoderma) and its management with

kakodumbara and manahshiladi lepa.Jamnagar 1993.

10. Dr.Kambale.S, Switra kustavar nidana parivarjana aushadhi (bavanchi) ani

aharacha parinama.Nanded 1996.

11. Dr.Prabhakar.Shinde, A Clinical study of the effect of Somarajyadi churnam (int)

and Somarajyadi lepa (ext) in Switra .Hyderabad 1996.

12. Dr Seeta Devi.P .A clinical study on the effect of lepa in Switra .Mysore 2003.

13. Dr.Venugopal CH, A clinical study on the effect of kaseesabadda ras (int) with

and without chitraka lepa in Switra (VITILIGO) Hyderabad 2003.

14. Dr.Mahantesh P.M, A Comprehensive management of kilasa kusta Vitiligo).Hubli

2006.


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NIRUKTI

The term switra is derived from “swith” dhatu meaning white colour. Rak pratyaya is

added and letter “kha” is deleted.It belongs to napunsaka gender.

Swith +ra = Switra40

Switra =Sweth varne switra

The term indicates a disease where white coloured patches appear on the skin.

Switra is analogous to the disease vitiligo in the contemporary medicine .The

term Vitiligo is derived from latin word “vitium” meaning defect .41 Documentation of

the word is present in the book De-Meedicina by the Roman Physician Celsus42.


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PARIBHASHA

The definition of Switra is given by all the ancient classics .The acharyas who have

defined switra primarily suggested that this is a disease related to impairment of colour.

The term Switra is derived from “sweth varne switra” meaning white colour.

Amarkosha defined switra as “Swetate twaganena Switram”43 meaning ‘white colour

of the skin’.

Shabda kalpa drumam defined it as “Swetate itihi” meaning white colour .44

Kashyapa samhita defined Switram as “Sweta bhavamicchanti switram” meaning

reflection of white colour .45

Sushruta defined it as “Twagatam eva aparisravi “one which involves only the skin and

has no oozing tendency.46

The essence of all the above mentioned, indicate Switra as a disease in which

hypopigmentation is a cardinal feature.

Vitiligo is defined as a dermatological disorder characterized by milky white patches

devoid of melanocytes .It bears resemblence in having a progressive tendency and

genetic predisposition.47


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SHAREERA RACHANA

Introduction: “Twak’ or the “Twacha” are the analogous names to identify the skin in

Ayurveda. It is one of the largest organs which cover the entire external surface area of

the body.

Twak is aptly defined as “Twach Samvarne” 48 meaning the one which covers. It

covers the entire external surface of the body protecting the underlying rakta, mamsa,

medo dhatus49. The skin forms a self renewing, self repairing interface between the body

and the environment.

Embryonic Development of Twak:- A perfect combination of healthy sukra and

sonitha leads to the formation of an healthy embryo50. The pancha maha bhutas act

accordingly on the embryo leading to the formation of various anga – pratyangas.

Amongst the five, Vayu helps in the division of the cells, and Tejo maha bhuta helps in

the maturation and specialization of the cells forming different layers of cells of different

organs. Sushruta opined that as the cream is formed over the boiling milk, the various

layers of the skin are also formed and deposited on the rapidly forming product of the

combination of sukra & sonitha.51

Vagbatta described that during the process of cooling (Processing) of the blood,

the layers of twak are formed, and the purity of the skin lies in the purity of blood.52

Sushruta described seven layers of the skin, Charaka53 and Vagbatta54 described six

layers of skin.

Twak is derived predominantly from vayu and akash mahabhutas and its

adhistana devata is vayu55. Twak is one of the pancha gnanedriyas56 and its indriyartha is

Sparsha57, its indriya buddi is Sparshana58.

The entire body is a combination of three doshas, Sapta dhatus and three malas59.

Skin also being a part of this body is composed of vata, pitta and kapha. It is an upadhatu

of mamsa dhatu. Sweda is excreted through the skin.


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The tridoshas have their respective role to play in the twak. The skin being the

seat of vata it does the sparsha grahana, 60 pitta helps in imparting the colour and luster51.

Kapha gives the mrudutwa and snigdatwa to the skin.62

In the process of formation of various dhatus, the mamsa dhatu is derived from

rakta dhatu.63 The prasada bhagha of mamsa dhatu is subdivided into vasa & twak.64

These two are nourished by the mamsa dhatu. Apart from receiving nourishment from its

parent dhatu, twak is also nourished by numerous rasavahinis. Sometimes the rasa and

twak become analogous, twak Sara person is considered as rasa Sara also65.

Twak is considered to be a rasaja bhava by the virtue of its property to reflect the

varna.66

LAYERS OF THE SKIN:

1st Layer: is named as “udakadhara”67 by charaka and is believed to contain watery

substance such as rasa or lasika (body lymph). Sushruta named it as ‘avabhasini’ which

measures 1/18vreehi; this layer reflects the colour and complexion of the skin68.

Vagbhatta named it as “bhasini”. It is the site for manifestation of sidma and

padmakantakam.

2nd Layer: is named as ‘asrgdhara’ by charaka as it contains blood capillaries. Sushruta

named it as “Lohita”. It measures 1/16 vreehi. Vagbhatta named it as “Lohini”.

Cutaneous infections like Tilakalaka, Nyaccha, and Vyanga are manifested here.

3rd Layer: Unnamed by charaka, Sushruta named it as “sweta” it measures 1/12 vreehi.

It is the site for manifestation of Charmadala, Ajagillika, and Mashaka.Charaka described

this layer to be the seat for Sidma & Kilasa.

4th Layer: Not named by charaka & Vagbhatta but explained it to be the site for all

varieties of kusta and dadru. Sushruta named it as ‘Tamra’ measuring about 1/8 th vreehi

and seat for various types of kusta and kilasa.


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5th Layer: Not named by Charaka and Vagbatta but explained diseases like alaji, and

vidradhi being manifested here. Sushruta named this layer “vedini” measuring about 1/6 th

of vreehi. And diseases like kusta and visarpa are explained here.

6th Layer: Not named by Charaka but Vagbhatta named it as “pranadhara” the supporter

of life and seat for diseases like arumshi. Excision of which leads to tremors and entering

to darkness. Any manifestations are deep rooted here and difficult to treat. Sushruta

named this layer as ‘Rohini’ which measures 1 vreehi. Grandhi, arbudas, apache, slipada,

galaganda are manifested here. All muscular outgrowths are noted here.

7th Layer: Named by sushruta as “Mamsadhara”. The deepest layer, thickness is double

the vreehi, and diseases like Bhagandara, Vidradhi are manifested here. All the diseases

involving mamsa and rakta dhathu are explained here.

According to Charaka69:

Table -1

S.No. Name of the Layer Function Diseases

1. Udaka dhara Protects the loss of body fluids -

2. Asragdhara Reservoir of blood -

3. Tritiya - Sidma, kilasa

4. Chaturtha - Dadru, Kusta

5. Panchami - Alaji, Vidradi

6. Shasti - Tremors anddarkness before eyes.


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According to Sushruta70:

Table -2

S.No. Name ofthe layer

Thickness Function Diseases

1. Avabhasini 1/18 Vreehi Reflection ofcolour &

complexion

Sidma, Padma Kantakam

2. Lohita 1/16 Vreehi - Tilakalaka, Nyaccha,Vyanga

3. Swetha 1/12 Vreehi - Charmadala, Ajagallika,Mashaka

4. Tamra 1/8 Vreehi - Kilasa & Kusta5. Vedini 1/6 Vreehi - Kusta & visarpa6. Rohini 1 Vreehi - Granthi, Apacchi, Arbuda,

Galaganda, Sleepada7. Mamsadara 2 Vreehi - Bhagandara, Vidradi,

Arsas

According to Astangahrudaya71:

Table -3

S.No. Nameof the layer

Function Diseases

1. Bhasini Expresses Colour and fiveshades of complexion

-

2. Lohini - -3. Swetha - -4. Tamra - -5. Vedini - -6. Rohini - -7. Mamsadhara - -


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ANATOMY OF THE SKIN

Among the three primary germ layers of the embryo, the epidermis is derived

from the ectoderm-the outer most primary germ layers. At the beginning of the second

month the ectoderm consists of simple cuboidal epithelium. These cells flatten and are

known as Periderm.

By the end of fourth month, all layers of the epidermis are formed and each layer

assumes its characteristic structure.

The dermis is derived from wandering mesodermal cells. The mesenchyme

becomes arranged in a zone beneath the ectoderm and there undergoes changes in the

connective tissues that form the dermis.

Nails develop during third month from ectoderm. Hairfollicles develop between

third & fourth month from the ectoderm. By the fifth and sixth month follicles produce

delicate hair called lanugo which usually shed before birth.

The secretory portions of sebaceous and sudoriferous glands are derived from

ectoderm. The connecting tissues and blood vessels associated with the glands develop

from mesoderm.

Microstructure of the Skin:

Epidermis: is a compound tissue consisting mainly of continuously self replacing

stratified keratinized squamous epithelium. The principle cells of which are called

Keratinocytes. Other Cellular elements of different developmental orgin within the

mature epidermis includes melanocytes or the pigment forming cells from embryonic

neural crest. Langercells are immunocompetent antigen presenting cells derived from

bone marrow. Other cells are Lymphocytes. These disparate cells are collectively

known as non-keratinocytes or epidermal immigrants. Neurally associated Merkel cells

are now thought to be modified Keratinocytes.


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Sensory nerve endings are also sparsely present within the epidermis. Each

component has an individual primary function, but the fact of there intimate spatial

associations and of functional interactions has led to the concept of epidermal symbionts.

The population of keratinocytes undergoes continuous renewal through out the

life a mitotic layer of cells at the base replacing those shed at the surface. As they move

away from the base of the epidermis, the keratinocytes undergo progressive changes in

shape and content full of protein keratin, a process known as keratinisation.

It is usual to divide the epidermis into number of strata from deep to superficial as

follows, S.basale, S.spinosum, S.granulosum, S.lucidum and S.corneum. The first three

of these layers are metabolically active and often grouped together as the stratum

malpighi. The more superficial strata of cells achieving terminal keratinazation

constitute the cornified zone.

1. Stratum basale: This includes the deepest layer of cells adjacent to the dermis and

appears to rest upon a continuous narrow ‘basement membrane’ which includes the basal

plasma membrane of the cell, a basal lamina consisting of lamina lucida and lamina

densa, and a dermal reticular lamina. This area is also known as epidermal – dermal

junction. The cytoplasm contains the common cellular organelles, melanosomes and

many cytoskeletal intermediate filaments. The plasma membranes of the opposed cells

are connected by desmosomes and the basal plasma membrane has hemidesmosomes.

Melanocytes, Langerhans cells and Merkelcells are interspread among the basal

keratinocytes.

2. Stratum spinosum (Prickle Cell Layer): This contains several layers of mature

keratinocytes packed closely and inter digitating by means of numerous projections and

indentations of the cell membrane which are linked by many desmosomes giving then

spiny appearance, hence also called as Prickle cell layer. The cytoplasm contains the

common organelles including some lysosomes and melanosomes. Langerhans cells and


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the occasional associated lymphocytes are the only non -keratinocytes present in the

stratum spinosum.

3. Stratum granulosum: In this stratum three to four layers of flattened cells with

extensive changes in Keratinocyte structure occurs . The nuclei become pycnotic and

began to disintegrate, the membraneous organelles such as mitocondria, golgi membranes

and ribosomes degenerate, and keratin filament bundles become more compact and

associated with Keratohyalin granules. Small round granules with a lamellar internal

structure also appear in the cytoplasm. The lamellar granules are concentrated deep to the

plasma membrane of the granular cell with which they fuse liberating their predominantly

lipid content in to the intercellular space not only of this stratum, but also into the space

between it and the stratum corneum. They form an important component of the

permeability barrier of the epidermis, langerhans cells may occasionally be seen at lower

levels of stratum granulosum.

4. Stratum lucidum: Only found in thick glabrous palmo-plantar skin, this layer

represents poorly understood stage in Keratinocyte differentiation. Ultrastructurally

resembles the transitional cell, an incompletely keratinized cell occasionally seen in the

innermost layer of the statum corneum of non-glabrous skin.

5. Stratum corneum: This stratum is the final product of epidermal differentiation or

Keratinazation. It consists of closely packed layers of flattened Polyhedral Corneocytes.

These cells overlap at their lateral margins and interlock with cells of opposed layers by

ridges, grooves and microvilli. In this skin the statum may be only a few cells deep, but in

thick skin it may be more than 50 cells deep. The interior of this corneocyte is devoid of

nucleus and membraneous organelles, consisting solely of a dense array of keratin

filaments embedded in an interfilmentous matrix partly composed of filaggrin derived

from keratohyalin granules.

Desquamation of the outer layers of the stratum corneum involves a poorly

understood loosening of attachments (desmosomes and inter cellular substances) between

the cells, probably involving enzyme action and is normally imperceptible, when


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execessive, it appears in hairy regions as dandruff and more massively in certain diseases

as peeling, scaling, and exfoliation. Langerhans cells are not present in the stratum

corneum and therefore are not desquamated.

Melanophages are macrophages which have ingested performed melanin and

melanphores or dermal melanocytes, within which melanin can be rapidly aggregated or

dispersed to change body colour in adaptation to environmental backgrounds.

Embryonic precursors of melanocytes migrate from the neural crest to enter the

epidermis as melanocytes from about eight gestational weeks. It is estimated that a single

melanocyte may be in functional intact via its dendrites with up to 30 Keratinocytes to

form an entity called the epidermal melanin unit. Melanocytes decrease significantly

in number in old age and are absent from grey hair.

EPIDERMAL MELANOCYTES AND SKIN PIGMENTATION

Melanocytes are melanin pigment forming cells derived from the neural crest and

widely distributed throughout the body in vertebrates. In humans they are present in the

epidermis and its appendages, in oral epithelium, some mucous membranes, the uveal

tract of the eyeball, parts of the middle and internal ear and in the leptomeninges at the

base of the brain. The cells of the retinal pigment epithelium, developed from the outer

wall of the optic cup, also produce melanin, and neurons in different locations within the

brain stem synthesize a variety of melanin called neuromelanin.

True melanins are complicated,high molecular weight polymers attached to a

structural protein (to form melanoproteins) and in humans there are two classes, the

brown black eumelanin and redyellow Phaeomelanin both derived from tyrosine

catalysed by the enzyme tyrozinase . The dermis is for the survival of the epidermis and

important morphogenetic signals are exchanged at the interface between the epidermal-

dermal junction during development and postnatally. The dermis can be divided into

superficial papillary layer, and a deeper reticular layer.


21

Dermis: The dermis is an irregular, moderately soft connective tissue, with a matrix

composed of an inter woven collageneous and elastic network in an amorphous ground

substance of glycosamino glycans, glycoproteins and bound water, which accommodates

nerves, blood vessels, lymphatics, epidermal appendages and a changing population of

cells. The dermis provides considerable strength to skin by virtue of the number and

arrangement of its collagen fibres, which give it tensile strength and it has elastic recoil,

because of its elastic fibres.

Layers of dermis:

1. Papillary Layer:- This is immediately deep to the epidermis and is specialized to

provide mechanical anchorage, metabolic support and trophic maintainance to the

overlying tissue as well as housing rich networks of sensory nerve endings and

blood vessels. Its superficial surface is marked by numerous papillae which

interdigitae with recesses in the base of the epidermis and form the dermal-

epidermal junction at the interface. The papillae have round or blunt apices which

may be divided into several cusps. In skin especially in regions with little

mechanical stress and minimal sensitivity, papillae are few and very small, while in

thick skin of the palm and sole of the foot, they are much larger, closely integrated,

and arranged in curved parallel lines following the pattern of ridges and grooves

typical of these surfaces. Lying under each epidermal ridge are two longitudinal

rows of papillae or either side of epidermal retepegs through which the sweat ducts

pass on the way to the surface. Each papilla contains dense collagen fibres, elastic

fibrils, microfibrils, attached to the basal lamina. Also present in thick hairless skin

meissner’s corpuscular nerve endings.

2. Reticular Layer: This merges with the deep aspect of the papillary layer. Its

bundles of collagen fibres are thick than those in the papillary layer and interlace

with them and with each other form a strong yet deformable three dimensional

lattice in which many fibres are parallel to each other and within which lies a

variable number of elastic fibres. The Orientation of the collagenfibres may be

related to the direction of action of the mechanical forces to which the dermis is

subjected and may be involved in the development of the skin surface lines.


22

ULTRASTRUCTURE OF MELANOGENESIS:

Melanocyte is a dendrite non-keratinocyte, lacking desmosomal contacts with

apposed keratinocytes. The nucleus is large round and euchromatic.

In the cytoplasm are intermediate filaments, a prominent golgi complex and

vesicles, associated granular endoplasmic reticulum, mitochondria and coated vesicles

together with a characteristic marker organelle, the melanosome.

The melanosome is a membrane bound structure which undergoes a sequence of

four developmental stages during which melanin is synthesized and deposited within it by

the tyrosine – tyrosinase reaction.

Stage –I Stage I melanosome is spherical vacuole, derived probably from the rough

endoplasmic reticulum, and containing filamento - amorphous structural protein and

vesiculo globular bodies.

Stage-II Stage II Eumelanosomes become spherical or ellipsoid and the inner

matrix becomes organized into filamentous sheets exhibiting a 9nm periodicity.

Stage-III At Stage III melanin begins to be deposited on the innersheets, gradually

observing their arrangement, until densely pigmented.

Stage-IV is reached, exhibiting no other internal structures apart from non-

melanized vesiculo globular bodies. Phaeomelanosomes retain their spherical shape

throughout all stages.


23

In most active melanocytes, melanosomes of the four stages are present. When

mature, stage IV melanosomes move into the dendrites along the surfaces of

microtubules and are transferred to keratinocytes by a special type of phagocytosis, with

subsequent liberation of melanosomes into the keratinocytes cytoplasm.

Hence colour of the skin plays a vital role in protecting the humans from various

physical, chemical agents and harmful effect of sunlight.

APPENDAGES OF THE SKIN:

Organs that develop from the embryonic epidermis – hair, sweat glands,

sebaceous glands, nails ceruminous glands, have a host of important functions to

perform. Hair and nails protect the body. The sweat glands help regulate body

temperature. The sebaceous glands produce an oily substance the sebum and ceruminous

glands provide waxy secretion in the ear canal. Skin along with its appendages forms the

integumentary system72-73.


24

SHAREERA KRIYA

Ayurveda defines “Shareera” as “Sheeryate iti Shareeram” means the one which

constantly undergoes wear and tear. This applies to all the organs which constitute the

shareera, particularly the skin.

As defined by Shabdakalpadrumam. “Twachati Samvrunoti medo shonithadikam

iti”74 Twak covers the underlying rakta, mamsa, medo dhatus. Twak not only covers the

entire body area but also forms a strong physical barrier against microbial invasion. It

protects the body against mechanical, chemical, thermal, osmotic and photo damage. It is

major site of inter communication between the body and environment.

Second vital function of the twak is to impart Varna or the colour to the body and

its structures. It reflects the luster and brilliance present in it.

The Varna of an individual is determined in the embryonic stage of life. It is a

rasaja bhava75. The tejomahabhuta is the main factor in determining the varna76. The kind

of food taken during pregnancy also determines the colour. The four prakrut varnas

formed by the combination of different mahabhutas.

Tejo+Jala = Gouravarna

Tejo+Prithvi = Krishna varna

Prithvi + Akash = Krishna – Shyama

Jala + Akash = Goura – Shyam

Charaka has attributed the Varna aspect to the udana vata (one among

panchavidha vatas). 77 The vital functions of Pitta are mentioned as production of normal

and abnormal temperature in the body as well as normal or abnormal colour of the

Skin 78.

Among the five types of Pitta, imparting colour to the skin is a specialized

function of the Bhrajakapitta79. As pitta is involved in the above said function, kapha

builds the texture of the skin making it supple, shiny and strong.80


25

There are two major aspects of varna-(i) Prabha (brilliance of the skin) (ii) Chaya

(Substratum of the colour) Prabha is of 7 types- rakta, Peeta, Sita, Syava, Harita,

Pandura, Asita. Prabha specifies the colour of an individual. Chaya is of 5 types,

according to the panchamahabutas 81. Nabhasi, Vayavi, Agneeyi, Ambasi, Parthivi and is

the substratum of the colour. Prabha is reflected to farther distance but chaya can be

appreciated only from a close view. Prabha and chaya are inseparable aspects of Varna

and their reflection is the vital function of Prakrit pitta. In a deranged state, pitta exhibits

abnormal colours.

Amongst the dhatus, twak is closely related to rasadhatu. It derives nutrition from

the rasadhatu through its channels. The texture of the skin is depended on the quality of

nutrition provided 82

Sweda, which is a mala of medodhatu, is expelled out through skin. But in normal

state it acts like a dhatu. It is held in the skin, thereby moisturizing it83.

Tridoshas have their own specific properties by the virtue of which they perform

various functions. “Ushma” 84 is the inherent property of pitta, which enables it perform

thermoregulation and helps in eliciting the lustre of the skin85

Applied aspect:

In ksheena avastha of pitta “Prabhahani” is noticed 86

If pitta prahopakara diet is consumed it vitiates pitta causing digestion of the cells

producing colour to the hair leading to a condition called “Palityam”87

In a vitiated state vata, pitta and kapha exhibit black, yellow and white colour

respectively.88


26

BHARAJAKA PITTA & ITS FUNCTIONS:

It has been specified by sushruta that production of colour, exhibition of luster of

skin are the functions of Bhrajakapitta 89

The word Bhrajaka is derived from “Bhraj Dhatu meaning “Deepti” or “Kanti”

‘Sushruta’ mentioned that Bhrajaka pitta resides in the skin. ‘Dalhana’ Commented that

Bhrajakapitta resides in the bahyatwak i.e. avabhasini. 90 Hence it is mentioned in the

reference of avabhasini that its main function is reflection of colour & luster.

Vagbatta also stated that Bhrajaka pitta is located in the skin and reflects the

radiance of the skin.91 Arunadutta commented that Bhrajaka pitta performs functions like

“deepana” “Pachana” of the substances used for abhyanga, lepa, Parisheka92

Chakrapani mentioned that variations in the body temperature and colour are the

functions of bhrajaka pitta93.

Dalhana stated absorption and digestion of the substances used together with oils

and decoctions used for sprinkling over the body is also done by the Bhrajakapitta.

Bhela Samhita has also described the function of Bhrajakapitta as providing

ushma and Prabha to the body94 .Hence it can be concluded that Bhrajaka pitta resides in

the avabhasini the first layer of twak and performs vital function like.

Providing luster and brilliance to the skin.

Helps in thermoregulation of the body.

Capable fo presystemic metabolism of drugs and other substances applied

topically through the process of “abhyanga” “parisheka” “avagahana” & “lepa”.

Applied aspect: Any derangement in the Bhrajakapitta functions leads to alteration of

skin colour and impaired thermo regulation. In the present disease switram, pathology is

noted due to the impairment of this pitta.


27

The third vital function of twak is thermo regulation. By the virtue of pitta

(Bhrajaka) located in the skin this function is performed. “The Ushma” property of pitta

aides in this function. Any derangement of pitta leads to “mandoanala” condition and

“Sheetam” 95 abnormal cold sensation to the body.

The fourth important function of twak is being a sensory organ. Twak is one

among the pancha gyanendriyas97. It is seat for the vata97. And “Sparsha” or the tactile

sensation is the inherent property of vata98 among the panchavidha vatas; the Pranavata

controls all the indriyas99. All kinds of sensations like touch, temperature, pain, pleasure

are perceived by the skin.

The fifth function of the skin is excretion. It is the channel for the excretion of

sweda which is considered as a mala of the body. If sweda is not generated sufficiently it

leads to bad odour, Cracks in the skin and hairfall.100

Sixth function of the twak is to act like channel or marga. Twak is categorized

under shakha101 along with other dhatus and shakha is classified under bahyaroga

marga102 .This rogamarga help in manifestation of the diseases and prognosis can be

known. Certain shodhana procedures are done to transfer the dhoshas from shaka to

kosta. Hence skin or twak also acts as a channel. It also lodges the nakha and smashru

which are the malas of asthi.

Hence, it can be said that the twak is a tridoshaja bhava in which vata acts as a

initiative principle pitta acts a metabolic principle and kapha is a preservative principle.


28

PHYSIOLOGY OF THE SKIN

The skin is the largest organ of the body, being on the surface and continually

exposed to injury. It has to be both strong and supple to resist the wear and tear. It forms

the integumentary system along with its derivatives like hair, nails, sweat and sebaceous

glands.

It forms about 8% of the total body mass and its surface area varies with height

and weight.

Functions of the skin:

1. Protection: The skin covers the entire body. It forms self renewing and self

repairing interface between the body and its environment it is major site of inter

communication in both directions between the two. Within limits it forms an

effective barrier against microbial invasion, and has properties which can protect

against mechanical, chemical, osmotic, thermal and photo damage.

2. Thermoregulation:- In response to high environmental temperature of strenuous

exercise, the evaporation of the sweat from the skin surface lowers an elevated

body temperature to normal. In response to low environmental temperature

production of sweat is decreased, which helps to conserve heat. Apart from this,

changes in the blood flow also regulate body temperature. The rich vasculature of

the skin has a generous rescue to meet the requirements of wounding and repair,

so common on surface. Dilatation can increase the flood flow 100 fold, assisting

the thermo regulation.

3. Sensation: Skin is a major sense organ, richly supplied by nerve terminals and

specialized receptors for touch, temperature, pain, pleasure stimuli.

4. Excretion: Besides removing heat and some water from the body, sweat is also a

vehicle for excretion of small amounts of salts and several organic compounds.


29

5. Synthesis of Vitamin D: It can be regarded as endocrine organ as it carries out

many biochemical synthetic processes (Boyce 1994) including formation of

vitamin D. It can synthesize vitamin D from calciferol in the presence of sunlight.

Apart from synthesizing vitamin D it also helps in the synthesis of cytokines and

growth factors. Cytokines include inter leukins, interferons.

6. Immunity: It is an important site of immuno-surveillance against the entry of

antigens and initiation of primary immune response.

7. Frictional property: Skin has good frictional properties, assisting in locomotion

and manipulation by its texture. It is elastic, and can be stretched and compressed

within limits. It is capable of absorption and excretion and selectively and

regionally permeable to a variety of chemical substances.

8. Skin Colour: The colour of human skin derives from and varies with the amount

of blood (and its degree of oxygenation) in the cutaneous circulation, the

thickness of the stratum corneum and the certainty of specialized cells producing

the pigment melanin. Melanin has protective role against ultraviolet radiation, and

acts as a scavenger of harmful free radicals produced under this and other

circumstances. Racial variations in the colour are mainly due to the differences in

the amount, type, distribution of melanin and are genetically determined.

The anterior pituitary gland or the adeno hypophysis secretes hormones that

regulate a wide range of bodily activities including skin pigmentation. Some cortiotrophs

of remnants of pars intermedia secrete MSH – melanocytes stimulating hormone which

effects the skin pigmentation. MSH increases skin pigmentation by stimulating the

dispersion of melanin granules in melanocytes in amphibians. Its exact role in humans is

unknown.

Three pigments, melanin, carotene and haemoglobin give colour to the skin.

Melanin is located mostly in the epidermis, carotene in dermis and haemoglobin in the

red blood corpuscles.


30

The amount of melanin varies the skin colour. Melanocytes are most plentiful in

the nucous membrane, penis, nipple of the breast, areola, face and he extremities. The

numbers of melanocytes are same in all the races but the amount of melanin produced

decides the colour.

Melanocytes synthesize melanin from the amino acid tyrosine, in the presence of

an enzyme tyrosinase in an organelle melanosome. Exposure to ultraviolet radiation

increases the enzymatic activity leading to the darkness of the skin which further protects

the body from ultraviolet radiation.

In this condition called VITILIGO there is partial or complete loss of melanocytes

from patches of skin thereby producing hypopigmented spots. The colour of the hair is

also due to the substance melanin, absence of which causes white colour of the hair. The

cells melanocytes are scattered in the matrix of the bulb of the hair.

TYROSINASE, AND SYNTHESIS OF MELANINS:

Tyrosinase is a copper containing metallo enzyme, present in the form of several

isozymes, which catalyses initial stages of the synthesis of tyrosine – melanin.

It is formed by ribosomes on the granular endoplasmic reticulum, conveyed to the

golgi complex, glycosylated and incorporated into coated vesicles which attach to

the limiting membrane of the stage I melanosome, liberating active enzyme.


31

ILLUSTRATION-1:

The first two steps include oxidation of tyrosine to DOPA

OXIDATION

TYROSINE DOPA

TYROSINASE

Oxidation of DOPA to Dopaquinone

OXIDATION

DOPA DOPAQUINONE

TYROSINASE

In eumelanin synthesis, dopachrome is formed converted into dihydroxyindoles

and 5-6 dihydroxy indoles, 2-dicarboxylic acid.

The final stages in the pathway to melanin essentially involves complex

polymerizations in which tyrosinase may again be involved.

In phaeo melanin synthesis, the amino acid cysteine is added to dopaquinone to

form 5-S cysteinyldopa.

Most natural melanins are mixture of eumelanins and phaeomelanin

Dopaquinone Dopachrome

dihydroxyindoles

Dopachrome Oxidoreductase

Dopachrome tautomerase

5-6 dihydroxy indoles and2-dicarboxylic acid


32

FUNCTIONS OF MELANINS:

Melanin has biophysical and biochemical properties related to its functions in the

skin.

It protects against the damaging effects of the ultra violet radiation on DNA

through its special absorptive electron-photon coupling and amorphous

semiconductor properties, whereby it can absorb any different types of energy and

dissipate them in the form of vibrational modes or heat.

Its redox capacity makes it an efficient scavenger of damaging free radicals,

however generated, and its ability to bind to a variety of metal ions and drugs

suffest it can act as an anti toxic agent.

However, if the energy input is too great, these properties can be expressed in the

output of toxins activated, chemical species which can be damaging.

Another disadvantage is that a high concentration of melanin in relation to

incident solar UV may adversely affect synthesis of vitamin D.

DETERMINATION AND CONTROL OF MELANIN PIGMENTATION:

Melanin Pigmentation of human skin can be analysed in two bases (1)

Constitutive (2) facultative

Constitutive pigmentation is the intrinsic level, genetically determined.

Facultative pigmentation comprises reversible changes induced by environmental

agents eg: UV and X-radiation, chemicals and hormonal influences.

Genetics: Specific genes can influence differentiation of neural crest cells into

melanoblasts, and also melano blast migration to the skin, their differentiation

with melanocytes and morphological features of these such as shape, size, and


33

length of dendrites, which in turn determine the size of the pool of keratinocytes

to which each cell transfers its melanosomes.

Other genes acting primarily within the melanocyte control the synthesis of

tyrosinase, its type and activity, the type of melanin synthesized the size, shape,

protein structure and number of melanosomes, their degree of melanization and

their rate of transfer to keratinocytes.

Constitutive melanin pigmentation in man is probably under similar precise

genetic control.

Racial variations in pigmentation are due to differences in melanocyte

morphology and activity of melanocytes than to numerical differences.

In heavily pigmented skins the cells tend to be larger, more dendritic and to

contain more and larger Stage III and IV melanosomes than melanocytes.

Ultraviolet radiation: The response of the melanin pigmentary system to

ultraviolet varies with genetic and constitutional factors. It includes immediate

tanning, or pigment darkening, which can occur within few minutes due to photo

oxidation of preexisting melanin.

Delayed tanning occurs after about 48hrs and involves stimulation of new

melanogenesis within the melanocytes, and transfer of additional melanosomes to

keratinocytes. There may also be some increase in size of active melanocytes and

their numbers.

Lower frequency UV band induces synthesis of keratinocytes of b-FGF, as well

as inter leukin I which induces them to produce melanocyte stimulating

hormone a known stimulant of melanogenesis.

Hormonal Influences: In amphibians MSH from the anterior lobe of the

hypophysis and melatonin, a skin lightening hormone secreted by the pineal, are

involved in pigmentary alterations.


34

Their importance as normal regulatory factors in man is unclear.

In pregnancy, higher levels of circulating Oestrogens and progesterone are

responsible for the increased melanization of the face, abdominal and genital skin

and the nipple and areola.

A number of other factors operating within the epidermis such as interleukins,

arachidonic acid, prostaglandins and various cytokines, also affect melanogenesis.

Level of pigmentation at anytime represents a balance between a large number of

competing influences between constitutive and facultative, and these must be

taken into account in the analysis and diagnosis of hypo and hyperpigmentary

disorders103.


35

NIDANA

Nidana is defined as the etiological factors responsible for causing the disease104

All the diseases affecting the skin in particular are described under one heading “kusta

rogas”. As switra also affects the skin it is described in this chapter.

All the acharyas have mentioned a common nidana for kusta and switra.105

Acharya charaka has mentioned a vishesha nidana for switra.106

The etiological factor can be sub divided into

a. Aharaja nidana

b. Viharaja nidan

c. Chikista sambandhi

d. Anyaja

a. Aharaja nidan:

Vagbatta mentioned, a pregnant women consuming excessive kaphakara ahara,

the baby shall be affected with switra.107

Viruddha ahara

Mithyahara

Asatmya bhojana

Ahita bhojana

Adhika matra Bhojana

Ajeerna anantara bhojanam

Vidhi viruddha ahara sevanam

Kuvidhi of langhana

Sheetala – ushna ahara sevanam

Drava, snigdha, guru padarthas

Gramya, anupa, jaleeyamamsa sevanam, anantharam dugda sevanam

Navanna, dadhi, matsya, lavana, amla, masha, mulaka, pisti, tila, ksheera, Guda

sevanam


36

Tila, guda, dudga sevanam

Chilachima variety of fish108.

Seven dietery factors (7) specially mentioned by vangasena109

Tila, Taila, Kulatthi, Valmika roga, Lingaroga, Mahisha dadhi, Vruntakam.

b. Viharaja Nidan

Chardi, Mala-mutradi vegadharana

Ati vyayamam

Ati Santapasevanam

Vyayamam in ajeernaavastha

Mithya vihara

Diva swapnam

Garma srama, Bhayarthanam sheethambu sevanam.

c. Chikista sambandhi Nidana:

Vagbatta mentioned usage of savisha jalouka in rakta mokshana leads to switra at

that site 110

Snehapana anantaram doing vyayamama,or vyavayam leads to skin diseases111

Suppression of vamana vegas or doing vyayamam or maithuna after vamana leads

to skin diseases112.

Panchakarma apacharas specifically produces skin diseases113

Taking apakwa Vajra, Vaikrantha, Nag, Loha, Hingula, Rasakarpur, Tutha leads

to skin diseases114.

Apakwa Hartal bhasma and Vanga bhasma leads to switra specifically.115

Vaidya Nimittija:

Snehapan after attaining samyak snigdha lakshnas causes sneha vyapat which

leads to kustarogas116.

Doing dushita rakta stambana leads to kilasa and kusta117


37

d. Anya nidana:

In adibala pravrutti Sukra – shonitha beeja doshas leads to kusta rogas in the

progeny118

Manasika causes like bhaya, krodha leads to skin diseases119

Dadga and kshatas produce switra120

Bhoja mentioned vrana and parasparsha to be the cause for switra121

Manu smriti described stealing of clothes and wealth leads to switra122

Harita samhita mentioned stealing of silver leads to switra123

Kashyapa mentions abstinence from yagnas, yagas, Homas, Bali, Improper athidi

sevana leads to switra.124

Papakarmas of previous births

Brahmana, Stri, Sajjana, go hatya

Disrespecting parents, insulting Gods

Having died of skin disease in the previous birth125

Vishesha Nidana specially mentioned by charaka126

Viruddha annapana sevana

Vacham asatyam

Papakarmas

Krutagna bhavas

Ninda suranam

Guru garshanam

Poorva kruta karmas


38

Aharaja Nidana:

Table – 4

S.No. Nidana C.S. S.S A.H M.Ni B.P Va.S

1. Garbhini consuming excessivekaphakara ahara

- - + - - -

2. Virudha ahara + + + + + +

3. Mithyahara - + + - - +

4. Asatmya Bhojan - + - - - -

5. Ahita Bhojan - + - - - -

6. Adhika matra Bhojan - - - + - +

7. Ajeernam anantara Bhojanam - + - + + +

8. Vidhi virudha ahara sevana - - - - + -

9. Kuvidhi of Langana - - - - - +

10. Sheetala – Ushna Ahara Sevanam - - - + + +

11. Drava – Snigdha – Guru padartha - + - + + +

12. Tila guda – dugda sevanam - - - + + +

13. Chilachima variety of fish + - - - - -

14. Gramya, anupa, jaleeyamamsasevanam,Anantaram dugda sevanam

- + - - - -

15. Navanna, dadhi, Matsya Lavana, Amla,Masha, Mulaka, Pisti, tila, Ksheera,Gud sevanam.

- - - + + +

Viharaja Nidana:Table - 5S.No. Nidana C.S. S.S A.H M.Ni B.P Va.S

1. Chardi, Mala-mutradi vegadharana - + - + + +2. Ati vyayayam - - - - - +3. Ati santapasevanam - - - + + +4. Vyavayam in ajeernavastha - - - - + +5. Mithya vihara - - + - - -6. Diva swapnam - - - + + +7. Garma, Srama, Bhayarthanam

sheethambu sevanam- + - + + +


39

Chikitsa Sambandhi Nidan:

Table - 6

S.No. Nidana C.S. S.S A.H M.Ni B.P Va.S1. Savisha Jalouka Prayog - - + + - -2. Snehapana anantaravyayamam or

maithun- + - - - -

3. Suppression of vamanadi vegas - - - + - +4. Doing vyayama or maithun after

vamana- + - - - -

5. Panchakarma apacharas - - - + + -6. Snehapana after attaining samyak

snigdha lakshanas+ - - - - -

7. Dushitha raktha stambhana + - - - - -

Anya Nidan:

Table - 7

S.No. Nidana C.S. S.S A.H M.N B.P Va.S M.S B.J Ka

1. Sukra shonitha beejadoshas

- + - - - - - - -

2. Bhaya, Krodha - - - + + - - - -

3. Kshata, Dagda - - + - - - - - -

4. Vranas - - - - - - - + -

5. Para sparsha - - - - - - - + -

6. Stealing of clothes &

Wealth

- - - - - - + - -

7. Abstinence fromyagna, homa, bali

- - - - - - - - +

8. Papakarmas ofprevious births

+ + + - - - - - -

9. Brahmana, Stri,Sajjana go Hatya

- + + + - - - - -

10. Vipra guru garshana + - - - + + - - -

11. Vacham asatyam + - - - - - - - -

12. Ninda suranam + - + - - - - - -

13. Having died of skindiseases in previousbirth

- + - - - - - - -


40

ETIOLOGY

The etiology of vitiligo is unknown but triggering / precipitating factors areidentified.

Triggering / Precipitating factors:

It is difficult to precisely define the triggering factors for vitiligo. Neverthless it

is essential to elicit the details of history of emotional stress, drug intake, infections,

trauma / injury (Koebner’s phenomenon) 127 existant prior to the development of vitiligo

lesions .128-130

It is believed that major oxidative stress occurs in vitiligo skin, which is

evidenced by low catalase levels and cellular vacuolization in the epidermis .131-132

several factors may contribute to the oxidative stress, thus leading to the accumulation of

epidermal hydrogen peroxide. The presence of the hydrogen peroxide can be

demonstrated invivo by using non-invasive Fourier transform Raman Spectro

Scopy133-134

ILLUSTRATION-2:

VITILIGO TRIGGERING / PRECIPITATING FACTORS ,

THEIR ROLE IN PATHOGENESIS135-138

Triggering Molecular level Genetic factorsFactors Changes

1. Nutritional Deficiency

2. Emotional stress Biochemical changes Normal Skin

3. Drugs

4. Infections Enzymatic Disturbances Previtiligo

5. Focal sepsis and toxins Auto Immunity and VitiligoImmune dysfunction

6. Exposure to chemical

7. Oxidative stress Epidermal hydrogen peroxide VITILIGOaccumulation


41

POORVARUPAS

Poorvarupas are defined as the prodromal symptoms of a disease to bemanifested.

Madhukosh commentary defined poorvarupas as Bhavi Vyadhi Prabodhakas139

Generally the poorvarupas are only indicators of a particular disease to be manifested.

Some times they are avyaktam not present at all and at times they are minimally

exhibited.140. The disease switram does not exhibit any poorvarupas, but as it has the

same causative factors like that of kusta141, the poorva rupas exhibited by kusta rogas can

be considered for switram occasionally.

Kusta Poorvarupas:

Sparsha Agnanam142

Atiswedam

Aswedam

Vivarnyam

Loma harsha

Kharatwam

Kandu

Toda

Srama143

Klama

Shula in vrana

Sheegrautpatti

Chira Stithiti

Daha

Suptata

Ruksham

Pipasa


42

Gouravam

Doubalyam

Vepathu

Pidaka

Arunshi

Ativedana

Kota utpatti

Ati bhrama

Ati kopanam 144

Asruja Karshanyam


43

RUPA

Rupa can be defined as the clinical features of the manifested disease. They are

the subjective evidences of a disease. They are exhibited only after the complete

manifestation of a disease. In the Shatkriyakalas the rupas are exhibited in the

vyaktavasta145. Dalhana commented that the rupas are exhibited after the completion of

Dosha – dushya samurchana and the pratyatmaka lingam or the cardinal symptom is first

exhibited.

Eswarasena’s commentary on Madhava nidan defined rupam146

“Vyadhi hi Swarupam…….

Tad Vyaktam Tadrupam.

Madhukosh defined rupam as147

“Utpanna vyadhi bodhakameva lingam rupam”

In switram, according to definition of kashyapa 148 expressions of white colour

patches on the body is the Pratyatmaka linga of switram.

Sushruta defined the rupas as “Twagtam eva aparisravi”149. The patch involves

the skin and has no oozing tendency

Vishista dosha lakshanas:

According to classical texts the vataja, pittaja, sleshmaja types of switram have

been mentioned. The tridoshas invade rakta, mamsa, and medodhatus respectively and

produce lakshanas accordingly.


44

Vataja:

Mandala

Aruna varnam or rakta varnam

Ruksham

Sparsha katinatvam

Parusham

Keshanashanam

Paridwamsi (Romapatrari)

Pittaja

Tamra Varnam

Kamala Patravat

Daham

Roma Vidwamsam

Sleshmaja

Swetavarnam

Snigdam

Stulam

Kandu yuktam

Guru

Ghanam

Charaka mentioned three varieties of the disease by the virtue of involvement of

dhatus150.

Daruna: When rakta dhatu is invaded by vata dosha it exhibits raktavarna151

Aruna: Mamsadhatu invaded by Pitta dosha it exhibits tamravarna

Switra: Medodhatu invaded by kapha dosha it exhibits swethavarna


45

Rupas:

Table -8

S.No. Lakshanas C.S S.S152 A.H153 M.Ni154 Sha.Sha B.P

Vataja

1. Mandalam - + - + - -

2. Arunavarnam - + + + - -

3. Raktavarnam + - - - - +

4. Rooksham - - + - - +

5. Sparsha katinatvam - + - + - -

6. Parusham - + - + - -

7. Keshanashanam - + - + - -

8. Paridwamsi - + - + - -

Pittaja

1. Tamravarnam + - + - - +

2. Kamalapatravat - + + + - +

3. Daham - + + + - +

4. Romavidvamsam - - + - - +

Sleshmaja

1. Swetavarnam + + + + - +

2. Snigdam - + - + - -

3. Stulam - + - + - -

4. Kandu yuktam - + + + - +

5. Guru - - + - - +

6. Ghanam - - + - - +


46

CLINICAL FEATURES

EPIDEMIOLOGY:

Vitiligo occurs world wide with an overall prevalence of 1%. However, its

incidence ranges from 0.1 >to 8.8% 155-161. The highest incidence of the condition has

been recorded in India followed by Mexico & Japan.

Behl et.al162-163 had organized camps in rural areas and industrial pockets in India

to evaluate the status of vitiligo. Its incidence was found to be higher in villagers living

near dyeing, printing, carpet industries. A higher incidence of vitiligo in such areas may

be due to inclusion of cases with chemically induced depigmentation by industrial

phenols, quinone’s which might have a completely different pathomechanism. Its

incidence however was relatively low amongst those residing adjoining copper mines.

SEX INCIDENCE:

Adults and children of both sexes are equally affected although the greater

number of reports among females is probably due to the greater social consequences to

women and girls affected by this condition164-171

AGE INCIDENCE:

Almost half the patients present before the age of 20 years and nearly 70-80%

before the age of 30 years.172-176

FAMILY HISTORY:

The proportion of patients with positive family history varies from one part of the

world to another. In India, in particular, it ranges from 6.25-18%. In some studies it is as

high as 40%. The mode of transmission of vitiligo is quite complex. It is probably

polygenic with a variable penetrance177-181


47

PERCENTAGE OF INCIDENCE:

1947 - Calcutta / India - 6%

1958 - Vellore / India - 4%

1969 - Amaravati/ India - 8%

1972 - Delhi / India - 8.8%

1974 - Goa / India - 2.9%

1988 - Delhi / India - 1.25%

The difference in its incidence may be due to higher reporting of vitiligo in population

where apparent colour contrast may force them to seek an early consultation.

CLINICAL FEATURES:

Vitiligo is characterized by the appearance of patchy discolouration evident in the

form of typical chalky – white or milky white macules.

The macules are round and oval in shape with scalloped margins 182-183

The size of the macules may vary from few mm to several cms with the lesions

affecting the skin and or mucous membrances.

The lesions are asymptomatic although itching, burning may precede or

accompany the onset of lesions in few patients .184-185

Vitiligo is a slow and progressive disease and may have remissions and

exacerbations correlating with trigerring events 186-187

Occassionally the lesions of vitiligo may begin to form around a pigmented

naevus188(Sutton’s nevus, Leucoderma aquisitum centrifugum) and then go on to affect

distant regions 189.


48

Although any part of the skin or mucous membrane is amenable to develop

vitiligo, the disease has a predilection for normal hyperpigmented regions such as the

face, groin, axillae, areola, and genitalia.

Furthermore lesions may develop in areas like, ankles, elbows, knees, which are

subjected to repeated trauma / friction, an outcome of koebner’s phenomenon190.

In the event of extensive disease the lesions are symmetrically distributed 191-193

with an exclusive dermatomal distribution or mucous membrane involvement 194-196

Lip-tip syndrome, another variant of vitiligo is characterized by depigmentation

fo the terminal phalanges and the lips.

CLINICAL VARIANTS:

1. Trichrome Vitiligo: Recognized by the presence of a narrow to broad

intermediate colour zone between vitiligo macule and normal pigmented

surrounding skin. It is a variant of unstable vitiligo 197.

2. Quadrichrome Vitiligo: It is well documented fourth colour in vitiligo lesions,

usually seen in darker skin types. A macular perifollicular or marginal hyper

pigmentation is its salient feature and denotes a repigmentating disease.

3. Penta chrome vitiligo: Infrequently encountered variant in which there is a

sequential display of white, tan, brown, blue-gray hyperpigmentation and normal

skin. Black Skinned individual are predisposed to have this disorder198

4. Blue vitiligo: It usually corresponds to vitiligo macules occurring at the site of

post inflammatory hypermelanosis 199.

5. Inflammatory Vitiligo: It is an entity which may reveal an erythematous, raised

border in a vitiligo macule with frequent itching / oozing. These can be induced

by aggressive therapy200-202.


49

CLINICAL FEATURES OF VARIOUS TYPES OF VITILIGO:

1. Localized:

Focal: One or more macules in one area, but not clearly as in segmental or

Zosteriform distribution.

Segmental: One or more macules in quasidermatomal pattern.

Mucosal: Involvement of mucosal membranes alone.

2. Generalized

Acrofacial: Involvement of distal extremities and face.

Vulgaris: Scattered macules over the body.

Mixed: Acrofacial and vulgaris involvement or segmental and acrofacial.

3. Universal: Complete or nearly complete depigmentation.

According to progression and prognosis

Segmental: Has an early onset in life, spreads rapidly in affected area. The cause may arrest

and depigmented patches can persist unchanged for the life.

Vitiligo Zosteriformis: Macules distributed along a dermatome or lines of body

cleavage.

Non Segmental:

Shows poor prognosis. Includes all types of vitiligo, except segmental type.

Vitiligo _areata: 1 or 2 macules (Focal, Localized or partial).

Vitiligo acrofacialis : Macules affecting face and tips of hands and feet.

Vitiligo vulgaris: Scattered macules over the body.

Vitiligo mucosal: Involvement of mucosal membranes alone.


50

According to clinical stages:

Progressive Vitiligo: Developing new lesions .

Increasing old lesions

Ill defined border of lesion

Quiescent stage: No appearance of new lesions

Stationary old lesions

Well defined, hyperpigmented borders

ASSOCIATIONS OF VITILIGO:

Cutaneous associations203-210

Premature graying of hair

Leucotricha

Halo nevus

Lichen planus

Alopecia areata

Occasionally other skin disorders like Dermatitis herpetiformis, Giant congenital

melanocytic nevus, Chronic urticaria, Malignant melanoma have been seen in association

with vitiligo.

Other interesting autoimmune associations include Morphea, and Hashimoto’s

thyrioditis 211.

While presenting strong direct and indirect evidence of auto immune etiology of

alopecia areata, Hordinsky and Ericson212 stressed its association with vitiligo in many

patients.


51

Occular associations:

Vogt-Koyanagi-Harada syndrome213-218 refers to full constellation of vitiligo,

Poliosis and Alopecia with pan uvetis and auditory and neurological manifestations.

However iris, retinal pigmentary abnormalities may be present as isolated

findings in vitiligo patients. Choroidal abnormalities and irites may also be present 219-221

Systemic associations:

Hypo / hyper thyroidism, Diabetes mellitus, Addisions disease, Pernicious

anaemia, Lymphoma, Leukemia, HIV, Autoimmune poly endocrinopathy ,Candidiasis

,Ectodermal dystrophy.

CHILDHOOD VITILIGO:

Morphological characteristics in childhood vitiligo are more or less identical to

those of adult onset vitiligo. Interestingly there has been steady increase in the evidence

of child hood vitiligo during past two decades222.

CONTACT VITILIGO:

Contact vitiligo is an acquired leucoderma as a result of repeated topical or

systemic exposure to variety of chemicals223. These chemicals are mainly alley phenols,

catechols used in manufacturing plastics, resins, synthetics, rubber, paints, petroleum,

deodorants, germicides, insectides, photographic chemicals, varnishes etc., These

chemicals are also present in certain objects like footware, plastic watch strap and

bindis.224-225


52

SAMPRAPTI

Samprapti is defined as the phenomenon of dosha-dushya samurcchana226. The

complete process of manifestation of a disease is explained in this context.

The nidana and samprapti for kusta and switra are similar 227. The whole process

of samprapti can be understood through shatkriyakalas228

Sanchaya

Prakopa Dosha Prakopa avastha

Prasara

Stanasamshryam Dosha – dusya samurcchana

Vyakti Vyadhi utpatti avastha

Bheda

The knowledge of samprapti is essential to break the chain of pathogenesis to

prevent further progression of the disease and to implement specific treatment at different

stages of pathogenesis229.

1. SANCHAYAM: is the accumulation of vitiated doshas in their respective places230.

The doshas remain in equilibrium, unless disturbed by external causes.

Viruddha ahara-vihara, Manasika karanas like Bhaya, krodha, papakarnas, sadvrut

apacharas are the endogenous causes.

Kshata, dagda, vranas, Savishajaloukaprayoga are the exogenous causes. The

exogenous and endogenous causes are responsible for the vitiation of doshas.

Viruddha ahara produces amavisha which is antagonistic to the dhatus, there by

leads to various disease.231

Adhika amla, lavana, ushna, teekshana dravyas cause pitta prakopa leading to

rakta dusti 232


53

Virudha vihara, diwaswapnam, atisantapasevanam causes pitta prakopa233

Suppression of natural urges causes vitiation of apanavata and it travels in

pratilomagati disturbs samanavata which in turn disturbs udana vata (responsible

for Varna).

Bhaya, kroda increase rajogunam in the body, which in turn causes vata-pitta

prakopa

Papakarmas, sadvrut apacharas leads to psycho-somatic disturbances, leads to

vitiation of vata pitta doshas234.

In agantuja karanas, directly twakdusti occurs and lakshanas are exhibited, later

on the doshas are vitiated.235

2. PRAKOPA: Prakopa the next stage of sanchaya. The accumulation of vitiated doshas

continues and the doshas are ready to rise above their respective stanas236.

Nidana Factors

Sanchaya Prakopa

Are continued

3. PRASARA: This is the stage where the vitiated doshas get dislodged from their

respective places and start spreading all over the body through siras or channels. In

switra, the vitiated vata, pitta, kapha spread in the body through “Tiryagata Siras” 237

which implies urdwa, adho, tiryak Siras. The doshas spread in all the directions238.

4. STANA SAMSHRAYAM: The most important phase of shatkriyakalas where the

major event “Samprapti” occurs239. Dosha – dushya samurcchana and vyadhi purvarupas

are exhibited in this stage


54

Doshas implies the vitiated vata, pitta, kapha and dushyas are twak, rakta, mamsa,

and lasika in kusta, and rakta, mamsa, medo dhatus in switra.

Switra is considered as “Tridhatu Samshrayam”240 which means involvement

of tridoshas and tridhatus (rakta, mamsa, and medodhatus) in the pathogenesis of the

disease241.

The vitiated doshas while moving in the body reach particular dhatus, by the

virtue of obstruction of that particular srotas. They get lodged in that dhatus.242.

The doshas cause “Shithilatwam” of rakta, mamsa, medodhatus and are

expressed out on to the surface i.e. twak. The term “Bahirnischarantou” (bahya desha

prasarantou) is used to denote the mechanism of outward movement of vitiated doshas.243

Charaka mentioned “doshopaghata”244 (being affected by the vitiated doshas) in this

context. The doshas reach “Twak” where they get settled. The twak becomes the place

for stanasamshrayam.

The fourth layer “Tamra” is the site for switra roga.245

No purva rupas are mentioned but as nidana is same for kusta and switra, some

purvarupas of kusta may occasionally appear.

5. VYAKTAVASTHA: The stage of exhibiting the lakshanas of the manifested

disease246. “Mandalas” and “Twak vivarnyam” are seen at the site of manifestation of

vitiated doshas in the skin.

In switra “Sweta Varnam” of twak is seen as a pratyatmaka lingam247.

Switra Produces discolouration of skin only, it does not cause destruction,

putrifaction of dhatus or exudation hence it is “aparisravi” and this feature differentiates

it from Kusta.248

In agantuja karanas like dagdas, kshata, vrana, directly twak dusti occurs causing

“Twak Vaivarnyam” and after that doshas get vitiated.


55

6. BHEDAVASTHA: The stage of complications or upadravas. If timely intervention is

not done leads to complete depigmentation of the body. Vagbhatta considered switra as

medical emergency as, if not treated on time spreads all over the body and makes it

asadya249.

The disease may go beyond medodhatu, and makes it asadya if not treated

timely.250

Three types of switra are present due to particular dosha predominance and

produce their respective colour on the patch 251

Vataja Involves raktadhatu Raktavarnam

Pittaja Involves mamsadhatu Tamra varnam

Sleshmaja Involves medodhatu Sweta Varnam

Types of Samprapti

Sankhya - 3

Vikalpa - Though sannipatika vyadhi, Ekadoshaja bhedas are alsomentioned

Pradhanya - Switra is a swatantravyadhi

Bala - Depending upon the state of nidana, dosha, dushyas in each

case

Kala - Vyadhi kala not mentioned


56

SAMPRAPTI GHATAKAS

Doshas : Pittapradhana tridosha

Dushya : Rakta, mamsa, medo dhatus

Agni : Jataragni, dhatwagni

Ama : Agnimandyam, dhatwagni mandyam

Udbhavastan : Amapakwashyam

Sanchara : Tiryakgata siras

Srotas : Rasa, rakta, mamsa, medo

Srotodusti : Sanga

Adhistana : 4th Layer of twak “Tamra”

Vyaktastana : Twak

Rogamarga : Bahya

Vyadhi Swabhava : Chirakari


57

ILLUSTRATION-3:

FLOW CHART

NIDANA

BEEJADOSHAS AHARAJA VIHARAJA MANSIKA PAPAKARMAS VRANA

DAGDA

KSHATAS

BEEJA BHAJA AGNIMANDYAM

AFFECTED

AMA UTPATTI

DOSHA DUSTI

VATA, PITTA, KAPHA

BEEJA BHAGA

AVAYAVA TIRYAKGATA SIRAS

RAKTA, MAMSA, MEDO DHATUS

BAHYAMARGA GAMANTOU

STANASAMSHRAYAM

TWAK DUSTI

BHRAJAKA PITTA DUSTI

SWETA VARNAM

SWITRAM


58

PATHOGENESIS OF VITILIGO

There are several diseases marked by lack of pigment in the skin that is grossly

referred to as leucoderma. Some are caused by an inability of melanocytes to produce

melanin, while others are caused by melanocytes either not being present or being

destroyed. The latter are the pathology for the disease VITILIGO.

Vitiligo is a progressive disease in which the melanocytes are gradually destroyed

causing unpigmented areas on the skin. The exact etiology of vitiligo is unknown, but

four main theories exist to explain the pathogenesis of it.

a. Autoimmune hypothesis

b. The neural hypothesis

c. The self destruct hypothesis

d. The growth factor defect hypothesis

It is believed that vitiligo is a polygenic trait and that a convergence theory,

combining elements of different theories is the most accurate etiology.

Vitiligo is not a physically damaging disease. But effects are social and

psychological especially for dark skinned races

a. Auto - immune theory: There is great anecdotal evidence that an auto immune

disorder cause the destruction of melanocytes, and this is accepted as the common cause

of vitiligo

Vitiligo appears in conjunction with several other auto immune disorders, such as

Juvenile diabetes, Addisions disease, Pernicious anaemia and additionally organ specific

antibodies.

If the immune system raises antibodies or cytotoxic T-cells to damage

melanocytes, the mode of action the cells take against the melanocytes could be apoptosis

induction directly against melanocytes or Ig induced Compliment.


59

There is histological evidence in vitiligo patients that apoptosis is occurring in

unpigmented skin lesions. There is damage to melanocytes and keratinocytes.

Melanocytes exhibit nuclear shrinking, vacuolization, loss of dendrites, and

detachment.

b. Neural Theory: The Peripheral nerve endings may secrete substance that is cytotoxic

to melanocytes and cause their destruction.

This is supported by segmental variety of vitiligo which occurs in specific

dermatomes, indicating the skin is possibly affected by nerves of specific dermatomes.

Vitiligo appears with certain neurological disorders such as encephalitis, trauma

that cause peripheral nerve damage.

Nerve endings in depigmented areas were seen to produce abnormal neuro

peptides, nerve growth factors, and displayed axonal degeneration, these abnormal

chemicals may be toxic to melanocytes.

Depigmented areas showed some abnormal autonomic functions, such as

increased adrenergic toxins, increased norepinepherine, and an increased concentration of

catecholamines. These data then suggested that neurotransmitter release could, have an

affect on melanocyte destruction and depigmentation.

c. Self destruct theory: It is known that some of the intracellular pre-melanogenesis

metabolites are toxic to melanocytes such as dopa, and dopachrome. Normally

melanocytes possess cellular measures to counteract these toxic substances and are

destroyed by leakage of metabolites into the cytoplasm and eventually cell lysis.

There is evidence, that certain hydroquinone derivatives that are similar to these

intra cellular metabolites cause leucoderma.


60

d. Growth factor Defect hypothesis : It was noted that growth defects of melanocytes

were partially corrected by adding a growth factors to their culture suggesting that growth

defects may be part of pathology of vitiligo.

e. Genetic Influences: There does appear to be a strong genetic influence in vitiligo. A

positive family history has been reported in about 20% of patients.

It does not progress via simple Mendelian pattern but more likely is coded

polygenically.

There is some evidence both proving and disproving involvement of HLA system

in occurrence of vitiligo.

Hence, it is believed that genetic factors play a key role in the pathogenesis of

vitiligo.

f. Convergence Theory: Researchers have begun to lean towards multifaceted etiology,

for vilitigo. This theory states that genetic influences have a role in causing vitiligo in

addition to other elements, such as stress, accumulation of toxic compounds, infection,

auto immunity, mutations, impaired melanocytes proliferation.


61

SWITRA – BHEDAS

The classification of switra gives the information about of the types of the disease.

It is an attribute of Sankhya samprapti. Classifications are based on different criteria like

Nidan Doshas, Ashraya dhatus and Sadya – asadyata.

I. Based on Nidan: 252 Bhoja classified switra into two types.

1. Doshaja: (endogenous Origin) again sub divided into

a. Atmaja

b. Paraja

2. Vranaja (Exogenous Origin)

II. Based on Doshas: 253

1. Vataja

2. Pittaja

3. Sleshmaja

III. Based on Ashraya Dhatus: 254

1. Accroding to charaka Baluki tantra255

Rakta ashrita Daruna Daruna

Mamsa ashrita Aruna Varuna

Medo ashrita switra switra

IV. Based on Sadhya – asadhyata: 256

1. Sadhya-Curable

2. Asadhya-incurable

Kashyapa257 mentioned 5 types of switra but has not mentioned names or clinical

features. Bhela 258 has mentioned switra to be one among eleven kshudra kustas.


62

Switra Bhedas:

Table -9

S.No. Types C.S. S.S A.H M.Ni Sa.s B.P B.J Ka.S B.S Bh

3 3 3 3 3 3 2 5 - 3

1. Doshaja - - - - - - + - - -

2. Vranaja - - - - - - + - - -

3. Vataja - + + + + + - - - -

4. Pittaja - + + + + + - - - -

5. Sleshmaja - + + + + + - - - -

6. Raktashrita + - - - - - - - - +

7. Mamsashrita + - - - - - - - - +

8. Midho asshrita + - - - - - - - - +

9. Sadya + + + + + + - - - -

10. Asadya + + + + + + - - - -


63

CLASSIFICATION OF VITILIGO

The classification system is important because of special significance assigned to

each type of vitiligo

I. Based on distribution:

1. Localised259: a) focal

b) Segmental

c) Mucosal

2. Generalized: a) Acrofacial

b) Vulgaris

c) Mixed

3. Universal

II.Based on Progression and prognosis: 260

1. Segmental: a) Vitiligo zosteriformis

2. Non Segmental: a) Vitiligo areata

b)Vitiligo acrofacialis

c) Vitiligo Vulgaris

d) Vitiligo mucosal

III. Based on Clinical Stages:261

1. Progressive Vitiligo

2. Quiescent Vitiligo


64

SAPEKSHA NIDAN

Sapeksha nidan, otherwise called has vyadhi vyavacchedaka nidan is the

differential diagnosis aspect of the disease. The knowledge is essiential to diagnose a

disease and to implement specific treatment.

In all the classics, the nidana of switra and kusta rogas are mentioned to be

same,262 but they differ in the symptomatic aspect.

Arunadutta specified that, the vitiated doshas affects the dhatus, eats up the hair,

skin, ligaments and cartilages in the kustarogas but these sequential events do not take

place in switra263.

Switra has to be differentiated from sidma kusta which is one of the mahakusta264

because of its close resemblance with the former.

Sapeksha Nidana:

Table - 10

S.No. Features Switra Sidma

1. Classified into Independent Mahakustas

2. Doshas involved Vata, Pitta, Kapha265` Vata-kapha266

3. Dhatus affected Rakta, mamsa, medo dhatus Twak, rakta, Mamsa,lasika

4. Skin layer involved 4th layer Tamra 1st layer avabhasini

5. Poorvarupas Not present Present

6.

a.

Roopas (Clinical features

Colour

White colour patches White, reddish brownpatches(Alabu-Pushpavarnam267

b. Areas involved Anywhere through out thebody

Mainly found on chestand back

c. Extent of layers involved “Twagatam only thesuperficial epidermis isinvolved

Dermis is involved

d. Appearance Centrally hypopigmentedwith hyperpigmented border

External margins arethin, fissured with


65

reddish brown or whitecolour centrally

e. Elevation Patch at the skin level, notelevated

Mildly elevated margins

f. Scales Not present When rubbed produce adust like material (RajoGrushtam)

g. Pain Not present Mild pain present onrubbing

h. Itching Not present Present when in contactwith sweat

i. Hair involved The hair of the patch mayturn white (Leucotrichia)

Hair not involved

j. Oozing tendency “Aparisravi” no oozingtendency.

Little purulentdischarges present inchronic stages

k. External causes May be Produced by dagda,vrana, kshatas also

Not due to these factors

l. Symmetry Symmetrical andasymmetrical patchespresent

Mostly asymmetricalpatches present

m. Sensation Not altered Sensation may bealtered

n. Prognosis The deeper the dhatuinvolved, the diseasebecomes incurable

Sadya roga268


66

DIFFERENTIAL DIAGNOSIS OF VITILIGO

Generalised vitiligo must be distinguished from Piebaldism, Waarden burg’s

syndrome, Woolf’s syndrome and Ziprokowski-margolis syndrome.

Piebaldism:

Is congenital

Stable and spares the dorsal spine

Hyperpigmented macules are present in white patches

A white forlock is also present on forehead

Characteristic distribution pattern

Waarden burg’s syndrome:

Autosomal disorder

Includes hearing defects

Has characteristic eye features, fundi may be hypopigmented

Along with white forelock, premature graying of scalp, hair, eyebrows, cilia and a

dappled appearance of the skin is seen.

Forehead, neck, chest, abdomen, anterior knees, arms, dorsa of hands are

commonly involved

Woolf’s syndrome:

Piebalism

Deafness

Ziprokowski-margolis syndrome:

Rare congenital syndrome

Occurs in males only

Deaf – mutism

Heterochromic irides

Piebald like hypomelanosis of skin


67

Round, oval or geographic hypopigmented macules

Occurs mainly on extremities and trunk

Segmental vitiligo must be distinguished from Nevus depigmentosus, Tuberous

sclerosis, Hypomelanosis of Ito.

Nevus depigmentosus:

Rare, congenital, non familial

Stable quasidermatomal leucoderma

Unilateral macules of varied size

Lesions are white to tan colour with regular or serrated margins

Lesions mostly on trunk, lower abdomen, proximal extremities but may involve

face and neck

Quasinevoid macules with irregular, serrated, feathered margins

Tuberous sclerosis:

Uncommon neurocutaneous syndrome

Appears during early life

Classical triad – adenoma sebaceum, seizures, mental retardation preceded by the

appearance of white macules

White macules, polygonal and lance ovate in shape.

White macules appear on trunk, lower extremities upper extremities, head and

neck.

CNS, heart, kidney, liver, thyroid, testes and gastrointestinal systems involved

Hypomelanosis of Ito:

Bilateral irregularly shaped leucoderma

Mainly on trunk and extremities

Randomly distributed with whorled or streaked configuration

Margins are serrated and blurred

Hypopigmentation may be progressive


68

A solitary vitiligo lesion must be distinguished from, Tinea versicolor, Pitryriasis alba,

Idiopathic guttate hypomelanosis, Post inflammatory hypomelanosis, Chemical

depigmentation, Vagabond leucoderma, Vogt-koyanagi-Harada syndrome,

Scleroderma

1. Tinea versicolor:

Occurrence on the upper chest, not amelanotic, scaling positive for fungi.

Lesions raised with hyperpigmented borders.

2. Pitryriasis alba:

Not amelanotic, faint margins, erythema and scaling.

3. Idiopathic guttate hypomelanosis:

Small, sharp margins, usually on arms, legs

4. Post inflammatory hypomelanosis:

History of presence of characteristic rash

5. Chemical depigmentation:

History of industrial exposure and small white macules at the site of contact

6. Vagabond leucoderma:

Is a leucoderma of older ill-kept men with history of poor hygiene, poor diet and

chronic alcohol abuse.

Depigmented patches are found in diffuse, light brown hypopigmented patches

around waist and groin.

The arms, legs, face are less involved

Attributed to multiple ectoparasitic infections.


69

7. Vogt-koyanagi-Harada syndrome:

Rare multi system disease

Characterised by uveites, alopecia, poliosis

The first stage is the meningo encephalitic phase

Second is the ophthalmic stage

Third stage is vitiligo, poliosis, alopecia which marks the convalescent stage

8. Scleroderma:

A vitiligo like hypomelanosis

Lesions primarly on the upper trunk and distal extremities

Lesions amelanotic, with perfollicular spearing which resembles repigmenting

vitiligo269


70

SADHYA –ASADHYATA

Sadhya – asadhyata is the prognostic aspect of a disease. They are the prabhava

bheda of a roga270. Prognosis is determined by the lakshnas of the disease exhibited by

the patient.

Switra involves rakta mamsa and medhodatus. The deeper the involvement of

the dhatus the prognosis becomes worse. In this context, Acharya vagbatta has specified

the sadhya - asadhyata based on the colour of the patch. Rakta Varna or Aruna Varna are

sadhya, Tamra Varna becomes kasta sadhya and Sweta Varna becomes atishaya asadhya.

As the disease penetrates the deeper dhatus it becomes asadhya.271

Charaka mentioned a person who has followed vamana – virechana, rakta

mokshana regime completely, who takes sattu regularly and whose papakarmas are over,

such case is sadhya.272

Kashyapa273 and Bhela 274 have mentioned switra to be asadhya vyadhi.

Sadhya lakshnas:

Nutana or recent onset (less than one year)

Hair not dis coloured into Rakta varna 275

Patch which is very superficial – Tanu

White in colour or panduvarna

Mild elevation in the centre of the patch276

If the disease is still present in the twak, rakta and mamsa 277

Patch small in size 278

Less in number

Patches not adjoining each other

Hair not turned into white colour279


71

Asadhya lakshnas:

If the disease is present for more than one year280

Hair discoloured into rakta varna, sweta varna

Patches large in size

Numerous patches all over the body

Patches adjoining each other

If the disease enters beyond medodhatu281

If guhyastan i.e. genitals involved, palms and soles, osta ie lips involved

If the patch is due to dagda, vranas, kshata282

Sadhya lakshnas:

Table -11S.No. Lakshnas C.S. S.S A.H M.Ni B.P

1. Nutana or recent onset (less than one year) + - + + +

2. Hair not dis coloured into Rakta varna + - + - -

3. Patch which is very superficial – Tanu + - + - +

4. White in colour or panduvarna + - - - -

5. Mild elevation in the centre of the patch + - - - -

6. If the disease is still present in the twak, rakta andmamsa

- + - - -

7. Patch small in size - - + - -

8. Less in number - - + + -

9. Patches not adjoining each other - - + + +

10. Hair not turned into white colour - - + + +


72

Asadhya lakshnas:

Table -12

S.No. Lakshnas C.S

.

S.S A.H M.Ni B.P

1. If the disease is present for more than one year + - - + -

2. Hair discoloured into rakta varna, sweta varna + - - - -

3. Patches large in size + - - + -

4. Numerous patches all over the body + - - + -

5. Patches adjoining each other + - - + -

6. If the disease enters beyond medodhatu - + - - -

7. If guhyastan i.e. genitals involved, palms and soles,osta ie lips involved

- - + + +

8. If the patch is due to dagda, vranas, kshata - - - + +


73

PROGNOSIS

a. Positive family history: A positive family history is associated with progression and

shows poor signs of prognosis.

b. Mucosal involvement: The site affected most commonly on the limbs and mucosae.

The next affected sites are face and trunk. Bad prognosis was observed in patients having

mucosal involvement. In mucosal involvement lip involvement is very high. The order of

occurance in lips, genetalia, nipple, buccal mucosa, gingivae, alveolar margins. It is

worth while to state that mucosal vitiligo is of poor prognostic value.

c. Koebner’s phenomenon: A trauma leading to hypopigmented patch defines this term.

Subjects with Isomorphic Koebner’s phenomenon showed poor prognosis.

d. Non - Segmental vitiligo: Among this, vitiligo vulgaris is the commonest type

followed by acro-facial and mucosal. The non-segmental type of vitiligo is considered to

be of autoimmune origin. Hence this type is a poor prognostic indicator that portends

disease progression. Amongst all forms V. Vulgaris is more predominant.

e.Trichrome sign: Has an intermediate zone of hypochromia, located between the

achromic centre and peripheral unaffected skin. Shows poor prognosis.

f. Leucotrichia: leucotrichia may indicate poor prognosis in regard to repigmentation.

There has been good prognosis in segmental type of vitiligo. The age at

presentation does not have much significance. But the mean age of presentation is around

26-30 years. It may also start at young age in subjects with strong family history.283


74

CHIKISTA

Chikista is defined as roga nidana pratikara charya284. It is vyadhi harana kriya285.

The Phenomenon which restores the normalcy in the equilibrium among the doshas,

dhatus and malas286.

The primary step, in treatment of a disease is the prevention or abstinence from

the etiological factors287. The nidana of switra suggests viruddha ahara – vihara,

papakarmas, and misconduct to be the vital causes for the manifestation of disease.

The treatment aspect includes three types of therapies to combat the disease288

1. Daiva Vyapashray chikista – spiritual therapy

2. Yukti vyapashray chikista - rational therapy

3. Satvavajaya chikista – psychological therapy

Vagbhatta mentioned switra to be a medical emergency due to its bheebhatsa

nature and tendency to turn asadya at the earliest, hence timely medical intervention is

necessary. 289

1. Daiva Vyapashray chikista – spiritual therapy:

The spiritual therapy consists of recitation of mantras, wearing roots and gems290

Performing auspicious acts, offering gifts, oblations to the fire God.

Following religious precepts, atonement, fastings, invoke blessings, falling on the

feet of Gods, pilgrimages.

Spiritual therapies have empirical powers to eradicate diseases instanteously.

Such therapies are related to the blessings and influence of the Gods.

All the items enumerated under the spiritual therapy are effective in eradication of

diseases only the to divine influences


75

2. Yukti vyapashray chikista - rational therapy: consists of wise administration of

diet and drugs. This is sub – divided into

a. Antah parimarjan chikista:

The drugs or diet taken internally to alleviate the disease.

In switra roga, a person is made to undergo all the shodhana procedures first.

After patient is fully evacuated, samsrama karma is done as primary step of

treatment by giving malapu ras (Kakodumbara) along with gudam291.

The mixture should be given according to the balam of the rogi. After that he

should be exposed to the sun. This procedure to be continued for 3 days.

During this event if patient feels thirsty, peya is given to quench his thirst .292

By doing the above patient develops blisters on the patches all over the body.

The blisters should be pricked with kantakam to release the fluid in it.

After all the blisters are opened, a kwath prepared from bark of kakodumbara,

priyangu, asan, and shatapushpa should be given early in the mornings for 15

days 293

Otherwise, Phanitham prepared from palasa kshara can also be given294

All the yogas beneficial in kusta rogaas, are recommended in switra also

Sprinkling khadira kwatha externally on the body or taking it internally or

even drinking khadira udaka is very beneficial in switra295

A person should be exposed to sun continuously for 1 week after taking

Bakuchi churnam internally, pathya being dugda sevanam296


76

Gomutram is very useful in switra roga. Trikatu, Chitraka, madhu added in

gomutram and stored in a jar of ghee for 15 days and then taking it is very

beneficial297

b. Bahirparimarjana chikista: Applications over the body are included in this category

Manahsilaadi lepam298

Burnt bone of as mixed with kadali kshara, cow’s blood and applied as a

paste299

Kshara of Jati (Malathi) flowers mixed with elephant’s ichor, applied

externally300

Nilotpala, kusta, saindhavalavana mixed in elephant’s urine

Seeds of Bakuchi and mulaka grounded in ‘Cow’s urine

Kakodumbara, bakuchi, chitraka, powdered with cow’s urine301

Manashila powdered with peacock’s bile makes an effective paste in switra

The seeds of bakuchi, cow’s bile, loha bhasma, rasanjana, souveeranjana,

pippali, together made into paste and applied externally 302

c. shastra pranidhan: all the surgical therapies are included here

Doing rakta mokshana is one therapy advised in switra

3. Satvavajaya chikista – psychological therapy: The satwavajaya chikista

includes virteous conduct of a person. The psychological therapy is restraint of

mind from the ahita or unwholesome objects.

Normally the mind, including the sensefaculties remains undisturbed.


77

In order to retain this condition one should make efforts to maintain a healthy

mind. This is achieved invariably by examining with intellect, not deviating from

the generally approved principles, not breaking the code of conduct or sadrut303

Respecting Gods,, Brahmins, preceptors, elderly people

Offering oblation to fire

Performing sandhya twice

Observing personal hygiene

Having faith and devotion towards teachers, gurus, and those who have

accomplished spiritual knowledge or perfection.

Be friendly to all creatures

Reconcile the angry

Controller of intolerance

Be of peaceful disposition

Conquer the roots of attachment

All the above acts help to maintain the psycho – somatic equilibrium, thus giving

health to a person304. The importance of these therapies is evident by the statement “a

person who has undergone shodhana procedures by vamana, virechana, raktamokshana,

who has been taking sattu as his regular diet, whose body is roughened and whose

papakarmas are decreasing by following the spiritual and virteous conduct, the disease

gets cured in such person305


78

TREATMENT

The main goal of treating vitiligo is to improve appearance. Therapy for vitiligo

takes a long time; it is usually continued for 6 to 18 months. The choice of therapy

depends on the number of white patches, their size, and location and how widespread

they are. Each patient responds differently to therapy and a particular treatment may not

work for everyone.

Current treatment options for vitiligo include:

1. Medical

2. Surgical

3. Adjuvant therapies

1. Medical therapies: Include most of which are applied topically

a) Topical Steroid therapy: Steroid creams are helpful in repigmentation, particularly if

they are applied in the initial stages of the disease. Cortico steroids are a group of drugs

similar to hormones which are produced by adrenal glands.

Mild topical steroid creams are prescribed for children under 10 years and

stronger for adults. They should be applied for 3 months to expect results and this is

simplest and safest treatment for vitiligo but not as effective as Psoralen

photochemotherapy.

There are side effects like skin shrinkage and skin striae in areas particularly

where skin is thin. They can be minimized by using weaker formulations of steroid

creams in these areas.

b. Psoralen Photochemotherapy: also known as Psoralen and ultraviolet A Therapy or

PUVA therapy.


79

The most effective treatment for vitiligo available. The goal of PUVA is to

repigment the white patches. Though time consuming yields better results but care must

be taken to avoid side effects which some times can be severe.

Psoralen is a drug that contains chemical that react with ultraviolet light to cause

darkening of the skin.

The treatment involves taking Psoralen by mouth (Oral) or by applying it on the

skin (topically) this is followed by carefully timed exposure to sunlight.

Topical Psoralen therapy: is used for small number of patches affecting a limited part

of the body, it is also used for children 2 yrs old or older who have localized patches of

vitiligo.

Oral Psoralen therapy: used for people with extensive vitiligo and for people who do

not respond to topical PUVA treatment. Advised for children above 10 years as young

children have the risk of developing cataracts.

c. Depigmentation: This treatment involves fading the rest of the skin on the body to

match the areas that are already white. For more than 50% involvement depigmentation is

the best treatment options.

Patients apply the drug monobenzyl ether of hydroquinone twice a day to

pigmented areas until they match the already depigmented areas.

2. Surgical therapies: All surgical therapies are considered only after proper medical

therapy is provided. These therapies are time consuming and expensive. They are

appropriate only for carefully selected patients.

a. Autologous skin Grafts: The doctor removes skin from one area of your body and

attaches it to another area. This type of skin grafting is useful for small patches.

Treatment with grafting takes time, and is costly.


80

b. Skin grafts using blisters: In this procedure the doctor creates blisters on your

pigmented skin by using heat suction or freezing cold. The tops of the blisters are then

cut out and transplanted to a depigmented skin area.

c. Micropigmentation: (Tatooing) : This procedure involves implanting pigment into

the skin with a special surgical instrument. This works best for lip area.

d. Autologous melanocyte transplants: In this procedure, the doctor takes a sample of

your normal pigmented skin and places it in a laboratory dish containing a special cell

culture solution to grow melanocytes. When the melanocytes in the culture solution have

multiplied, the doctor transplants them into depigmented areas.

3. Adjuvant therapies: In addition to medical and surgical therapies, there are many

things you can do to minimize the appearance of white patches and cope with emotional

aspects of vitiligo.

a. Sunscreens: People who have vitiligo, particularly those fair skinned should use

sunscreens to protect from both UVA and UVB forms of ultraviolet light. Sunscreens

also minimize tanning which makes the contrast between normal and depigmented skin

less noticeable.

b. Cosmetics: Some patients cover the depigmented patches with stains, makeup,

selftanning lotions. These cosmetic products are effective for people whose vitiligo is

limited to exposed areas of the body. Self tanning lotions have an advantage over makeup

in that the colour will last for several days and will not come off with washing.

c. Counselling and support groups: many people with vitiligo find it helpful to get

counselling from a mental health professional. A mental health counselor can also offer

support and help in coping with vitiligo.


81

PATHYA – APATHYA

Pathya – apathyas are the list of indicative and preventive measures to be

followed by a person afflicted by a disease. Pathya – apathyas are of great importance to

the patient to stay healthy and avoid further progression of the disease. In the ayurvedic

classics, acharyas have mentioned pathya – apathya for all the diseases. As the nidana is

same for kusta and switra, the pathya – apathyas also remain same.

Pathya:

1. Ahara:

Shali rice (Oriza sativa)

Shastik rice (Oriza sativa)

Yava ( Barly)

Godhuma (Wheat)

Koradoosh ( Paspalum scrobiculatum)

Shyamak (Echinochlova frumentacea)

Uddalaka ( wild variety of Paspalum scrobiculatum

The above mentioned grains should be one year old and matured

Mudga (Phaseolus radiatus)

Adaki arhar (Cajanus cajan)

Soups to be prepared from the above two

Flesh of Jangala animals devoid of fatty matter

2. Vihara:

To be sincere and to be dutiful to God, Teachers, Gurus,

To offer prayers, perform yagna, homas, give donation to poor and needy.

3. Aushadha:

Nimba

Bhalltaka


82

Manduka parni (Centella asiatica)

Avalaguja (Psorhalia Corylifolia)

Adusa (Adathoda vasica)

Flowers of Arka (Calotropis procera)

Medicated oil prepared from sarshapa (Brassica nigra)

Medicated ghee prepared from chakramarda (Cassia tora), Patola (Trichosanthes

dioca)

Body of the patient can be anoinated with vajraka taila, Khadira kashaya,

Argwadhadi group fo drugs, power or paste.306

Apathya:

1. Ahara:

Mamsa (Flesh of birds)

Vasa (Oily part of flesh)

Dugdha (Milk)

Dadhi (Curd)

Tila taila (Seasame oil)

Kulatta (Dolichos biflorus)

Masha (Phaseolus mungo)

Nishpav (Dolichos lablab)

Preparations of sugar and Jaggery

Pisti

Amla (Articles having sour taste)

Viruddha ahara (incompatible food)

Vidahi (Food which can cause obstruction to channels)

Vidagda (food which cause acidic eructations)307

Arundutta mentioned that prohibition from aetiological factors constitutes the actual

treatment of disease. Although meat of all kinds may be prohibited but meat if not

incompatible may be permitted.308


83

2. Vihara:

Adhika matra bhojanam

Food taken during ajeernam

Diva swapnam

Vegadharana

Ativyayamam

Ativyavayam

Abusing elders, gurus, teachers


84

CRITERIA FOR DRUG SELECTION

The present drug “Dhatri-Khadira Kwatham” has been taken from

“Kustarogadhikar” of “Bhaishajya Ratnavali”, a contemporary textbook of 19th 309

century A.D.

The compound has two drugs – Khadira and Amlaki, Madhu as anupana.

Both the above mentioned drugs are non-controversial, unadulterated, easily

available, and economical

It is a simple combination and easy to prepare and use.

Both are sheeta Virya dravyas hence best pitta shamakas, and indicated in

kustarogas.

“Khadira” is mentioned as “Kustagnanam”310. It is equally beneficial in swithra

also.

The use of Khadira Kashaya or Khadira udaka internally and externally is highly

recommended in swithra311. Hence to know its action, on pigmentation in the present

disease is the main purpose for the selection.

Amlaki, the best rasayanam312, easy to use highly beneficial for the body to

restore health and improve immunity.

Apart from this, it has mild laxative effect which is very beneficial in the

treatment.

Regular use of amlaki destroys diseases like Swithra and Prameha313

Ultimately the principle “Swasthasya Swasthya rakshanam, aturasya vikara

prashamanam” is achieved through these two drugs.

Khadira helps in treating the disease, amlaki helps in restoring the health.


85

DESCRIPTION OF INDIVIDUAL DRUGS

KHADHIRA:

Latin Name : Acacia catechu

Family : Leguminosae – Mimosaceae - (Vatadi Varga)

Charaka : Kustagna, Kashayaskanda

Sushruta : Salasaradi Gana

VERNACULAR NAMES:

English : Black Catechu, Cutch Tree

Hindi : Katha, Khair, Khair babul

Telugu : Kasu, Khadiramu, Mallasandra, Podala Manu, Sandra,

Sundara

Sanskrit : Bahushalya, Balapatra, Bala putra, Balatanaya,

Dantadhavana, Gayatri, Homa, Hima Shalya, Khadira,

Karkati, Kantaki, Kusthari, Kustarahita, Medya, Tiktasara,

Saradruma, Sushalya, Pathidruma, Vakrantaka, Yagnanga,

Yagnika, Yapadru

Morphology: A moderate sized tree of 9-12 mts hight. Bark is dark coloured, rough.

Young shoots are dark brown or purple glaborous. Leaves 2-pinnate.

Bark: The part used in the present study. The bark is bitter and acrid, cooling, astringent

to the bowls, antihelmenthic, antidysentric, antipyretic, cures itching, sore throat,

bronchitis, indigestion, heaviness, ulcers, boils, Psoriasis, inflammations, leprosy,

anemia, Leucoderma, also given in elephantiasis, urinary discharges, strengthens teeth.


86

PROPERTIES:

Rasa : Tikta, Kashaya

Guna : Laghu, Ruksha

Virya : Sheeta

Vipaka : Katu

Karma : Kapha-Pittahara, Medogna, Dipana, Dantya

MAJOR CHEMICAL CONSTITUENTS:

Heart wood : Catechani, Catechutannic acid

Wood : I-epicatchin, Afzelchin, Gossypetin, Procyanidin, taxifolin

Gum : L-Arabinose, D-galactose, D-Rhamnose

RESEARCH WORK DONE ON ACACIA CATECHU:

1. A Medicinal extract of Acacia Catechu and Scutelleria baicalensis at as a dual

inhibitor of cyclooxygenase and 5-lipooxygenase to reduce inflammation

Ref: Burnett BP JiaQ.ZhaoY.levy RM.

J.Med Food 2007 Sep; 10 (3) 442-51

2. Medicinal Plant extra acts as anti-Escheria coli 0157: H7 agents and their effects

on bacterial cell aggregation.

Ref: Voravunthikunchai SP.Linsuwan S.

J.Food Prot 2006 Oct; 69(10) : 2336-41

3. Determination of the predominant catechins in Acacia Catechu by liquid

Chromatography / electrospray ionization – mass spectrometry.

Ref: Shen.D. WuQ. Wang M. Yang Y. Lavoie E J. Simon JE

J. Agric Food Chem 2006 May; 3 54(9): 3219 -24

4. Final report of the safety assessment of Acacia Catechu Gum.

Ref: Int.J.Toxicol 2005; 24 suppl. 3:75-118.


87

5. Effective Medicinal plants against enterohaemorrghic eschercia Coli.0157:H7.

Ref: J.Ethnopharma col.2004 Sep; 94(1) 49-54

6. Antimicrobial Evaluation of some medicinal plants for their anti – enteric

potential against multi – drug resistant salmonella typhi

Ref: Rani P. Khullar N. Phytother Res 2004 Aug; 18(8) : 670-3

7. In vitro plantlet regeneration from seedling nodal explant of Acacia Catechu.

Ref: Sahani.R.Guptha Sc.Indian J.Exp Biol 2002 Sep; 04(9):1050-5

8. Preliminary observations on leukemia specific agglutinoins from seeds.

Ref: Agarwal S.Agarwal SS.

Indian J. Med Res 1990 Feb; 92:38-42

9. Antifertility activity of traditional contraceptive pill comprising Acacia Catechu

Ref: Azad Chowdhary A.K

Indian J. Med Res 1984 Sep; 80:372-4

10. Hypotensive action of Acacia Catechu.

Ref: J.S.K. Sham, K.W.Chiu, P.K.T.Pang,

Planta Med 1984; 50:177-180


88

AMLAKI:Latin Name : Emblica officinalis

Family : Euphobiaceae (Haritakyadi Varga)

Charaka : Vayasthapana, Virechanopaga

Sushruta ; Triphala, Parushakadi

VERNACULAR NAMES:

English : Emblic myrobalan Tree

Hindi : Amlaki, Amla, Amlika

Telugu : Amlakamu, Amalaki, Usiri, Usirikaya, Nelli, Pullayusirika

Sanskrit : Adiphala, Akara, Amalaki, Amrita, Amrita Phala,

Bahuphali, Dhatri, Dhatrika, Dhatriphala, Shriphala,

Vayastha, Tishya, Sriphali, Vrishya, Rochani, Karshaphala,

Kayastha.

Morphology: A deciduous small or middle sized tree with crooked trunk and spreading

branches, bark greenish grey, peeling off in Conchoidal flakes. Branchlets glaborous

leaves sub-sessile.

Fruit: The part used in the drug given in the present study. The fruit is acrid, sour, bitter,

sweetish, cooling, carminative, alterative, laxative, tonic, antipyretic, and useful in

burning sensations, urinary discharges, thirst, leprosy, piles, and anaemia.

Properties:

Rasa : Amlapradhana Pancharasas (except lavana)

Guna : Guru, Snigdha

Virya : Sheeta

Vipaka : Madhura

Karma : Tridoshahara, Vayasthapana, Rasayana, Chakushya,

Vrusya, Keshya.


89

Major Chemical Constituents :

Fruit: Vit-C, Phyllembin, Tinolic Acid, indole, acetic Acid, Phyllembic acids & Salts,Ellagic acid, Corilagin.

RESEARCH WORK DONE ON EMBLICA OFFICINALIS:

1. Hypolipidaemic effect and anti atherosclerotic effects of fruit juice of Emblica

Officinalis in cholesterol fed rabbits.

Ref: Ritu Mathur, Arti Sharma, Mira Varma

J. Ethnopharmacology Vol 50 (2) 1996 pgs 61-68

2. Detoxifies the body, regulates digestion, helps to increase lean body mass &

reduce fats. A natural source of vitamin C.

Ref: Dr. Manish, Chakrapani Ayurvedic Clinic & Research Centre

3. Antitumor activity of Emblica Officinalis

Ref: Jeena K. Jose, Girija Kuttana nd Ramadasan Kuttan.

J. Ethnopharmacology vol 75; issues 2-3, May 2001 Pg 65-69

4. Flavinoids from Emblica Officinalis and Mangifera Indica effectiveness for

dyslipidemia

Ref: L. Anila and N.R. Vijayalakshmi

J. Ethnopharmacology vol 79 issue:1, Feb 2002 pg 81-87.

5. Hepatoprotective activity of Emblica Officinalis

Ref: Jeena K. Jose and Ramadasan Kuttan

J. Ethnopharmacology vol.72 (1-2) Sep 2002 pg 135-140

6. Cytoprotective and immuno modulating properties of Amla (Emblica Officinalis)

on lymphocytes and in-vitro study.

Ref: M. Saiam; D Neetu Yogesh B. Anju P.

J. Ethnopharmacology vol.81 (1) June 2002 Pg 5-10


90

MADHU:

There are 8 types of Madhu - Makshika, Bhramara, Ksaudra, Pauthika chatra,

Ardya, Audalaka, and Dalam.

Best anupana, has good yogavahi nature

Properties: Sheeta, Laghu, Swadu, Ruksha, Gnahi, Lekhana, Netrahitakara,

Agnideepaka, Swarakara, Vrana Sodhana, Ropana, Srotoshodhaka, Varnya, Medhya,

Vrishya, Visada, Ruchikara, Kusta-arsas, Raktapitta, Kapha, Prameha, Klama, Krimi,

Medohara, Swasa, Kasa, Hikka, Malabaddahara, Alpavatakara,

Rasa : Madhura Rasa, Kashaya anurasa

Guna : Laghu, Ruksha

Veerya : Sheeta Virya

Vipaka : Katu


91

METHOD OF DRUG PREPARATION

The present yogam is a combination of Khadira and Amlaki

The bark of Khadira, fruits of Amlaki are used in the preparation

Barks of Khadira, fruits of amlaki are collected, through the herb collector; they

are dried under shade, to restore their medicinal properties.

Khadira bark is pounded into coarse powder & weighed. Equal quantity of amlaki

fruit is pounded and added to it.

The powder is made into kwath churam. It is stored in a neat, dry container and

packed accordingly.

The Kwath form is administered to the patient.

Dose : 30ml Tid

Madhu as anupana


92

METHODOLOGY

The study was conducted in the Department of Kayachikitsa, Govt. Ayurvedic

Hospital, Erragadda,Hyderabad between 6-3-07 to 31.1.08

Aim: To assess the efficacy of Dhatri – Khadira kwath in causing pigmentation in white

patches of switra.

Source of Data : Patients of either sex aged between 5-70 years diagnosed as switra

were selected from OPD of Govt.Ayurvedic Hospital, Erragadda, Hyderabad.

Sampling Method and Research Design: The study was conducted as an open trial

study with randomized selection of 30 patients of either sex within age groups 5-70 years

suffering from switra were included.

Informed consent from all patients was obtained prior to the study. A complete

history was taken through a special proforma including age of onset, duration, family

history of switra, H/o consangnious marriage of parents, any personal or family history of

systemic diseases. A thorough dermatological examination was conducted on the

patients.

Inclusion criteria:-

Patients of either sex with sweta varna mandalas (i.e. milky white patches,

centrally hypopigmented with sharp circumscribed borders).

Patients aged between 5-70 years

Chronicity less than 6 years.

Exclusion criteria: as per ICD-10, L00-L99 skin and sub-cutaneous diseases,

L80-Vitiligo

Patients below 5 years and above 70 years

Certain conditions originating in the perinatal period (P00-P96)


93

Certain infectious and parasitic diseases – (B00-B99)

Complications of pregnancy and childbirth (O00-O99)

Endocrinal, nutritional and metabolic diseases (E00-E90)

Congenital malformations, deformities and chromosomal abnormalities (Q00-Q99)

Neoplasms (C00-D48)

Systemic connective tissue disorders (M30-M36)

With other skin diseases like Psoriasis, Eczema which interfere with the treatment.

With Psychiatric problems like Psychosis, mania, OCD, Schizophrenia

Investigations: Following investigations were done prior to the study.

CBP

ESR

RBS

CUE

Diagnostic Criteria: Swetavarna mandalas with or without other features of switra

Intervention:

Drug: Dhatri – Khadira kwath

Dose: 30ml tid, followed by madhu as anupana

Route: Oral

Duration: 45 days

Followup: 2 months

Assessment criteria:

The assessment was made on the colour, number and size of the mandalas which were

observed before starting the treatment, during and after the treatment.

Change in the colour of mandalas

Change in number of mandalas

Change in the size of mandalas

To assess the improvement in the colour the following grading was given


94

C0 – Normal skin colour

C1 – Tanned brown

C2 – Light brown

C3 – Dark pink

C4 – Light pink

C5 – White colour

The data obtained before and after treatment were analysed. The complete results

of treatment were ascertained in terms of,

I. Colour of the mandalas:

1-25% - Mild Response

26-50% - Moderate Response

51-75% - Marked Response

76-100% - Excellent Response

0 - No Response

II. Number of Mandalas:





0 - No Response

III. Size of Mandalas:





0 - No Response


95

Overall effect of therapy was assessed based on the following groups





0 - No Response

In this study subjects were classified into 5 groups mild, moderate, marked

excellent and No response groups. If the symptoms of a patient decrease by 1-25% he is

put in mild group, if the patient has decrease in symptoms by 26-50% he is placed in

moderate group, subject with relief of symptoms by 51-75% he is placed in marked

group. If patient has relief by more than 75% he is placed in excellent group. There are

patients with no relief of symptoms who are placed in no response group.


96

OBSERVATIONS

ACCORDING TO THE INCIDENCES

Table – 13 Showing incidence of age:

Sl.No. Age(in years) No. of Patients %

1. 0-10 yrs 6 20%

2. 11-20 yrs 7 23.33%

3. 21-30 yrs 6 20%

4. 31-40 yrs 4 13.33%

5. 41-50 yrs 1 3.33%

6. 51-60 yrs 4 13.33%

7. 61-70 yrs 2 6.66%

Among 30 patients taken for the study maximum number of patients fall under

11-20 yrs group.

Highest percentage of study population includes females 56.66%

Table – 15 Incidence of Habitat:

Sl.No. Habitat No. of Patients %

1. Rural 2 6.6%

2. Urban 23 76.6%

3. Town 5 16.66%

Majority of the subjects came from urban areas 76.6%


97

6

7

6

4

1

4

2

0

1

2

3

4

5

6

7

NO OF PATIENTS

0 TO 10 11 TO 20 21 TO 30 31 TO 40 41 TO 50 51 TO 60 61 TO 70YRS

AGE OF THE PATIENT

Series1

INCIDENCE OF SEX

MALES43%

FEMALES57%

MALES FEMALES

2

23

5

0

5

10

15

20

25

NO OF PATIENTS

RURAL URBAN TOWNHABITAT

INCIDENCE OF HABITAT

Series1


98

Table – 16 Incidence of Religion:

Sl.No. Religion No. of Patients %

1. Hindu 21 70%

2. Muslim 6 20%

3. Christian 3 10%

Majority of the subjects belong to Hindu community 70%.

Table – 17 Incidence of Marital Status:

Sl.No. Marital Status No. of Patients %

1. Married 13 43.33%

2. Un-married 17 56.66%

Most of the patients taken for clinical study were un-married 56.66%.

Table – 18 Incidence of Diet:

Sl.No. Diet No. of Patients %

1. Mixed 23 76.66%

2. Veg 7 23.33%

Veg: Vegetarian diet

Majority of the subjects had mixed diet 76.66%

Table – 19 Incidence of Socio - Economic Status:

Sl.No. Age(in years) No. of Patients %

1. LIG 13 43.33%

2. MIG 17 56.66%

3. HIG 0 0

LIG: Low income group (below 10,000/-),

MIG: Middle income group (10,000/- to 20,000/-),

HIG: High income group (20,000/- and above)

Majority of the subjects belong to middle income group


99

21

6

3

0

5

10

15

20

25

NO OF PATIENTS

HINDU MUSLIM CHRISTIANRELEGION

INCIDENCE OF RELEGION

Series1

MARITAL STATUS

MARRIED43%

UNMARRIED57%

MARRIED UNMARRIED


100

INCIDENCE OF DIET

MIXED77%

VEG23%

MIXED VEG

13

17

0

0

2

4

6

8

10

12

14

16

18

NO OF PATIENTS

LIG MIG HIG

SOCIO -ECONOMIC STATUS

Series1


101

Table – 20 Incidence of Occupation:

Sl.No. Occupation No. of Patients %

1. Agriculture 1 3.33%

2. Private Employees 2 6.6%

3. Business 2 6.66%

4. Electrician 1 3.33%

5. Student 16 53.33%

6. Housewife 6 20.00%

7. Carpenter 1 3.33%

8. Watchman 1 3.33%

Majority of the patients belonged to student community 53.33%

Table – 21 Incidence of Colour of the patients:

Sl.No. Colour of pt No. of Patients %

1. Fair 9 30%

2. Wheatish 14 46.66%

3. Black 7 23.33%

Majority of the subjects were wheatish skinned people 46.66%.

Table – 22 Incidence of Origin of the disease:

Sl.No. Origin No. of Patients %

1. Doshaja 28 93.33%

2. Vranaja 2 6.66%

The origin of the disease due to external causes were found in two subjects 6.66% and in

majority of subjects the cause was endogenous 93.33%


102

1

2 2

1

16

6

1 1

0

2

4

6

8

10

12

14

16

NO OF PATIENTS

AGRICULTURE BUSINESS STUDENT CARPENTEROCCUPATION

INCIDENCE OF OCCUPATION

Series1

9

14

7

0

2

4

6

8

10

12

14

NO OF PATIENTS

FAIR WHEATISH BLACK

COLOUR OF THE PATIENT

Series1

ORIGIN OF DISEASE

DOSHAJA93%

VRANAJA7%

DOSHAJA VRANAJA


103

Table – 23 Incidence of Prakriti:

Sl.No. Prakriti No. of Patients %

1. VP 9 30%

2. PK 5 16.66%

3. KV 1 3.33%

4. PV 9 30%

5. VK 3 10%

6. KP 3 10%

VP= Vata pitta, PK= Pitta kapha, KV= Kapha vata, PV= Pitta vata, VK= Vata Kapha,KP= Kapha pitta.Among 30 patients, majority of them belonged to vatapitta and Pitta vata prakruti 30%.

Table – 24 Incidence of Family History:

Sl.No. Family History No. of Patients %

1. Present 1 3.33%

2. Absent 29 96.66%

Majority of the patients did not present with a family history 96.66%.

Table – 25 Incidence of Stress:

Sl.No. Stress No. of Patients %

1. Present 7 23.33%

2. Absent 23 76.66%

Majority of the patients did not present with history of stress 76.66%.

Table – 26 Incidence of Consangnious Marriage of parents:

Sl.No. Cong.Marriage No. of Patients %

1. Presnet 6 20%

2. Absent 24 80%

Majority of patients did not present with history of consangious marriage of parents 80%.


104

9

5

1

9

3 3

0

1

2

3

4

5

6

7

8

9

NO OF PATIENTS

VP PK KV PV VK KP

PRAKRUTI

Series1

FAMILY HISTORY

present3%

absent97%

present absent

STRESS

PRESENT23%

ABSENT77%

PRESENT ABSENT


105

Table – 27 Incidence Chronicity:

Sl.No. Chronicity No. of Patients %

1. 1month – 1 yr 20 66.66%

2. 2 -3 yrs 6 19.99%

3. 4-5 yrs 3 10%

4. 6-7 1 3.33%

Majority of the patients taken for the study had chronicity of disease from 1 month to 1

year 66.66%.

Table – 28 Incidence of Old/New cases:

Sl.No. Old/New cases: No. of Patients %

1. Old 15 50%

2. New 15 50%

Among 30 cases taken for the study 15 patients were new and 15 patients were old who

already received treatment else were.

Table – 29 Incidence of age of first onset:

Sl.No. Age(of first onset) No. of Patients %

1. 0-10 yrs 7 23.33%

2. 11-20 yrs 8 26.66%

3. 21-30 yrs 4 13.33%

4. 31-40 yrs 4 13.33%

5. 41-50 yrs 1 3.33%

6. 51-60 yrs 4 13.33%

7. 61-70 yrs 2 6.66%

In majority of patients disease started before the age of 20 yrs 49.99%


106

H/O CONSANGNIOUS MARRIAGE

PRESENT20%

ABSENT80%

PRESENT ABSENT

20

6

3

1

0

2

4

6

8

10

12

14

16

18

20

NO OF PATIENTS

1MON-1YR 2YR-3YR 4YR-5YR 6YR-7YR

CHRONICITY OF THE DISEASE

Series1

OLD/NEW CASES

OLD50%

NEW50%

OLD NEW


107

Table – 30 Site of first onset:

Sl.No. Site (of first onset) No. of Patients %

1. Scalp 0 0

2. Face 11 36.66%

3. Neck 0 0

4. Chest 1 3.33%

5. Abdomen 2 6.66%

6. Back 4 13.33%

7. Upper limbs 2 6.66%

8. Lower limbs 9 30%

9. Genitals 1 3.33%

In majority of subjects face was the site of first onset 36.66% followed by lower limbs

30%

Table – 31 Nidanam:

Sl.No. Ahara nidanam No. ofPatients

%

1. Adika ushna, teekshana ahara sevana 1 3.33%

2. Amla, lavana, katurasa sevana 5 16.66%

3. Madura rasa sevana 3 10%

4. Adhika dadhi 4 13.33%

5. Adika mamsa 5 16.66%

6. Dumrapana 1 3.33%

7. Masha and mulakas 1 3.33%

8. Dadi and mamsa 1 3.33%

9. Nothing particular 9 30%

Among 30 subjects 9 patients did not have any particular eating habits in excessive 30%.


108

7

8

4 4

1

4

2

0

1

2

3

4

5

6

7

8

NO OF PATIENTS

0 TO 10 11 TO 20 21 TO 30 31 TO 40 41 TO 50 51 TO 60 61 TO 70

AGE IN YEARS

AGE AT FIRST ONSET

Series1

0

11

0

1

2

4

2

9

1

0

2

4

6

8

10

12

NO OF PATIENTS

SCALP NECK ABDOMEN UPP.LIMB GENITALS

SITE

SITE OF FIRST ONSET

Series1


109

Table – 32 Types:

Sl.No. Types No. of Patients %

1. Localized 26 86.66%

2. Generalized 4 13.33%

3. Universal 0 0

Among 30 subjects taken for the study 26 of them presented with localized type of

vitiligo 86.66%

Table – 33 Nature of spread:

Sl.No. Spread No. of Patients %

1. Gradual spread 29 96.66%

2. Sudden spread 1 3.33%

3. Stable 0 0

Among 30 subjects 29 of them presented with gradual spread of the disease 96.66%.

Table – 34 Symmetry of the patches:

Sl.No. Symmetry No. of Patients %

1. Symmetrical 15 50%

2. A symmetrical 15 50%

Among 30 subjects 15 patients presented with symmetrical patches and 15 presented with

asymmetrical patches 50%

Table – 35 Leucotrichia:

Sl.No. Leucotrichia No. of Patients %

1. Present 5 16.66%

2. Absent 25 83.33%

Among 30 subjects 25 of them did not have leucotrichia (hair not involved) 83.33%


110

26

40

0

5

10

15

20

25

30

NO OFPATIENTS

LOCALIZED GENERALIZED UNIVERSAL

TYPES OF VITILIGO

Series1

29

10

0

5

10

15

20

25

30

NO OF PATIENTS

GRADUAL SUDDEN STABLENATURE OF SPREAD

NATURE OF SPREAD

Series1


111

Table – 36 Colour of the patches:

Sl.No. Colour of the patches No. of Patients %

1. White colour (C5) 23 76.66%

2. Light Pink (C4) 5 16.66%

3. Dark pink (C3) 2 6.66%

4. Light Brown (C2) 0 0

5. Tanned brown (C1) 0 0

Among 30 subjects 23 of them presented with white coloured patches 76.66%

Table – 37 Number of patches:

Sl.No. Number of patches No. of Patients %

1. 1-5 27 90%

2. 6-10 1 3.33%

3. Above 10 2 6.66%

Among 30 subjects 27 of them had 1-5 number of patches on them 90%

Table – 38 Size of patches (for 24 patients only):

Sl.No. Size of patches No. of Patients %

1. 1-15cm 19 82.6%

2. 16-30cm 2 8.68%

3. 31-45cm 1 4.34%

4. 46-60cm 0 0

5. 61-75cm 1 4.34%

6. 76-90cm 0 0

7. Above 90cm 1 4.34%

Among 30 subjects 19 of them presented with patches between 1-15cm size 82.60%


112

19

2

1

0

1

0

1

0

2

4

6

8

10

12

14

16

18

20

NO OF PATIENTS

1-15 cms 16-30 cms 31-45 cms 46-60cms 61-75 cms 76-90 cms above 90 cmsSIZE IN CMS

SIZE OF THE PATCHES

Series1

23

5

2

0 0

0

5

10

15

20

25

NO OF PATIENTS

C5 C4 C3 C2 C1

COLOUR OF THE PATCHES

27

12

0

5

10

15

20

25

30

NO OF PATIENTS

1 TO 5 6 TO 10 ABOVE 10NO OF PATCHES

NO OF PATCHES


113

Table – 39 Aggravating factors:

Sl.No. Aggravating factors No. ofPatients

%

1. Exposure to sun 4 13.33%

2. Contact with chemicals 1 3.33%

3. Application of Cosmetics 0 0

4. Intake of milk 1 3.33%

5. Intake of curd 2 6.66%

6. Non-veg diet 2 6.66%

7. Nothing particular 20 66.66%

Among 30 subjects 20 of them had no specific aggravating factors 66.66%

Table – 40 History of Allergy:

Sl.No. History of Allergy No. ofPatients

%

1. Food 1 3.33

2. Drugs 0 0

3. Dust 1 3.33

4. Nothing particular 28 93.33

Among 30 subjects 28 of them had no specific History of Allergies 93.33%


114

RESULTS

Table – 41 Responded / Not responded:

Sl.No. Parameter Responded % Notresponded

%

1. Colour 24 80% 6 20%

2. Number 3 10% 27 90%

3. Size (for24 Pts) 11 45.8% 13 54.1%

Amont 30 subjects 24 patients responded in colour and 6 did not respond, 3 patients

responded in number and 27 did not respond, out of 24 patients 11 responded in size and

13 did not respond.

Table – 42 Response in the Colour of Patches:

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 11 6 7 0 6

Among 30 subjects 11 showed mild response, 6 moderate, 7 marked and 0 excellent

response in colour. 6 patients showed no response in colour.

Table – 43 Response in the Number of Patches:

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 0 2 1 0 27

Among 30 subjects 0 showed mild response, 2 showed moderate response, 1 showed

marked improvement, 0 showed excellent response. 27 patients showed no response in

the number of patches


115

RESPONSE IN COLOUR

RESPONDED80%

NOTRESPONDED20%

RESPONDED NOTRESPONDED

11

6

7

0

0

2

4

6

8

10

12

NO OF PATIENTS

1-25% 26-50% 51-75% 76-100%

% RELIEF

RESPONSE IN COLOUR

Series1


116

RESPONSE IN NUMBER

RESPONDED10%

NOTRESPONDED90%

RESPONDED NOTRESPONDED

A

0

2

1

0

0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

1.8

2

NO OF PATIENTS

1-25% 26-50% 51-75% 76-100%% RELIEF

RESPONSE IN NUMBER

Series1


117

RESPONSE TO SIZE

RESPONDED46%

NOT.RESPONDED54%

RESPONDED NOT.RESPONDED

3

6

1 1

0

1

2

3

4

5

6

NO OF PATIENTS

1-25% 26-50% 51-75% 76-100%% RELIEF

RESPONSE IN SIZE

Series1


118

Table – 44 Response in the Size of Patches (for 24 patients only):

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 3 6 1 1 13

Among 30 subjects 3 showed mild Response, 6 showed moderate Response, 1 showed

marked improvement, 1 showed excellent Response. 13 patients showed no Response in

the size of patches

Table – 45 Overall Results:

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 18 4 2 0 6

Among 30 subjects 18 showed mild response ,4 showed moderate response, 2 showed

marked improvement, 0 showed excellent response after the clinical study, and 6 patients

did not respond to the treatment at all.

Table – 46 Results:

VARIABLE MALESN=13

FEMALESN=17

Age (Mean Age) 27.1 yrs 28.58 yrs

Habitat – Urban 76.92 % 76.47 %

Habitat – Town 15.38 % 17.65 %

Habitat – Rural 7.69 % 5.8%

Diet – Vegetarian 38.46 % 11.26 %

Diet - Mixed 61.54 % 88.24 %

Types – Localized 92.31 % 82.35 %

Generalized 7.69 % 17.65 %


119

18

4

2

0

6

0

2

4

6

8

10

12

14

16

18

NOOFPATIENTS

1-25% 26-50% 51-75% 76-100% 0RESPONSE%RESPONSE

OVERALLRESULTS

Series1


120

Table – 47 Statistical Analysis of the Results :

PARAMETER MEAN MEAN

DIFF.

STD

DEV

STD

ERR

t

Value

p

Value

REMARKS

COLOUR BT 4.44 0.84 0.48 0.08 6.6 < 0.0001 SIGNIFICANT

COLOUR AT 3.6 1.1 0.2

NUMBER BT 1.66 0.28 2.23 0.41 1.7 <0.35 NOTSIGNIFICANT

NUMBER AT 1.38 1.94 0.36

SIZE BT 12.36 0.02 24.4 4.45 2.05 <0.1 NOTSIGNIFICANT

SIZE AT 12.34 24.3 4.2


121

DISCUSSION

About the Disease: Switra is an ancient malady due to its references being cited in the

Vedas. It is evident that people suffered from this disease from times unknown. A similar

condition like switra was prevalent in other civilizations across the globe. This is evident

from, the description of the disease available in their respective literature. It was called

“Kilas” in Tibet, “Bohak” in Arabia “Zorak” in Jerusalem, “Shirabito” in Japan,

Hence it can be said that this disease was prevalent across the globe not restricting to

particular country or race. Since ancient times attempts were made to combat the disease.

Switra can be well correlated to VITILIGO in contemporary medicine.

Switra and vitiligo have similar clinical features and presentation of the disease.

Both the diseases are related to hypopigmentation. Vitiligo is the most commonly aquired

hypomelanosis. The prevalence of the disease is 1% World wide.

In a society where attractiveness is positively related to expectations of further

success, happiness and satisfaction in marital relationships, it is not surprising that any

visible illness like switra can make the afflicted person experience high levels of self

conciousness and low self – esteem.

The etiology of vitiligo remains unknown, only the Triggering / Precipitating

factors are identified, among which nutritional deficiency, emotional stress infections,

exposure to chemicals are included. The etiology of Switra is given as incompatible diet,

misconduct, improper life style. The essence of both remains same i.e. misconduct,

improper life style indirectly leads to stress which disturbs the harmony between the body

and mind. Stress plays an important role in dermatological diseases. Incompatible diet

leads to disturbances in the metabolism and causes accumulations of toxins in the body,

in directly leads to nutritional deficiency. Vitiligo (Non - segmental type) is considered of

auto immune origin.

.


122

During this study no prodromal symptoms are mentioned for both switra and

vitiligo and the same was noticed in the study.

The pratyatmaka linga “Swetavarna mandalas” were clearly evident. Patients

sought medical attention when they noticed white coloured patches on the skin. As per

the definition of Sushruta, 30 switra is “Twagatam” and “Aprasravi”accordingly in

subjects the skin was only involved, no pain or secretions were noticed. Vitiligo is also

presented as milky white patches, centrally hypopigmented with sharp circumscribed

borders and mostly asymptomatic. The clinical features of vataja, pittaja, sleshmaja could

not be found in the patients as described in the texts. The macules were found to be of

round, oval shape and some macules were irregular in shape. The size of macules mostly

varied from 1-15cm. The mucous membranes were affected and lips were mostly among

the affected mucosal surfaces. Although any part of the skin or mucous membrane is

amenable to develop vitiligo the disease has a predilection for normal, hyperpigmented

regions such as face, groin, axillae, areola, and genitalia. The same was observed that the

face was the first site of onset in many patients.

Further, lesions may develop in areas like ankles, elbows, knees, which are

subjected to repeated trauma or friction according to texts and the same has been

observed in the patients whose first site of onset were limbs the areas generally involved

were the knees, or elbows or ankles. Lip – tip syndrome characterized by depigmentation

of terminal phalanges was not encountered during the study.

Clinical variants of vitiligo were not seen in subjects of the study. Among the

various types of Vitiligo, maximum prevalent type was localized – focal and segmental

forms. The non - segmental form, which is a generalized type, was also seen in the

patients in less percentage.


123

Discussion on Drug Review: The drug taken for the clinical study is “Dhatri – Khadira

Kwath” selected from Baishaijya Ratnavali. It basically contains Dhatri i.e. Amlaki and

Khadira. The main aim for selecting the drug is to find a simple panaceae for a disease

like switra. The form of administration is kwath form which has high efficacy. Both the

drugs are easily available, non-controversial, unadulterated and economical. The kwath

churnam was given to the patients sufficient for every 15 days for a total duration of 45

days. The patients were advised to take 1 tsp (5grms) of honey each time after taking the

medicine. Before starting the treatment patients were advised to take Triphala Churnam

for virechanam. Khadira is the best kustahara dravya. Many instances have quoted

khadira to be beneficial in switra also. Works on Bakuchi, Kakodumbara, Chitraka, and

Kaseesabaddaras have been conducted but efficacy of khadira in causing pigmentation

has not been studied. Moreover Amlaki is the best rasayana, pitta shamaka and improves

the efficacy of the formulation.

Probable mode of action: Khadira is the Sheeta Virya Dravya having tikta, Kashaya

rasas. Has best Pitta Shamaka and rakta shodaka property. As Rakta and pitta

(Interlinked with each other) are both vitiated in switra Khadira acts best in this aspect.

Amlaki also is sheeta virya dravya with pancharasas (Except Lavana). It is the

best source of vitamin C. Helps to build immunity, and may hinder the autoimmune

reaction in the body. It is also best pitta shamaka. Generally the oxidants which are the

outcome of metabolic reactions are accumulated in the skin which can be shown through

Fourier – Raman spectroscopy. These oxidants are responsible for the harmful changes in

the skin. Amlaki has the best anti - oxidant property which can counter the effects of

toxins in the skin.

Discussion on Methodology: The study was conducted in the Dept of Kayachikitsa,

Govt.Ayurvedic Hospital, Erragadda, Hyderabad. The main aim was to assess the

efficacy of Dhatri- Khadira Kwatha in causing pigmentation in white patches of switra.


124

A total of 34 patients were incorporated, 4 patients were dropouts, 30 patients

completed the treatment schedule. The patients had to come for a review for every 15

days. And the improvement in the condition was assessed accordingly. Patients of either

sex aged between 5-70 yrs were randomly selected into a group, and an open trial was

conducted. Prior to the trial an informed consent from all the patients was obtained. A

thorough dermatological examination and a detailed history were taken through a special

case sheet.

Inclusion Criteria: Patients of either sex were included in the study to know the

incidence of the disease among males and females. Patients aged 5yrs were the lowerlimit

and 70 yrs the higher limit. To know the increase in the incidence of childhood vitiligo

the lower limit was taken and higher limit to know the incidence of switra in elderly

people.

Chronicity less than 6 yrs was taken to assess the response of patches to the

treatment. Generally above 6yrs of chronicity the patches do not respond to the treatment

and in some cases there may be complete depigmentation.(Fitzpatrick)

Exclusion criteria: The exclusion criteria were followed from ICD-10. L00-L99-Skin

and sub-cutaneous disease. L80 vitiligo; shows the exclusion criteria for vitiligo. Patients

below 5yrs are too young to take the medicine and above 70yrs also may not be able to

take the medicine.

Other skin diseases like Psoriasis and Eczema interfere with the treatment hence

they are excluded. The psychiatric problems like psychosis etc makes the patient unfit for

this treatment.

Investigations: There are no special laboratory investigations to diagnose switra. As a

part of routine examination CBP, ESR, RBS, CUE were done prior to the study.

Diagnostic Criteria: Swetavarna mandalas on the skin and mucosal surfaces with or

without other features of switra.


125

Assessment criteria: The assessment was based on three clinical parameters, the colour,

number and size of the mandalas, which was observed before, during and after the

treatment. To assess the improvement in the colour, grading was given. C0- Normal Skin

colour, C1-Tanned Brown Colour, C2 – Light Brown Colour, C3- Dark Pink, C4 – Light

Pink, C5 – White Colour. All the patients did not present with white coloured patches.

Some had light pink, others had darkpink colour in the patches. During the treatment the

improvement was assessed like change of colour from white to light pink and so on. The

grading was given to assess the stepwise changes in the colour.

The complte results of the treatment were ascertained in terms of 5 groups. If the

symptoms of a patient decrease by 1-25% he is put in mild response group, if the patient

had decrease in symptoms by 26-50% he is placed in moderate response group, if the

patient had relief of symptoms by 51-75% he is placed in marked response group. If the

relief is more than 75% he is placed in excellent response group. If no know relief of

symptoms is seen they are placed in no response group.

Discussion on observations: A total of 34 patients were incorporated among whom, 4

were dropouts and 30 completed the treatment schedule. The following discussion on

observations is based on them.

Age groups: Among 30 patients, 6 of them (20%) were below the age of 10 yrs. 7

patients (23.33%) were below the age of 20yrs. From past two decades there is a sharp

rise in the incidence of childhood vitiligo (Behl) and the same was observed in this study.

Sex: Both males and females were taken for the study. The disease affects both the sexes

equally. But the percentage of female patients (56.66) in this study is higher than men. It

can be attributed to the social stigma and embarrassment caused due to depigmentation

and thus making female patients seek medical attention earlier than males.

Religion: Higher percentage of the subjects 70% belonged to Hindu community.

Generally in particular communities the dietary habits vary, which may be the cause for

the disease, to evaluate that, religion was taken into consideration.


126

Marital Status: Among 30 subjects, unmarried patients were more in number 17,

(56.66%).

Diet: The higher incidence of the disease was found in subjects with mixed diet 23

patients (76.66%). Generally taking non - vegetarian diet may accelerate the onset of the

disease.

Socio Economic Status: The subjects were classified into three groups depending on

their income level. Less thanRs.10,000/- were grouped into Low income group,

Rs.10,000-20,000/- Middle income group and aboutRs.20,000/- High income group.

Majority of subjects 17 (56.66%) belonged to Middle income group.

Habitat: Incidence of the disease is high in the rural population (Behl), among the 30

subjects taken for the study; a high incidence is seen in the urban population -23 patients

(76.6%) Rapid phenomenon of urbanisation which leads to life style changes and dietary

disorders might have resulted in the higher incidence in urban people.

Occupation: Switra may be produced as one of the occupational hazard. Occupation has

a direct influence on the disease. Occupation which includes contact with chemicals, or

printers, dyers, have chance of acquiring switra. In the present study majority of them

were students 16 (53.33%).

Colour of the patients: Generally vitiligo affects all the races equally, but the dark

skinned people are more prone to display due to the colour contrast. India is a tropical

country where we find more of wheatish to dark coloured people. In the study the

incidence of switra was found more in wheatish skinned people 14 (46.66 %.)

Origin of the disease: Switra has a doshaja (Endogenous) origin and vranaja origin

(Exogenous). Generally due to intake of incompatible diet and other factors disease may

be produced and due to external causes likes vranas due to accidents, burns, chemical

contacts or trauma Switra may be produced. Among 30 patients 28 of them (93.33%) are

of endogenous origin and 2 (6.66%) had exogenous origin. Among which 1 patient


127

acquired the disease due to burns with spirit and other due to trauma (Koebner’s

phenomenon). The origin of the disease due to trauma also holds significance.

Prakriti: among 30 patients, majority of the patients 9 (30%) with switra belonged to

Vata – Pitta prakriti followed by Pitta-Vata prakriti (30%) The incidence was more in

people with vata and pitta features.

Family History: The proportion of patients with positive family history varies from one

part of the world to another. In India, in particular it ranges from 6.25 – 18%. In some

studies it is as high as 40% (Behl). In the present study the incidence of family history

was 3.33% only. The absence was 96.66% it cannot be generalized, but the polygenic and

variable penetrance of the disease can be known.

History of Consangnious marriage: Among 30 subjects only 6 of them (20%)

presented with a history of consangnious marriage of parents, 24 of them (80%) had no

history.

Stress: Though stress is said to be one of the triggering factors for the disease

(Srivastava), in the present study only 7 of them presented with history of stress (23.33%)

Chronicity: Majority of the subjects, 20 of them (66.66%) had chronicity below 1 year.

The higher the chronicity, it was observed that patients’ response to treatment decreased.

The highest chronicity of the study was 6 yrs. But no severe depigmentation was noticed.

,

Old/New: Among 30 patients’ 15 patients were new cases, who started treatment with

the trial drug and 15 cases were old who previously took treatment elsewhere.

Age of first onset: Almost half the patients presented before the age of 20yrs and nearly

70-80% before the age of 30 yrs (Lerner and Nor Bend). In the present study , 50% of the

patients presented before the age of 20 yrs , 13.33% before the age 30yrs and 13.33%

before 40yrs. It is seen in majority of the patients that the disease presented before the

second decade of life and the incidence decreased in the subjects with age above 50yrs.


128

Nidanam: As per Ayurvedic texts the ahara – vihara nidana plays an important role in

the disease. Description about the cause of the disease due to adhika amla, lavana, dadhi,

dugda, masha, pisti sevana is mentioned. In the present study majority of them 9 (30%)

did not have any particular dietary habits as mentioned above. But 16.66% patients had

history of excessive consumption of meat and 16.66% had history of excessive curd

intake.

Site of first onset: The disease has a predilection for normal hyperpigmented regions

such as face, groin, axillae, areola, and genetalia. Further lesions may develop in areas

like ankles, elbows, knees, which are subjected to repeated trauma or friction (Behl) and

the same was observed in the clinical study that about 11 patients 36.6% face was the

first site of onset and 9 patients 30% had lowerlimbs as first site of onset. In patients with

lowerlimbs were involved the patches developed at the site of knees, ankles and

bonyprominences of medial malleolus. Very less patients 1 (3.33%) presented genitals as

first site of onset.

Types: There are three types of vitiligo, localized, generalized and universal. The

localized forms includes focal, segmental and mucosal, the generalised includes the non-

segmental, universal where complete depigmentation occurs. In the present study

majority of patients 26 (86.66%) were of localized types 4 patients were of generalized

type(13.33%).No patients with universal type were seen.

Nature of spread : In 29 (96.66%) patients the lesions had gradual spread ,only one

patient had sudden spread of the patches immediately after attaining puberty. Lesions

stable for many years was not found in any patients.

Symmetry of the patches: The shape of the patches was taken into account. Equal

number of patients had symmetrical 50% and asymmetrical patches 50%. Mostly round

and oval were prevalent in symmetrical types.


129

Leucotrichia: Hair over the patch may or may not turn white (Behl) But if hair turns

white indicates poor prognosis. In the present study only 5 patients presented with

leucotrichia. Among whom only 2 patinets responded to the treatment.

History of Allergy: H/o dust allergy was found in 1 patient 3.33%, 1 patient had food

allergy (particularly to bananas, Brinjalas) majority of them 28 (93.33%) had no H/o

allergy.

Aggravating factors: A couple of observations regarding the aggravating factors were

made during the clinical study. Majority of them 20pts (66.66%) did not have any

aggravating factors, but 4 pts observed redness of patch, burnings sensation when

exposed to sun. 2 pts (6.66%) observed intake of non-veg diet particularly chicken and

fish resulted in increase in the size of the patch, 2 patients observed taking curd caused

intense itching in the patches, the same was observed by 2pts, that taking milk caused

itching in the patches.

Colour of the patches: Among 30 patients 23 (76.6%) of them presented with white

coloured patches. 5 pts presented with light pink coloured patches, 2 pts presented with

dark pink coloured patches. Probably the application of topical creams might have lead to

the change in the colour. Old cases presented with the about two coloured patches.

Number of patches: Among 30 patients 27 (90%) of them had patches between 1-5 in

number only 1 patient had between 6-10, and 2pts had patches above 10 in number.

Size of the patches: The size measurement was possible for only 24 patients. 19

patients (82.6%) had patches ranging between 1-15cms. 2 patients has patches between

16-30 cm, 1 patient presented with patch size between 31-45 cms, 1 patient presented

with 61-75cms, above 90cms – 1 patient.


130

Discussion on Results: The results were analysed statistically by paired‘t’ test from the

observations made during and after the clinical study. The mean age of the study

population is 28 yrs. Mean age of female population is 28.58yrs. Majority of the subjects

had mixed diet, more than females, males were vegetarians. Highest percentage of the

study population came from urban areas. In females the disease was more of systemic

type.

Colour of the patches: Among 30 patients, 24 patients (80%) responded in colour, 6

patients (20%) did not respond in the colour. The patients who have undergone complete

treatment schedule showed marvelleous improvement in the colour of the patches. The

patient came every 15 days for a review. Each time patient noticed marked changes in the

colour of patch. In the first 15 days the colour changed to light pink, in some it even

turned into darkpink. In patients who have already taken treatment elsewhere presented

with light and darkpink patches initially. In those subjects after 30 days brown

pigmentation spots were noticed .After 45 days the pigmentation improved noticeably.

Two kinds of pigmentation changes were noticed during the study. In some cases

pigmentation started from periphery bringing about changes in the size, such is peripheral

repigmentation. In some case pigmentation spots were seen around the hair follicles in

the center of the patch, gradually growing in size and changing the symmetry of the

patch, such is perifollicular repigmentation. The statistical analysis shows P<0.0001

which is significant.

Among the 24 patients responded, 11 patients showed mild response, 6 showed

moderate response, 7 showed marked response, no patients showed excellent response.

Number of patches: Among 30 patients majority of them, 27 presented with 1-5 no on

their body. 1 patient had patches in between 6-10 and 2 patients had more than 10 patches

on the body. After the treatment schedule, the patients did not show much response in the

number. But patients who responded showed moderate and marked response.


131

Of 30 patients only 3 responded in number and 27 numbers did not show any

response in change of number of patches. Out of 3, 2 patients showed moderate response,

1 patient showed marked response. No patient showed excellent response.

The statistical analysis shows P<0.35 which is not – significant. There were

changes noticed in the patch but there was no change in the number of patches. The

patients in whom the number decreased were of recent onset and small in size. But

among few who responded in number, their response was remarkable.

Size of the patches: Among 24 patients, 19 patients had patches of size in between 1-15

cms, 2 patients had size in between 16-30 cms. 1 patient had 31-45cms, 1 patient had

patch ranging between 61-75cms, and 1 patient above 90 cms.

After completing the treatment schedule 11 patients (45.8%) responded in size, 13

patients (54.1%) did not respond. Among the 11 patients 3 showed mild response, 6

showed moderate response, 1 showed marked response, 1 patient showed excellent

response.

The change in the size of the patches was depended on the colour changes. The

repigmentation occurring in the white patches brough about the difference in size.

Peripheral repigmentation caused Shrinkage in the size and perifollicular repigmentation

brought about changes in symmetry (shape) which automatically brought difference in

the size

The statistical analysis shows P<0.1 which is notsignificant. But the response

seen in the size of the patches in duration of 45 days is commendable.

During the clinical study, in the first 15 days majority of them started showing

changes in the patches. The colour change was prominent, but there was no change in the

number and size.


132

After 30 days, the colour grading improved; the change in the colour was

even more remarkable. Pigmentation spots in the centre of patch were seen in some

patients and in few, changes from periphery were noticed. No change in the number

noticed.

After completion of 45 days – changes in the colour was even more satisfactory. Size

differences in the patches were clearly evident. Small patches of 1-3 cms disappeared and

some faded due to the pigmentation. They were not as prominent as before. Change in

number but only in 3 patients was noticed. The improvements were noticed in patients

with less chronicity, fresh cases with small sized patches. And the type was more of

localized type. In cases where the buccal mucosa was involved changes in colour was

remarkable.

During the treatment patients noticed many factors that caused irritation, itching,

burning sensation and increase in size. No blisters or oozing was noticed. Initially

patients experienced nausea, while taking the medicine but after a week the feeling

disappeared. Patients were advised for followup of 2 months. Only 12 patients had

regular followup. The changes that took after completion of treatment schedule persisted

after 2 months also. No new findings took place. No patients were Diabetic,

Hypertensive or Asthamatic hence no changes were recorded in those aspects.

Overall, from the clinical study conducted on 30 patients for duration of 45 days

satisfactorily with negligible side effects 18 patients showed mild response, 4 patients

showed moderate response, 2 patients showed marked response, no patients showed

excellent response. 6 patients showed no response to treatment at all. The initial results

are promising depending upon the response in colour, number and size. Some more time

is needed to establish the results.

Limitations of the study:


133

1. As the study does not have a control group, any categorical statements about the

success attribution to drug cannot be made.

2. The duration of the study is very short, it would have been better if the duration

was for a longer period to establish the results even more effectively.

3. As the sample size is very small (30pts) any significant findings found in the

study cannot be generalized to the population.

Recommendations for the future study:

1. Study to be conducted on larger samples.

2. To do a comparative study between a control group and test group with medicine

taken internally.

3. To do a comparative study between a control group taking medicine internally

and externally and test group taking medicine only internally.

4. To take a longer duration of time for clinical study.

5. To scientifically probe the action of Khadira on melanocytes.


134

CONCLUSION

From the discussion based on this study, it becomes nearly conclusive that,

Switra is a pittapradhana tridoshaja, twak vikara. Sweta Varna mandalas appear

on the skin suggestive of the disease.

It has historical background suggestive that many people suffered from this

disease since times unknown.

Based on the clinical features it can be well correlated to vitiligo of contemporary

medicine.

The prevalence of the disease is 1% world wide, affecting males and females

equally, but incidence of females is higher due to the social stigma and

embarrassment attached to the disease.

The incidence of childhood vitiligo is rapidly increasing from past two decades.

In the present study 20% of the patients were below 10 years.

The age of first onset, is before 20yrs, face and lowerlimbs are the site of first

appearance of the disease.

Family history and H/o consangnious marriage of parents had little role to play in

the etiology. Many of the patients had no specific incompatible dietary habits, in

most of the cases etiology was unknown.

Koebner’s Phenomenon was noticed in two patients as etiology. Leucotrichia also

was not seen in majority of patients.

Certain foods caused itching, increase in size of the patches, exposure to sun

caused redness and burning sensations in the patches.


135

Early detection and short duration of the disease, small sized patches, good

prognosis is seen.

The drug proved to be beneficial as promising results were noticed initially in

response of colour and size. No much change in number was noticed.

Out of 30 patients – 18 patients showed mild response, 4 patients moderate

response, 2 marked response and 6 members did not respond to the treatment.

Better results can be established with “Dhatri-Khadira Kwath” if study is

conducted on larger samples, for a longer duration in a comparative fashion by

enthusiastic scholars.


136

SUMMARY

A clinical study was undertaken to evaluate or assess the efficacy of ‘Dhatri-

Khadira Kwath’ in the disease switra.

As the colour of the skin plays an important role in the lives of people, any visible

changes in the skin can make the afflicted person experience high levels of self –

conciousness and low self esteem. Patients are subjected to social embarrassment, there

by leading to psychological disturbances. Hence disease switra which is related to

hypopigmentation was selected for the study. Based on the clinical features it is well

correlated to vitiligo of contemporary science.

The etiology of the disease remains unknown. It is expected to develop as a

sequel to irregular dietary habits and life style changes. Genetic predisposition may also

account for the disease.

A comprehensive formula “Dhatri-Khadira Kwath” selected from Bhaishajya

Ratnavali was used in the clinical study. A total of 30 patients fulfilling the inclusion and

exclusion criteria were taken for the study for duration of 45 days.

The present literary work is divided into five parts which gives a detailed picture

of the disease, and clinical study.

Thte first part consists of review of literature where the literary aspect about the

historical background, anatomy, physiology of the affected part, etiology, clinical

features, differential diagnosis, prognosis, treatment and dietary restrictions are

explained.


137

The second part contains the drug review which includes the criteria for the

selection of drug, description of individual drugs and method of preparation has been

elaborated.

The third parts comprises of methodology, observations of the study and results of

the study.

Fourth part is mainly the discussion, conclusion and summary aspect of the study.

Fifth part relates to references, bibliography, annexure which includes, master

charts and special casesheet of the study.

The present study highlights the fact that, medicine taken orally could be

beneficial in the management of Switra.


138

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89. Su.Su 21/9-10

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91. A.H.Su 12/14

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96. Su.Sha 1/6

97. Su.Sha 1/10

98. Su.Sha 1/26

99. A.H. Su 12/4

100. A.H. Su 11/22

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107. A.H.Sha ¼

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Harada disease Immunohistological analysis of inflammatory site Gafes Arch

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Jr. Childhood Vitiligo. J Am Acad Dermatol 1987; 16:948-54.

223,224,225. Singh P, Singh J. Agarwal US, Bhagavan RK. Contact Vitiligo:

Etiology and treatment. Indian J.Dermatol Venerol Leprosol. 2003; 69:27-9


149

Samprapti:

226. A.H.Ni.1/8

227. A.H.Ni.14/2

228. Su.Su.21/36

229. Cha.Ni 5/22-23

230. A.H.Ni. 12/22

226. A.S.Su 9/7

227. Cha.Su 24/1-10

228. A.S. Su 9/26

229. Cha.Su 8/18

230. Cha.Su 11/45

231. A.H.Su. 12/23

232. Su.Ni.5/3

233. Su.Ni 5/3 Dalhana Commentary

234. Su.Su.21/23

235. A.H.Ni.14/37

236. A.H.Ni. 14-37 Arunadutta Commentary

237. Su.Su 24/10

238. A.H.Ni 14/1-3

239. Cha.Ni 5/3

240. Su.Sha 4/33

241. Su.Su 21/34 - Dalhana Commentary

242. Amarakosha

243. Su.Ni 5/17

244. A.H.Chi. 20/1

245. Su.Ni.5/28

246. Cha.Chi 7/177

Bhedas:

247. M.Ni 49/37-39

248. Su.Ni 5/17


150

249. Cha.Chi 7/174

250. M.Ni 49/37-39 – Bhalukitantra

251. Cha.Chi 7/175-176

252. Kashyapa samhita Kusta Rogadikar

253. Bhela samhita 6th Chapter

254. Fitzpatrick; Elsen; Wolf Dermatology in General Medicine,

255. Behl PN, Agarwal A, Srivastava G. Vitiligo In Behl PN Srivastava G editor,

practice of Dermatology 9th edition Pg 238-41

256. Behl PN, Agarwal A, Srivastava G. Vitiligo In Behl PN Srivastava G editor,

practice of Dermatology 9th edition Pg 238-41

Sapeksha Nidan:

257. M.Ni 49/37

258. A.H.Ni 14/5 – Arunadutta Commentary

259. Cha.Chi 7/13

260. Su.Ni 5/17

261. Cha.Chi 7/28

262. Cha.Chi 7/19

263. Cha.Chi 7/37

264. Fitz Patrick, Eisen, Klaus Disorders of Melanocytes – Dermatology in General

Medicine 3rd edition

Sadya-Asadyata:

265. Cha.Vi 6/3

266. A.H.Ni.14/39

267. Cha.Chi 7/172

268. Kashyapa Samhita Kusta chikitsa

269. Bhela Samhita 6/35

270. Cha.Chi 7/176

271. Cha.Chi 7/177

272. Su.Ni 5/28


151

273. A.H.Ni 14/40

274. M.Ni 49/40

275. Cha.Chi 7/175

276. Su.Ni.5/28

277. B.P. 54/47

278. Dermatology General Medicine Vol-1 3rd edition

Chikitsa:

279. Vaidyata Shabda Sindu

280. B.P. Purvakanda, 54th Chapter

281. Cha.Su 9/5

282. Su.utt 1/25

283. Cha.Su 11/54

284. A.H. Chi 20/1

285. Cha.Su 11/55

286. Cha.Chi 7/162

287. Cha.Chi 7/163

288. Cha.Chi 7/164

289. Cha.Chi 7/165

290. Cha.Chi 7/166

291. B.R. 54/56

292. A.H.Chi 20/7

293. Cha.Chi 1/167

294. Cha.Chi 1/168

295. Cha.Chi 1/169

296. Cha.Chi 1/170

297. Cha.Chi 1/171

298. Cha.Su 8/16

299. Cha.Su 8/18

300. Cha.Chi 7/172


152

Patya – Apatyas:

306. Su.Ni 9/5 – Dalhana Commentary

307. Su.Chi 9/4

308. A.H.Chi 19/25 – Arunadutta Commentary

Drug Review:

309. B.R 54/53

310. Cha.Su 25/40

311. Cha.Chi 7/166

312. B.P. Nigantu Haritak Kyadi varga/39 sloka

313. Cha.Chi 6/48


153

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159

POST GRADUATE DEPT. OF KAYACHIKITSADR.B.R.K.GOVT.AYURVEDIC MEDICAL COLLEGE, HYD-038.

“A CLINICAL STUDY ON THE EFFECT OF “DHATRI- KHADIRA KWATH”IN THE MANAGEMENT OF SWITRAM (VITILIGO)

SPECIAL CASE SHEET

Name : OP/IP No:Age : Pt.Code No. :Sex : Sp.Diagnosis:Address : Date of Research:

Drug Given:Occupation : Contact No:Marital Status :Religion / Nationality :

CASE HISTORY

1. Chief Complaint with duration :

2. Associated Symptoms :

3. History of Present Illness :

4. History of Past Illness

a. Medical Past History : DM/HTN/Br. Asthma /Anaemia / Hypo or Hyperthyroidism /koch’s /Any other Skin Disorders.

b. Surgical Past History :

5. Treatment Historya. Regarding Switram :

b. Other Illness :

6. Family Historya. Noint / Nuclearb. No. of Family Members present :c. H/o consangnious marriage in the family.d. Any member suffering with similar complaint.e. Any Psychological disturbance associated with the family.


160

7. Personal History:a. Socio-economics Status : LIG/MIC/HIGb. Diet : Veg/Mixed

Staple food:c. Nature of Job : Sedentery/Active/Labourious/Standing/Travellingd. Psychological Stress : Mid/Moderate/Severee. Timings : Day/Night/Late Nights/Shiftf. H/o.Allergy : Food/Drug/or Any otherg. Habits :h. Addictions :

8. Menstrual/Obestetric History:a. Menstrual Cycle :b. Marital Life :c. LCB :d. Any other disorders :

Physical Examinations:a. Height f. RRb. Weight g. Heartc. PR h. Lungsd. BP i. Abde. Temp

DASAVIDHA PARIKSHA:

a. Prakruti f. Satmyab. Vikruti g. Satwac. Saara h. Ahara Shakthi : i. Abhyaharanad. Samhananam ii. Jarana shakthie. Pramananam i. Vyayama Shakthi

j. Vayastah

ASHTASTANA PARIKSHA:

a. Nadi e. Shabdab. Muthram f. Sparshac. Malam g. Drikd. Jihwa h. Akriti

SROTO PARIKSHA:


161

EXAMINATION OF THE SKIN

i. AGE AT ONSET :

ii. DURATION :

iii. ETIOLOGY :a. Positive family historyb. Trauma ( Koebner’s Phenomenon )c. Incompatible foodd. Untimely sleeping habitse. Emotional disturbancesf. Stressg. Exposure to hot and cold climatesh. Consangnious marriagei. Any history of autoimmune disorderj. Drug allergy

iv. NATURE OF SPREAD:

a. Gradualb. Stablec. Sudden

v. TYPE OF LESION :

a. Symmetricalb. A symmetrical

vi. ANY H/O itching/oozing/inflammation:

vii. ANY AGGRAVATING/RELIEVING FACTORS:

viii. SITE INVOLVED:a. Faceb. Scalpc. Trunk

i. Chestii. Abdomeniii. Back

d. Limbsi. bony prominencesii. Upper limbsiii. Lower limbs

vi ORIGIN OF LESION:

I. a. Doshaja (endogenous)b. Vranaja (exogenous)


162

II.

VATAKA(rakta dhatu )

PITTAJA (mamsa) KAPHAJA(medo)

1. Mandala 1. Kamala parravat 1. Ghana

2. Ruksha 2. Daham 2. Guru

3. Parusham 3. Roma Vidwamsam 3. Kanduyuktam

4. Kesha Nashanam 4. Tamra Varnam 4. Swetavarnam

5. Aruna varnam

vii. TYPES OF DEVELOPMENT:

I Localized

a. Focal

b. Segmental

c. Mucosal

II. Generalized

a. Non-Segmental

b. Universal

INVESTIGATIONS:

a. CBP

B. ESR

C. RBS

TREATMENT SHEDULE:

Drug : Dhatri Khadira Kwatham for 45 days (Ref BR)

Dose : 30ml tid or 45 ml BD


163

DURING THE TREATMENT SCHEDULEBEFORE TREATMENT

15 days 30 days 45 daysLOCATION

Colour Number Area Colour Number Area Colour Number Area Colour Number Area

Face

Scalp

Trunk

i. Chest

ii. Abdomen

iii. Back

b. Limbs

i. Upperlimbs

ii. Lowerlimbs

ASSESSMENT OF THE RESULT : RESPONDED/NOT RESPONDED

Sign of the Guide Sign of Co-Guide Sign of PG Scholar


164

CONSENT FORM

I, Smt. / Sri.______________________________aged ___________ years have willingly

Accepted to take the medicine given as a drug trial as a part of research programme

scheduled for 45 days. Hence I shall continue the medicine for above said tenure with

full acceptance.

Signature of the Patient.________________________________________________________________________

NOTES

A CLINICAL STUDY ON THE EFFECT OF“DHATRI-KHADIRA KWATH” IN THE

MANAGEMENT OF “SWITHRAM”(VITILIGO)

BYDr.K.NAMRATA

Guide & SupervisorDr. Prakash Chander

M.D (Ayu)Professor & H.O.D., P.G.Unit (K.C)

Ayurmitra

TAyComprehended

Introduction

Swithra is a dermatological disorder having its referencescited in the Vedas.

The term is derived from “Sweth Varne” meaning whitecolour, & is a disease related to hypopigmentation

20-30% of skin diseases require serious attention & Switra isone among them.

Based on the clinical features, swithra can be correlated toVitiligo.

Vitiligo occurs world wide with an overall prevalence of 1%. Vitiligo on the face is ranked 17th by WHO in world’s most

Disabling diseases.

CONT..

The higher incidence of the condition has been recordedin India from Asia

The etiology of vitiligo remains unknown. It is expectedto be of autoimmune origin.

Dhatri-Khadira Kwath (B.R –kusta rogadikar)has beentaken for the present study to assess the efficacy incausing pigmentation in white patches of swithra.

SHAREERA RACHANA

Twak is defined as “Twach Samvarne” meaning the onewhich covers.

Sushruta mentioned seven layers of skin namely,Avabhasini, Lohitha, Swetha , Tamra, Vedini, Rohini,Mamsadhara.

Tamra is the seat for Kilasa or Swithra.Charaka has mentioned 6 layers of skin namely,

Udakadhara, Asragdhara, Tritiya, Chaturtha, Panchami,Shasti.

Tritiya is the seat for Kilasa or Swithra.

SHAREERA KRIYA

Twak covers the underlying rakta, mamsa, medo dhatus Twak imparts varna to the body. Imparting varna to the body is a specialized function of

the Bhrajakapitta.The third vital function of twak is thermo regulation by

the virtue of pitta . Other functions include –being a sense organ,acting as a

channel to excrete sweda. It belongs to bahya roga marga .

NIDANA

a. Aharaja nidan:Vagbatta mentioned, a pregnant women consuming

excessive kaphakara ahara, the baby shall be affectedwith switra.

Gramya, anupa, jaleeyamamsa sevanam, anantharamdugda sevanam, Navanna, dadhi, matsya, lavana, amla,masha, mulaka, pisti, tila, ksheera, Guda sevana.

b. Viharaja NidanChardi, Mala-mutradi vegadharana ,Ati vyayamam , Ati

Santapasevanam ,Vyayamam in ajeernaavasthaGarma srama, Bhayarthanam sheethambu sevanam.

CONT..

c. Chikista sambandhi Nidana:Vagbatta mentioned usage of savisha jalouka in rakta

mokshana leads to switra at that site 110

Doing dushita rakta stambana leads to kilasa and kustaVishesha Nidana specially mentioned by charakaViruddha annapana sevana ,Vacham asatyamPapa karmas ,Krutagna bhavasNinda suranam ,Guru garshanamPoorva kruta karmas

RUPA

Swetha Varna mandalas on the body is the pratyatmakalinga of switram.

It is Twagtam and aparisravi .vataja, pittaja, sleshmaja types of switram have beendescribed which invade rakta ,mamsa &medo dhatus

If the doshas are present in rakta dhatu they producerakta varna,

when in mamsa dhatu produce tamra varna,and in medodhatu produce swetha varna.

SAMPRAPTI GHATAKAS

Doshas : Pittapradhana tridosha Dushya : Rakta, mamsa, medo dhatus Agni : Jataragni, dhatwagni Ama : Agnimandyam, dhatwagni

mandyam Udbhavastan : Amapakwashyam Sanchara : Tiryakgata siras Srotas : Rasa, rakta, mamsa, medo Srotodusti : Sanga Adhistana : 4th Layer of twak “Tamra” Vyaktastana : Twak Rogamarga : Bahya Vyadhi Swabhava : Chirakari

SADHYA-ASADHYATA

The deeper the involvement of the dhatus the prognosisbecomes worse.

Rakta Varna or Aruna Varna are sadhya, Tamra Varna becomes kasta sadhya andSweta Varna becomes asadhya.Charaka mentioned a person who has followed vamana –

virechana, rakta mokshana regime completely, whotakes sattu regularly and whose papakarmas are over,such case is sadhya.

CHIKITSA

The treatment aspect includes three types of therapiesto combat the disease

Daiva Vyapashray chikista – spiritual therapyYukti vyapashray chikista - rational therapySatvavajaya chikista – psychological therapyCHIKITSA SUTRAM : In switra roga, a person is made to undergo all the

shodhana procedures first. After patient is fully evacuated, samsrama karma is done

as primarily by giving malapu ras (Kakodumbara) alongwith gudam.

CONT….

After that he should be exposed to the sun for 3 days. If patient feels thirsty, peya is given to quench his thirst . patient develops blisters on the patches all over the body. The

blisters should be pricked with kantakam to release the fluid init.

After all the blisters are opened, a kwath prepared from barkof kakodumbara, priyangu, asan, and shatapushpa should begiven early in the mornings for 15 days

Sprinkling khadira kwatha externally & taking it internally ordrinking khadira udaka is very beneficial in switra.

Gomutram is very useful in switra roga..

DRUG REVIEW

The present drug “Dhatri-Khadira Kwatham” has been takenfrom “Kustarogadhikar” of “Bhaishajya Ratnavali”,

The compound has two drugs – Khadira and Amlaki, Madhu asanupana.

The drugs are non-controversial, unadulterated, easilyavailable, and economical

It is a simple combination and easy to prepare and use. Khadira is mentioned as “Kustagnanam” The use of Khadira Kashaya or Khadira udaka internally and

externally is highly recommended in swithra.

CONT…

Khadira is the Sheeta Viryadravya having tikta, Kashayarasas.Tikta rasa has ama pachana &vishagna prop.Khadira has Pitta Shamaka and rakta shodaka property.As Rakta and pitta are both vitiated in switra Khadira actsbest in this aspect.

Amlaki also is sheeta virya dravya ,having best pittashamaka effect.

Amlaki, is the best rasayanam , for rasa and rakta dhatusHelps to build immunity, and may hinder the

autoimmune reactions in the body. Amlaki has the best anti - oxidant property which can

counter the effects of toxins in the skin

CONT

It has a mild laxative effect which is very beneficial inthe treatment.

Regular use of amlaki destroys diseases like Swithra andPrameha.

The form of administration is kwatha which has highefficacy

The bark of Khadira, fruits of Amlaki are used in thepreparation

Khadira bark is pounded into coarse powder & weighed.Equal quantity of amlaki fruit is pounded and added to it.

The powder is made into kwath churam.

KHADIRA BARK

AMLAKI FRUITS

DHATRI KHADIRA KWATH CHOORNAM

CLINICAL STUDY-METHODOLOGY The study was conducted in the Department of Kayachikitsa, Govt.

Ayurvedic Hospital, Erragadda,Hyderabad. Aim: To assess the efficacy of Dhatri – Khadira kwath in causing

pigmentation in white patches of switra. Source of Data : Patients of either sex aged between 5-70 years

diagnosed as switra were selected from OPD of Govt.AyurvedicHospital, Erragadda, Hyderabad.

Sampling Method and Research Design: The study was conductedas an open trial study with randomized selection of patients .

Informed consent from all patients was obtained prior to the study. A complete history was taken through a special proforma including

age of onset, duration, family history of switra, H/o consangniousmarriage of parents, any personal or family history of systemicdiseases.

INCUSION CRITERIA

Patients of either sex with sweta varna mandalas (i.e. milky whitepatches, centrally hypopigmented with sharp circumscribed borders).

Patients aged between 5-70 years Chronicity less than 6 years. Exclusion criteria: as per ICD-10, L00-L99 skin and sub-cutaneous

diseases, L80-Vitiligo Patients below 5 years and above 70 years Certain conditions originating in the perinatal period (P00-P96) Certain infectious and parasitic diseases – (B00-B99) Complications of pregnancy and childbirth (O00-O99) Endocrinal, nutritional and metabolic diseases (E00-E90). Neoplasms (C00-D48)&Systemic connective tissue disorders (M30-M36)

INVESTIGATIONS

Following investigations were done prior to the study.

CBP,ESR ,RBS ,CUEDiagnostic Criteria: Swetavarna mandalas with or

without other features of switra Intervention:Drug: Dhatri – Khadira kwathDose: 30ml tid, followed by madhu as anupanaRoute: OralDuration: 45 days

Assessment criteria

The assessment was made on the COLOUR , NUMBER and SIZE ofthe mandalas which were observed before, during and after thetreatment.

To assess the improvement in the colour the following grading wasgiven

C0 – Normal skin colour C1 – Tanned brown C2 – Light brown C3 – Dark pink C4 – Light pink C5 – White colour The data obtained before and after treatment were analysed.

CONT..

The complete results of treatment were ascertained in terms of, 1-25% - Mild Response 26-50% - Moderate Response 51-75% - Marked Response 76-100% - Excellent Response 0 - No Response If the symptoms of a patient decreased by 1-25% he is put in mild

group, decrease in symptoms by 26-50% he is placed in moderategroup,

Relief of symptoms by 51-75% he is placed in marked group, reliefby more than 75% he is placed in excellent group ,no relief ofsymptoms were placed in no response group.

OBSERVATIONS

INCIDENCE OF AGE: Maximum number of patients 7(23.3%)fall under11-20 yrs group.

INCIDENCE OF SEX : more of females 17(56.6%) INCIDENCE OF HABITAT: Majority of the subjects came from urban

areas 23 (76.6%) INCIDENCE OF RELIGION: Majority of the subjects belong to Hindu

community 21 (70%). INCIDENCE OF MARITAL STATUS: Most of the patients t were un-

married17( 56.66%). INCIDENCE OF DIET: Majority of the subjects had mixed diet 23 (

76.66%) INCIDENCE OF SOCIO-ECONOMIC STATUS: Majority of the subjects

belong to middle income group,17( 56.6%). INCIDENCE OF OCC:Majority of the patients belonged to student community 16(53.33%)

OBSERVATIONS

ORIGIN OF THE DISEASE: The origin of the disease due to externalcauses were found in two subjects 6.66% and in majority of subjectsthe cause was endogenous 28(93.33%)

COLOUR OF THE PT: Majority of the subjects were wheatishskinned people14( 46.66%)

PRAKRITI: Majority of them belonged to vatapitta and Pitta vataprakruti 30%.

FAMILY HISTORY: Majority of the patients did not present with afamily history 29(96.66%)

STRESS: Majority of the patients did not present with history ofstress 25(76.66%).

CONSANGNIOUS MARRIAGE OF PARENTS: Majority of patientsdid not present with history of consangious marriage of parents24(80%).

OBSERVATIONS

CHRONICITY : Most had chronicity of disease from 1 month to 1 year20(66.66%)

Old/New cases: 15 patients were new and 15 patients were old whoalready received treatment else were.

AGE OF ONSET: In majority of patients disease started before theage of 20 yrs 15(49.99%)

SITE OF ONSET: In majority of subjects face was the site of firstonset 11(36.66%) followed by lower limbs 9( 30%)

Nature of spread: Among 30 subjects 29 of them presented withgradual spread of the disease 96.66%

History of allergy: Among 30 subjects 28 of them had no specifichistory of Allergies 93.33%

OBSERVATIONS

Colour of the patches: Among 30 subjects 23 of thempresented with white coloured patches 76.66%

Number of patches: Among 30 subjects 27 of them had 1-5number of patches on them 90%

Size of Patches (for 24 patients only): 19 of them presentedwith patches between 1-15cm size 82.60%

OBSERVATIONS

BEFORE TREATMENT AFTER TREATMENT

BEFORE TREATMENT AFTER TREATMENT

RESULTSResponded/Not responded

Sl.No. Parameter Responded

% Notresponded

%

1. Colour 24 80% 6 20%

2. Number 3 10% 27 90%

3. Size (for24

Pts)

11 45.8% 13 54.1%

Response in the colour of the patches

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 11 6 7 0 6

Response in the number of patches

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 0 2 1 0 27

Response in the size of the patches

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 3 6 1 1 13

Overall Results

Sl.No. Mild

(1-25%)

Moderate(26-50%)

Marked(51-75%)

Excellent(76-100%)

Noresponse

1. 18 4 2 0 6

Statistical analysis of the results

PARAME

TER

MEAN MEAN

DIFF.

STD

DEV

STD

ERR

t

Value

p

Value

REMARK

S

COLOUR

BT

4.44 0.84 0.48 0.08 6.6 < 0.0001 SIGNIFIC

ANT

COLOUR

AT

3.6 1.1 0.2

NUMBER

BT

1.66 0.28 2.23 0.41 1.7 <0.35 NOTSIGNIFIC

ANT

NUMBER

AT

1.38 1.94 0.36

SIZE BT 12.36 0.02 24.4 4.45 2.05 <0.1 NOTSIGNIFIC

ANT

SIZE AT 12.34 24.3 4.2

DISCUSSION

Switra is an ancient malady due to its references being cited in theVedas.

Switra can be well correlated to Vitiligo as both have similar clinicalfeatures and presentation of the disease. Both the diseases arerelated to hypopigmentation.

The etiology of vitiligo remains unknown, only the Triggering /Precipitating factors are identified, among which nutritionaldeficiency, emotional stress ,infections, exposure to chemicals areincluded. The etiology of Switra is given as incompatible diet,misconduct, improper life style.

No prodromal symptoms were seen. Swetavarna mandalas” were clearly evident,

CONT…

switra is “Twagatam” and “Aprasravi”accordingly in subjects the skin wasonly involved, no pain or secretions were noticed.

The macules were found to be of round, oval and irregular in shape. Among the mucosal surfaces ,lips were commonly involved. There are no special laboratory investigations to diagnose switra. From past two decades there is a sharp rise in the incidence of childhood

vitiligo (Behl) and the same was observed in this study. It was noticed that non –veg diet accelerated the disease progression. The origin of the disease due to trauma also holds significance. The higher the chronicity, it was observed that patients’ response to

treatment decreased. pts observed redness of patch, burnings sensation when exposed to sun.

COLOUR OF PATCH

Two kinds of pigmentation changes were noticed during thestudy

pigmentation started from periphery bringing aboutchanges in the size, such is peripheral repigmentation.

In some cases pigmentation spots were seen around the hairfollicles in the center of the patch, gradually

growing in size and changing the symmetry of the patch,such is perifollicular repigmentation.

The statistical analysis shows P<0.0001 which is significant.

NUMBER OF PATCHES

Among 30 patients , 27 presented with 1-5 no on theirbody. 1 patient had patches in between 6-10 and 2patients had more than 10 patches on the body.

Out of 3, 2 patients showed moderate response, 1patient showed marked response. No patient showedexcellent response.

The statistical analysis shows P<0.35 which is not –significant.

SIZE OF PATCHES

The change in the size of the patches was depended onthe colour changes.

The repigmentation occurring in the white patchesbrough about the difference in size.

Peripheral repigmentation caused Shrinkage in the sizeand perifollicular repigmentation brought about changesin symmetry (shape) which automatically broughtdifference in the size

The statistical analysis shows P<0.1 which is not-significant. But the response seen in the size of thepatches in duration of 45 days is commendable.

CONT.. In the first 15 days majority of them started showing changes in the

patches. The colour change was prominent, but there was no changein the number and size.

After 30 days, the colour grading improved remarkably, but nochange in the number was noticed.

After completion of 45 days – changes in the colour was even moresatisfactory.

Size differences in the patches were evident. Small patches of 1-3cms disappeared and some faded due to the pigmentation.

The improvements were noticed in patients with less chronicity,fresh cases with small sized patches.

LIMITATIONS OF THE STUDY

As the study does not have a control group, anycategorical statements about the successattribution to drug cannot be made.

The duration of the study was short, it wouldhave been better if the duration was for a longerperiod to establish the results even moreeffectively.

As the sample size is very small (30pts) anysignificant findings found in the study cannot begeneralized to the population.

RECOMMENDATIONS

Study to be conducted on larger samples. To do a comparative study between a control

group and test group with medicine takeninternally.

To do a comparative study between a controlgroup taking medicine internally and externallyand test group taking medicine only internally.

To take a longer duration of time for clinicalstudy.

To scientifically probe the action of Khadira onmelanocytes.

CONCLUSION

Switra is a pittapradhana tridoshaja, twak vikara. Sweta Varna mandalas appear on the skin suggestive of the disease. Based on the clinical features it can be well correlated to vitiligo of

contemporary medicine. The prevalence of the disease is 1% world wide, affecting males and

females equally, but more commonly reported by females. The incidence of childhood vitiligo is rapidly increasing from past

two decades. The age of first onset is before 20yrs, face and lowerlimbs are the

site of first appearance of the disease. Family history and H/o consangnious marriage of parents had little

role to play in the etiology.

CONT…

The drug proved to be beneficial as promising results were noticedinitially in response of colour and size. No much change in numberwas noticed.

Out of 30 patients – 18 patients showed mild response, 4 patientsmoderate response, 2 marked response and 6 members did notrespond to the treatment.

Better results can be established with “Dhatri-Khadira Kwath” ifstudy is conducted on larger samples, for a longer duration in acomparative fashion by enthusiastic scholars.

SUMMARY

A clinical study was undertaken to assess the efficacy of ‘Dhatri-Khadira Kwath’ in the disease switra.

Switra is related to hypopigmentation was selected for the study. 30 pts of either sex were taken for the study duration of 45 days

fulfilling the inclusion and exclusion criteria Comprehensive formula “Dhatri-Khadira Kwath” selected from

Bhaishajya Ratnavali was used in the clinical study Three parameters were taken to assess the improvement –colour

,number ,size of the mandalas. The work is divided into five parts which gives a detailed picture of

the disease, and clinical study.

THANK YOU

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Research in any field is the most important section of development. Ayurveda is inservice is for ages to the needy mankind to relieve their ailments and recording the factsfor the future generations. At present the Ayurveda research scholar, developing theAyurveda and understanding under the limelight of contemporary scientific backgrounds.The plagiarism is more and more now a day in the scientific community. This ishappening as the researches of the various institutions are not available for the commonresearcher. We wish to control this plagiarism by contributing the dissertations forscientific community. If you find any thesis is a copy of the previous publication, we takethis issue to the university authorities for proper action. The solution to prevent copy catsis … http://ayurvedaresearch.wordpress.com/

Dr. Shiva Rama Prasad Kethamakka

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Switram kc020 hyd

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