Psoriasis + Pitiriasis Versikolor Ncbl+Emed

8/3/2019 Psoriasis + Pitiriasis Versikolor Ncbl+Emed

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http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001470/ diunduh tangggal 22-11-2011 http://emedicine.medscape.com/article/1091575-clinical

Psoriasis Plaque psoriasis

Last reviewed: November 8, 2010.

Psoriasis is a common skin condition that causes skin redness and irritation. Most people with psoriasis havethick, red skin with flaky, silver-white patches called scales . See also: Guttate psoriasis Causes, incidence, and risk factors

Psoriasis is a very common condition. The disorder may affect people of any age, but it most commonly beginsbetween ages 15 and 35.

The condition cannot be spread to others.

Psoriasis seems to be passed down through families. Doctors think it probably occurs when the body's immunesystem mistakes healthy cells for dangerous substances. See also: Inflammatory response

Skin cells grow deep in the skin and normally rise to the surface about once a month. In persons with psoriasis,this process is too fast (about 2 weeks instead of 4 weeks) and dead skin cells build up on the skin's surface.

The following may trigger an attack of psoriasis or make the condition more difficult to treat:

Bacteria or viral infections, including strep throat and upper respiratory infections

Dry air or dry skin

Injury to the skin, including cuts, burns, and insect bites

Some medicines, including antimalaria drugs, beta-blockers, and lithium

Stress

Too little sunlight

Too much sunlight (sunburn)

Too much alcohol

In general, psoriasis may be severe in people who have a weakened immune system. This may include personswho have:

AIDS

Autoimmune disorders (such as rheumatoid arthritis )

Cancer chemotherapyUp to one-third of people with psoriasis may also have arthritis, a condition known as psoriatic arthritis.

Symptoms

Psoriasis can appear suddenly or slowly. In many cases, psoriasis goes away and then flares up again repeatedlyover time.

People with psoriasis have irritated patches of skin. The redness is most often seen on the elbows, knees, andtrunk, but it can appear anywhere on the body. For example, there may be flaky patches on the scalp.

The skin patches or dots may be:

Itchy
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Dry and covered with silver, flaky skin (scales)

Pink-red in color (like the color of salmon)

Raised and thick

Other symptoms may include:

Genital lesions in males

Joint pain or aching (psoriatic arthritis)

Nail changes , including nail thickening, yellow-brown spots, dents (pits) on the nail surface, andseparation of the nail from the base

Severe dandruff on the scalp

Psoriasis may affect any or all parts of the skin. There are five main types of psoriasis:

Erythrodermic -- The skin redness is very intense and covers a large area.

Guttate -- Small, pink-red spots appear on the skin.

Inverse -- Skin redness and irritation occurs in the armpits, groin, and in between overlapping skin.

Plaque -- Thick, red patches of skin are covered by flaky, silver-white scales. This is the mostcommon type of psoriasis.

Pustular -- White blisters are surrounded by red, irritated skin.

Signs and tests

Your doctor will look at your skin. Diagnosis is usually based on what the skin looks like.

Sometimes, a skin biopsy is done to rule out other possible conditions. If you have joint pain, your doctor mayorder x-rays.Treatment

The goal of treatment is to control your symptoms and prevent infections.

In general, three treatment options are used for patients with psoriasis:

Topical medications such as lotions, ointments, creams, and shampoos

Body-wide (systemic) medications, which are pills or injections that affect the whole body, not justthe skin

Phototherapy, which uses light to treat psoriasis

Most cases of psoriasis are treated with medications that are placed directly on the skin or scalp:

Cortisone creams and ointments

Creams or ointments that contain coal tar or anthralin

Creams to remove the scaling (usually salicylic acid or lactic acid)

Dandruff shampoos (over-the-counter or prescription)

Moisturizers

Prescription medicines containing vitamin D or vitamin A (retinoids)

If you have an infection, your doctor will prescribe antibiotics.
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You may try the following self-care at home:

Oatmeal baths may be soothing and may help to loosen scales. You can use over-the-counter oatmealbath products. Or, you can mix 1 cup of oatmeal into a tub of warm water.

Sunlight may help your symptoms go away. Be careful not to get sunburned.

Relaxation and antistress techniques may be helpful. The link between stress and flares of psoriasis isnot well understood, however.

Some people may choose to have phototherapy.

Phototherapy is a medical treatment in which your skin is carefully exposed to ultraviolet light.

Phototherapy may be given alone or after you take a drug that makes the skin sensitive to light.

Phototherapy for psoriasis can be given as ultraviolet A (UVA) or ultraviolet B (UVB) light.

Persons with very severe psoriasis may receive medicines to suppress the body's immune response. Thesemedicines include methotrexate or cyclosporine. (Persons who have psoriatic arthritis may also receive these

drugs.) Retinoids such as acitretin can also be used.

Newer drugs called biologics specifically target the body's immune response, which is thought to play a role inpsoriasis. These drugs are used when other treatments do not work. Biologics approved for the treatment of psoriasis include:

Adalimumab (Humira)

Alefacept (Amevive)

Etanercept (Enbrel)

Infliximab (Remicade)

Stelara

Support Groups See: Psoriasis support group Expectations (prognosis)

Psoriasis is a life-long condition that can be controlled with treatment. It may go away for a long time and thenreturn. With appropriate treatment, it usually does not affect your general physical health.

Complications

Arthritis

Pain

Severe itching

Secondary skin infections

Side effects from medicines used to treat psoriasis

Skin cancer from light therapy

Calling your health care provider

Call your health care provider if you have symptoms of psoriasis or if the skin irritation continues despitetreatment.

Tell your doctor if you have joint pain or fever with your psoriasis attacks.
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If you have symptoms of arthritis, talk to your dermatologist or rheumatologist.

Go to the emergency room or call the local emergency number (such as 911) if you have a severe outbreak thatcovers all or most of your body.

Prevention

There is no known way to prevent psoriasis. Keeping the skin clean and moist and avoiding your specificpsoriasis triggers may help reduce the number of flare-ups.

Doctors recommend daily baths or showers for persons with psoriasis. Avoid scrubbing too hard, because thiscan irritate the skin and trigger an attack.

References 1. Gottlieb A, Korman NJ, Gordon KB, Feldman SR, Lebwohl M, Koo JY, et al. Guidelines for the

management of psoriasis and psoriatic arthritis. Section 2. Psoriatic arthritis: overview and guidelinesof care for treatment with an emphasis on biologics. J Am Acad Dermatol . 2008;58:851-864.[PubMed ]

2. Menter A, Korman NJ, Elmets Ca, Feldman SR, Gelfand JM, Gordon KB, et al. American Academyof Dermatology guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3.Guidelines of care for the management and treatment of psoriasis with topical therapies. J Am Acad

Dermatol . 2009;60:643-659. [PubMed ] 3. Menter A, Gottlieb A, Feldman SR, Voorhees ASV, Leonardi CL, Gordon KB, et al. Guidelines for

the management of psoriasis and psoriatic arthritis. Section 1. Overview of psoriasis and guidelinesof care for the treatment of psoriasis with biologics. J Am Acad Dermatol . 2008;5:826-850.[PubMed ]

4. Stern RS. Psoralen and ultraviolet a light therapy for psoriasis. N Engl J Med . 2007;357(7):682-690.[PubMed ]

Review Date: 11/8/2010.

Reviewed by: Kevin Berman, MD, PhD, Atlanta Center for Dermatologic Disease, Atlanta, GA. Review provided by

VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

A.D.A.M., Disclaimer

Copyright 2011, A.D.A.M., Inc.
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BackgroundTinea versicolor is a common, benign, superficial cutaneous fungal infection usually characterized byhypopigmented or hyperpigmented macules and patches on the chest and the back. In patients with apredisposition, tinea versicolor may chronically recur. The fungal infection is localized to the stratumcorneum.

PathophysiologyTinea versicolor is caused by the dimorphic, lipophilic organisms in the genus Malassezia, formerlyknown as Pityrosporum . Eleven species are recognized within this classification of yeasts, ofwhich Malassezia globosa and Malassezia furfur are the predominant species isolated in tineaversicolor .[1, 2, 3, 4, 5] Malassezia is extremely difficult to propagate in laboratory culture and is culturableonly in media enriched with C12- to C14-sized fatty acids. Malassezia is naturally found on the skinsurfaces of many animals, including humans. Indeed, it can be isolated in 18% of infants and 90-100% of adults.

The organism can be found on healthy skin and on skin regions demonstrating cutaneous disease. Inpatients with clinical disease, the organism is found in both the yeast (spore) stage and thefilamentous (hyphal) form. Factors that lead to the conversion of the saprophytic yeast to the parasitic,

mycelial morphologic form include a genetic predisposition; warm, humid environments;immunosuppression; malnutrition; and Cushing disease. Human peptide cathelicidin LL-37 plays arole in skin defense against this organism.

Even though Malassezia is a component of the normal flora, it can also be an opportunistic pathogen.The organism is considered to be a factor in other cutaneous diseases, including Pityrosporum folliculitis , confluent and reticulate papillomatosis , seborrheic dermatitis , and some forms of atopicdermatitis .

EpidemiologyFrequency

United States

Tinea versicolor occurs more frequently in areas with higher temperatures and higher relativehumidities. The national prevalence of this condition is 2-8% of the population. The exact incidence inthe United States is difficult to assess because many individuals who are affected may not seekmedical attention.

International

Tinea versicolor occurs worldwide, with prevalences reported to be as high as 50% in the humid, hotenvironment of Western Samoa and as low as 1.1% in the colder temperatures of Sweden.

Mortality/Morbidity

Tinea versicolor is a benign skin disease that causes scaly macules or papules on the skin. As thename implies ( versi means several), the condition can lead to discoloration of the skin, with colorsranging from white to red to brown. The condition is not considered to be contagious because thecausative fungal pathogen is a normal inhabitant of the skin.The skin of an individual who is affected by tinea versicolor may be either hypopigmented orhyperpigmented. In the case of hypopigmentation, tyrosinase inhibitors (resulting from the inhibitoryaction of tyrosinase of dicarboxylic acids formed through the oxidation of some unsaturated fatty acidsof skin surface lipids) competitively inhibit a necessary enzyme of melanocyte pigment formation. Inhyperpigmented macules in tinea versicolor, the organism induces an enlargement of melanosomesmade by melanocytes at the basal layer of the epidermis.Race

Although the alteration in skin pigmentation is more apparent in darker-skinned individuals, theincidence of tinea versicolor appears to be the same in all races.

Sex

Several studies have addressed the frequency of tinea versicolor based on sex, and no dominance ofeither sex is apparent.
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Age

In the United States, tinea versicolor is most common in persons aged 15-24 years, when thesebaceous glands are more active. The occurrence of tinea versicolor before puberty or after age 65years is uncommon .[6] In more tropical countries, age frequency varies; most cases involve peopleaged 10-19 years who live in warmer, humid countries, such as Liberia and India.

Proceed to Clinical Presentation

HistoryMost individuals with tinea versicolor report cosmetically disturbing, abnormal pigmentation.

The involved skin regions are usually the trunk, the back, the abdomen, and the proximalextremities. The face, the scalp, and the genitalia are less commonly involved.The color of each lesion varies from almost white to reddish brown or fawn colored.A fine, dustlike scale covers the lesions.

Tinea versicolor patients often report that the involved skin lesions fail to tan in the summer.Occasionally, a tinea versicolor patient also reports mild pruritus.Greater than 20% of tinea versicolor patients report a positive family history of the condition. Thissubset of patients records a higher rate of recurrence and longer duration of disease .[7] PhysicalTinea versicolor can present in 4 forms.

Tinea versicolor - Form 1o The most common appearance of the disease is as numerous, well-marginated, finely scaly, oval-

to-round macules scattered over the trunk and/or the chest, with occasional extension to the lowerpart of the abdomen, the neck, and the proximal extremities.

o The macules tend to coalesce, forming irregularly shaped patches of pigmentary alteration. As thename versicolor implies, the disease characteristically reveals a variance in skin hue. The involvedareas can be either darker or lighter than the surrounding skin.

o The condition is more noticeable during the summer months when the discrepancy in color from

the normal skin becomes more apparent.o Light scraping of the involved skin with a scalpel blade characteristically yields a copious amount

of keratin.Tinea versicolor - Form 2

o An inverse form of tinea versicolor also exists in which the condition has an entirely differentdistribution, affecting the flexural regions, the face, or isolated areas of the extremities. This formof tinea versicolor is more often seen in hosts who are immunocompromised.

o This form of the disease can be confused with candidiasis, seborrheic dermatitis, psoriasis,erythrasma, and dermatophyte infections.

Tinea versicolor - Form 3o The third form of Malassezia infections of the skin involves the hair follicle. This condition is

typically localized to the back, the chest, and the extremities.o This form can be clinically difficult to differentiate from bacterial folliculitis. The presentation

of Pityrosporum folliculitis is a perifollicular, erythematous papule or pustule.o Predisposing factors include diabetes, high humidity, steroid or antibiotic therapy, and

immunosuppressant therapy. Additionally, several reports reveal that M furfur also plays a rolein seborrheic dermatitis .

Tinea versicolor - Form 4o Another clinical presentation is multiple firm, 2- to 3-mm, monomorphic, red-brown, inflammatory

papules. These lesions may, or may not also demonstrate a fine white scale.o The lesions are usually found on the torso and are asymptomatic.o Histologically, the rash demonstrates not only fungal hyphae and spores in the stratum corneum,

but also an interface dermatitis in the superficial dermis . [8] CausesMost cases of tinea versicolor occur in healthy individuals with no immunologic deficiencies.

Nevertheless, several factors predispose some people to develop this condition. These factorsinclude genetic predisposition; warm, humid environments; immunosuppression; malnutrition; andCushing disease .[9, 10]
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The reason why this organism causes tinea versicolor in some individuals while remains as normalflora in others is not entirely known. Several factors, such as the organism's nutritional requirementsand the host's immune response to the organism, are significant.

The organism is lipophilic, and lipids are essential for growth in vitro and in vivo. Furthermore, themycelial stage can be induced in vitro by the addition of cholesterol and cholesterol esters to the

appropriate medium. Because the organism more rapidly colonizes humans during puberty when skinlipids are increased more than that of adolescent levels and tinea versicolor is manifested in sebum-rich areas (eg, chest, back), individual variations in skin surface lipids are hypothesized to play amajor role in disease pathogenesis. However, patients with tinea versicolor and control subjects donot demonstrate any quantitative or qualitative differences in skin surface lipids. Skin surface lipidsare significant for the normal presence of M furfur on human skin, but they probably play little role inthe pathogenesis of tinea versicolor.

Evidence has been accumulating to suggest that amino acids, rather than lipids, are critical for theappearance of the diseased state. In vitro, the amino acid asparagine stimulates the growth of theorganism, while another amino acid, glycine, induces hyphal formation. In vivo, the amino acid levelshave been shown to be increased in the uninvolved skin of patients with tinea versicolor in 2 separatestudies.

Another significant causative factor is the patient's immune system. Although sensitization against M furfur antigens is routinely present in the general population (as proven by lymphocyte transformationstudies), lymphocyte function on stimulation with the organism has been shown to be impaired inpatients who are affected. This outcome is similar to the situation of sensitization with Candida albicans . In short, cell-mediated immunity plays some role in disease causation.

Proceed to Differential Diagnoses Laboratory StudiesThe clinical presentation of tinea versicolor is distinctive, and the diagnosis is often made without anylaboratory documentation.

The ultraviolet black (Wood) light can be used to demonstrate the coppery-orange fluorescence oftinea versicolor. However, in some cases, the lesions appear darker than the unaffected skin under

the Wood light, but they do not fluoresce.The diagnosis is usually confirmed by potassium hydroxide (KOH) examination, which demonstratesthe characteristic short, cigar-butt hyphae that are present in the diseased state. The KOH finding ofspores with short mycelium has been referred to as the spaghetti and meatballs or the bacon andeggs sign of tinea versicolor. For better visualization, ink blue stain, Parker ink, methylene bluestain, or Swartz-Medrik stain can be added to the KOH preparation. Contrast stain containing 1%Chicago sky blue 6B and 8% KOH (as the clearing agent) achieves the greatest sensitivity andspecificity .[11] Special media are required for culture. Because the diagnosis is usually clinically suspected and canbe confirmed with a KOH preparation, cultures are rarely obtained.

With blood examination, no definitive deficiencies of normal antibodies or complement are present inpatients with tinea versicolor, but research continues in this area.

For example, although individuals who are affected reveal no specific antibody levels above those ofage-matched controls, M furfur antigens do elicit a specific immunoglobulin G response in patientswith seborrheic dermatitis and tinea versicolor detected by enzyme-linked immunosorbent assayand Western blotting assays.

M furfur does induce immunoglobulin A, immunoglobulin G, and immunoglobulin M antibodies, andit can activate complement via both the alternate pathway and the classical pathway.Various studies have found defects in lymphokine production, natural killer T cells, decreasedphytohemagglutinin and concanavalin A stimulation, interleukin 1, interleukin 10, and interferongamma production by lymphocytes in patients.Although these tests do not suggest an immunologic disorder, they do suggest a reduced bodyresponse to the specific fungal elements that produce tinea versicolor. Further assessment iswarranted.

Next Section: Histologic Findings
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Histologic FindingsThe organism that causes tinea versicolor is localized to the stratum corneum. M furfur can bedetected by hematoxylin and eosin (H&E) alone, although periodic acid-Schiff (PAS) or methenaminesilver staining are more confirmatory. On rare occurrences, the organism can approach the stratumgranulosum, and it can even be found inside keratinocytes . [12] The epidermis reveals mildhyperkeratosis and acanthosis, and a mild perivascular infiltrate is present in the dermis. Anacanthosis nigricans like epidermal change is noted in the papular variety, with dilated blood vesselsobserved in erythematous lesions.

Medical CarePatients should be informed that tinea versicolor is caused by a fungus that is normally present on theskin surface and is therefore not considered contagious. The condition does not leave any permanentscar or pigmentary changes, and any skin color alterations resolve within 1-2 months after treatmenthas been initiated. Recurrence is common, and prophylactic therapy may help reduce the high rate ofrecurrence.

Tinea versicolor can be successfully treated with various agents. Effective topical agents includeselenium sulfide, sodium sulfacetamide, ciclopiroxolamine , [13] as well as azole and allylamine

antifungals .[14, 15, 16]

Various regimens can be used. Selenium sulfide lotion is liberally applied toaffected areas of the skin daily for 2 weeks; each application is allowed to remain on the skin for atleast 10 minutes prior to being washed off. In resistant cases, overnight application can be helpful.Topical azole antifungals can be applied every night for 2 weeks. Weekly application of any of thetopical agents for the following few months may help prevent recurrence. In patients withwidespread disease, topical antifungal therapy can be expensive. Topical allylamines have beendemonstrated to be clinically and mycologically effective.Oral therapy is also effective for tinea versicolor and is often preferred by patients because it is moreconvenient and less time consuming. Of course, oral therapy can be used in consort with topicalregimens. Ketoconazole, fluconazole, and itraconazole are the preferred oral agents . [17, 18, 19] Variousdosing regimens have been used. With ketoconazole, a 10-day 200-mg daily therapy and as asingle-dose 400-mg treatment are popular, both with comparable results . [20] Fluconazole has beenoffered as a single 150- to 300-mg weekly dose for 2-4 weeks. Itraconazole is usually given at 200

mg/d for 7 days. Pramiconazole and sertaconazole have also been used in the management oftinea versicolor .[21, 22] Oral therapy does not prevent the high rate of recurrence, and treatment with oral ketoconazole or atopical agent may need to be repeated intermittently throughout the year. Because tinea versicoloris a benign condition and oral therapy is not without risk, the decision to treat with an oral agentshould be made only after a complete discussion of the risks involved .[23] In the case of oralterbinafine, some subgroups of M furfur apparently are not clinically responsive, although in vitrostudies suggest fungistatic activity .[24] Also, a regimen of 1 tablet a month of ketoconazole,fluconazole, and itraconazole has been used successfully to prophylactically prevent recurrences . [25] Also see the clinical trial, Ketoconazole Foam 2% for the Treatment of Versicolor .

Surgical CareReports describe successful treatment of tinea versicolor with 5-aminolevulinic acid photodynamictherapy .[

DietDietary alterations have not proved successful in the treatment of tinea versicolor.

Medication SummaryTinea versicolor responds well to both topical and oral antimycotic therapies. Many patients preferoral therapy because of its convenience.

AntifungalsClass Summary

Topical antifungals temporarily eradicate the condition, although treatment may need to beintermittently repeated to prevent recurrence. Oral therapy for tinea versicolor is convenient and
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effective, but it does not prevent recurrences. A once-monthly (for 6 mo) oral dose of fluconazole is apopular alternative.

View full drug information

Terbinafine topical (Lamisil)

Inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal cell death. Usemedication until symptoms significantly improve. Duration of treatment should be >1 wk but not >4 wk.


Clotrimazole topical

Broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability,causing fungal cell death. Reevaluate diagnosis if no clinical improvement after 4 wk.


Ketoconazole (Nizoral)

Both topical and systemic agent. Imidazole broad-spectrum antifungal agent; inhibits synthesis ofergosterol, causing cellular components to leak, resulting in fungal cell death. Achieves excellent skinlevels with minimal oral dosing. M furfur is eradicated by the presence of ketoconazole in outer skinlayers. Tinea versicolor is extremely rare in small children; thus, do not treat children aged < 10 y withoral ketoconazole for tinea versicolor.


Ciclopirox (Loprox)

Interferes with synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements infungal cells.


Butenafine (Mentax)

Damages fungal cell membranes causing fungal cell growth to arrest.


Naftifine (Naftin)

Broad-spectrum antifungal agent and synthetic allylamine derivative; may decrease the synthesis ofergosterol, which, in turn, inhibits fungal cell growth. If no clinical improvement after 4 wk, reevaluatethe patient.


Econazole (Spectazole)

Effective in cutaneous infections. Interferes with RNA and protein synthesis and metabolism. Disruptsfungal cell wall membrane permeability, causing fungal cell death.

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Oxiconazole (Oxistat)

Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeabilityis increased, causing nutrients to leak out and resulting in fungal cell death.

Further Outpatient CareTinea versicolor has a high rate of recurrence, and prophylactic treatment with topical or oral therapyon an intermittent basis is necessary to prevent recurrences in most cases.

\ PrognosisAlthough tinea versicolor is recurrent for some patients and, therefore, a chronic disease, thecondition remains treatable with the available remedies (see Medical Care and Medication). Thus, theprognosis is excellent.

Patient EducationPatients need to realize that tinea versicolor is caused by a fungus that is normally present on the skinsurface; thus, it is not considered a contagious disease. Sequelae from the disease are notpermanent, and any pigmentary alterations resolve entirely 1-2 months after treatment is initiated.Treatment is needed to remedy the condition and for prophylaxis to prevent

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