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Transcript of Ing3 Completed
THE RISK AND BENEFITS OF TEA IN GENERAL
HEALTH
Written by:
AYUNDA AFDAL
030. 09. 040
FACULTY OF MEDICINE
TRISAKTI UNIVERSITY
JAKARTA, DECEMBER 2012
ABSTRACT
All tea is produced from a plant called Camellia sinensis.1 The Camellia
Sinensis plant is native to Asia, but is currently cultivated around the world in
tropical and subtropical areas. With over 3,000 varieties, tea is the most
consumed beverage in the world after water.2 Tea can be divided into five basic
categories: black, green, oolong, white, and puerh.
Tea contains a large number of potentially bioactive chemicals, including
flavonoids (antioxidant), polyphenols, vitamins & mineral, theanine, caffeine,
and several polysaccharides, and a variety of health effects have been proposed
and investigated. Due to modern day environmental pollution fluoride and
aluminium have also been found to occur in tea. Tea also contains small
amounts of theobromine and theophylline. 3
Keywords : tea, antioxidant, flavinoids, polyphenols, vitamin & mineral,
theanine, caffeine.
INTRODUCTION
People have turned to tea to soothe body and soul for more than 5,000
years. In China, tea has served medicinal purposes since ancient times.
According to the November issue of Mayo Clinic Women's HealthSource,
modern science has confirmed potential health benefits of tea. 4
Tea is an aromatic beverage commonly prepared by pouring hot or
boiling water over cured leaves of the tea plant. All tea is produced from a plant
called Camellia sinensis.1 The Camellia Sinensis plant is native to Asia, but is
currently cultivated around the world in tropical and subtropical areas. With
over 3,000 varieties, tea is the most consumed beverage in the world after water.
The differences between teas arise from processing, growing conditions,
and geography. The fermentation process of these leaves also defines the
different types of teas. Black tea undergo long fermentation. Green and white
tea undergo the least processing and are steamed quickly. All teas contain
polyphenols. Tea can be divided into five basic categories: black, green, oolong,
white, and puerh.
Black tea is allowed to wither, which precedes a process called oxidation
(sometimes incorrectly referred to as fermentation) during which water
evaporates out of the leaf and the leaf absorbs more oxygen from the air. Black
teas usually undergo full oxidation, and the results are the characteristic dark
brown and black leaf, the typically more robust and pronounced flavors of black
teas, and, when brewed appropriately, a higher caffeine content compared to
other teas (50-65% of coffee, depending on the type and brewing technique).
Green tea is allowed to wither only slightly after being picked. Then the
oxidation process is stopped very quickly by firing (rapidly heating) the leaves.
Therefore, when brewed at lower temperatures and for less time, green teas tend
to have less caffeine (10-30% of coffee).
Oolong tea (also known as wulong tea) is allowed to undergo partial
oxidation. These teas have a caffeine content between that of green teas and
black teas. The flavor of oolong (wulong) teas is typically not as robust as
blacks or as subtle as greens, but has its own extremely fragrant and intriguing
tones. Oolongs (wulongs) are often compared to the taste and aroma of fresh
flowers or fresh fruit.
White teas are the most delicate of all teas. They are appreciated for their
subtlety, complexity, and natural sweetness. They are hand processed using the
youngest shoots of the tea plant, with no oxidation. When brewed correctly,
with a very low temperature and a short steeping time, white teas can produce
low amounts of caffeine.
Puerh is an aged black tea from China prized for its medicinal properties
and earthy flavor. It is perhaps the most mysterious of all tea. Until 1995 it was
illegal to import it into the U.S., and the process of its production is a closely
guarded state secret in China. It is very strong with an incredibly deep and rich
flavor, and no bitterness, and an element that could best be described as almost
peaty in flavor. 2
Tea contains a large number of potentially bioactive chemicals, including
flavonoids (antioxidant), polyphenols, vitamins & mineral, theanine, caffeine,
and several polysaccharides, and a variety of health effects have been proposed
and investigated. Due to modern day environmental pollution fluoride and
aluminium have also been found to occur in tea. Tea also contains small
amounts of theobromine and theophylline. 2
It has been suggested that green and black tea may protect against cancer,
though the catechins found in green tea are thought to be more effective in
preventing certain obesity-related cancers such as liver and colorectal while
both green and black tea may protect against cardiovascular disease. 3
Numerous recent epidemiological studies have been conducted to
investigate the effects of green tea consumption on the incidence of human
cancers. These studies suggest significant protective effects of green tea against
oral, pharyngeal, esophageal, prostate, digestive, urinary tract, pancreatic,
bladder, skin, lung, colon, breast, and liver cancers, and lower risk for cancer
metastasis and recurrence.6
Healthy consumption of two to three cups a day may reduce the chances
of heart attack and stroke. Drinking tea may keep the arteries smooth and clog-
free. Dr. Carrie Ruxton and colleagues at Kings College London found clear
evidence that drinking three to four cups of tea a day can cut the chances of
having a heart attack.3
DISCUSSION
Tea contains a large number of potentially bioactive chemicals, including
flavonoids (antioxidant), polyphenols, vitamins & mineral, theanine, caffeine,
and several polysaccharides, and a variety of health effects have been proposed
and investigated. Due to modern day environmental pollution fluoride and
aluminium have also been found to occur in tea. Tea also contains small
amounts of theobromine and theophylline. 3
Antioxidants counter the harmful effects of free radicals. Free radicals are
unstable molecules that attack other molecules in the body, leading to cell
damage. Antioxidants inhibit the oxidation reactions caused by free radicals,
thereby preventing damage to cells and tissues. The type and amount of
flavonoid contained in tea depends on the variety of leaf, growing environment,
processing, and brewing method. Green tea contains mostly simple flavonoids
called catechins while black tea contains more complex varieties called
theaflavins and thearubigins. Re3Scientists have demonstrated that flavonoids,
which are polyphenolic compounds, exhibit antioxidant activity. 14
Catechin is a flavan-3-ol, a type of natural phenol and antioxidant. It is a
plant secondary metabolite. It belongs to the group of flavan-3-ols (or simply
flavanols). It is often considered to belong to the family of flavonoids.
Catechins are highest in concentration in white and green teas, while black tea
has substantially fewer due to its oxidative preparation. The health benefits of
catechins have been studied extensively in humans and animal models. Many
studies on health benefits have been linked to the catechin content. According to
Norman Hollenberg, professor of medicine at Harvard Medical School,
epicatechin can reduce the risk of four of the major health problems: stroke,
heart failure, cancer and diabetes.
Polyphenol protect cells and body chemicals against damage caused by
free radicals, reactive atoms that contribute to tissue damage in the body.
Polyphenols is a kind of chemical that may protect against some common health
problems and possibly certain effects of aging. They can also block the action
of enzymes that cancers need for growth and they can deactivate substances that
promote the growth of cancers.
In addition, polyphenols also activate the key enzyme (AMP kinase) that
helps restore cellular ATP levels. At high enough levels, these chemical
substances can exert an anti-inflammatory effect by inhibiting the activation of
inducible inflammatory proteins that normally occurs once the innate immune
system has been activated. Blood levels of polyphenols will peak soon after
they are consumed, then decrease as they are metabolized or excreted from the
body. Some will not be absorbed into the bloodstream, but will merely pass
through the digestive tract. These are very important as well because they may
help to prevent colon cancer and such diseases.
Polyphenols actively work in the body to prevent certain disease
mechanisms from occuring. They work in the body to enhance health in
complex ways, and as such they are not simply antioxidants. Their specific
health-promoting actions are still being actively researched, and it is generally
recognized that polyphenols can reduce the risk factors for cardiovascular
disease and basically help to protect many body systems from the risks or
ravages of many types of chronic disease.
The following vitamins are naturally found in tea:
• Vitamin C – a recent study showed that black tea, green tea and oolong tea are
all extremely good sources of vitamin C, a potent antioxidant.
• Carotene, a precursor to vitamin A, has antioxidant and protective properties.
• Thiamine (vitamin B1) and pantothenic acid are necessary for the release of
energy from fat and carbohydrate. (pictured here)
• Vitamin B6 is involved in metabolism proteins
• Folic Acid plays a role in cell division.
Tea is a good source of essential minerals:
• Manganese is essential for bone growth and development.
• Potassium is vital for maintaining a healthy heart. It enables nerves and
muscles to function and regulates fluid levels within the cells. Deficiency
leads to erratic heartbeat and fatigue.
• Fluoride is the most successful agent against.tooth decay ever discovered. Tea
is one of the few natural sources of fluoride. High fluoride intake (daily
intakes over 2 mg for children, 4 mg adults) increases the risk
osteofluorosis and fractures.12
Theanine is an amino acid found in tea. Theanine has a chemical structure
very similar to glutamate, a naturally occurring amino acid in the body that
helps transmit nerve impulses in the brain. Theanine has been shown to reduce
mental and physical stress. Theanine also promotes alpha wave production in
the brain, which is the part of the brain that is stimulated during meditation.
Caffeine is a bitter, white crystalline xanthine alkaloid that acts as a
stimulant drug. In humans, caffeine acts as a central nervous system stimulant,
temporarily warding off drowsiness and restoring alertness, alleviating fatigue,
increasing wakefulness, and improving concentration and focus. Caffeine is
toxic at sufficiently high doses. Ordinary consumption can have low health
risks, even when carried on for years – there may be a modest protective effect
against some diseases, including certain types of cancer. Caffeine can have both
positive and negative effects on anxiety disorders. Some people experience
sleep disruption if they consume caffeine, especially during the evening hours,
but others show little disturbance and the effect of caffeine on sleep is highly
variable. 5.8
Effect on the body :
• Hormones- You can feel the effects of caffeine in your system within a few
minutes of ingesting it, and it stays on your system for many hours—it
has a half-life of four to six hours in your body. While in your body,
caffeine affects the following hormones:
• Adenosine- Can inhibit absorption of adenosine, which calms the body, which
can make you feel alert in the short run, but can cause sleep problems
later.
• Adrenaline- Caffeine injects adrenaline into your system, giving you a
temporary boost, but possibly making you fatigued and depressed later. If
you take more caffeine to counteract these effects, you end up spending
the day in an agitated state, and might find yourself jumpy and edgy by
night.
• Cortisol- Can increase the body’s levels of cortisol, the “stress hormone”,
which can lead to other health consequences ranging from weight gain
and moodiness to heart disease and diabetes.
• Dopamine- Caffeine increases dopamine levels in your system, acting in a
way similar to amphetamines, which can make you feel good after taking
it, but after it wears off you can feel ‘low’. It can also lead to a physical
dependence because of dopamine manipulation.
These changes caffeine makes in your physiology can have both positive
and negative consequences:
• Sleep.
Caffeine can affect your sleep by keeping you awake longer, thereby
shortening the amount of sleep you get, and giving you less time in the
restorative stages of sleep, which takes a toll on your level of alertness the
next day and overall health. Interestingly, though, caffeine doesn’t affect
the stages of sleep the way other stimulants do, so it’s a better choice than
speed or other ‘uppers’ to use if you need to stay awake.
• Weight.
Many experts believe that increased levels of cortisol lead to stronger
cravings for fat and carbohydrates, and cause the body to store fat in the
abdomen. (Abdominal fat carries with it greater health risks than other
types of fat.) Also, if increased cortisol levels lead to stronger cravings
for caffeine-laden foods, the body goes into a cycle that leads only to
worse health. The good news, though, is that caffeine can speed up
metabolism. Also, it can help the body break down fat about 30% more
efficiently if consumed prior to exercise. (You must be exercising to get
this benefit, though.) Additionally, caffeine can keep blood sugar levels
elevated, leaving you feeling less hungry.
• Exercise.
If caffeine elevates levels of cortisol and other hormones for a temporary
boost, after caffeine wears off, the body can feel fatigued and feelings of
mild to moderate depression can set in. This can make physical activity
more difficult. On the positive side, caffeine has been found to enhance
physical performance and endurance if it isn’t overused. This, combined
with its effect of fat burning during exercise, can actually enhance
workouts and enable you to get in better shape if you take it at the right
time.8
How the tea is actually prepared plays an important role in how much
caffeine makes it into your cup. Everything, from the amount of tea used to
water temperature and brewing time to whether the leaves are steeped loose, in
a tea bag, or strainer, becomes a factor. In general, though, more tea, hotter
water, and longer steeping all contribute to more caffeine pecup.
A report by the Department of Nutritional Services provides the
following ranges of caffeine content for a cup of tea made with loose leaves: 9
Beverage Caffeine
White Tea 6-25 mg
Green Tea 8-36 mg
Oolong Tea 12-55 mg
Black Tea 23-110 mg
For most healthy adults, moderate doses of caffeine — 200 to 300
milligrams (mg), or about two to four cups of brewed coffee a day — aren't
harmful. But some circumstances may warrant limiting or even ending your
caffeine routine.
Although moderate caffeine intake isn't likely to cause harm, too much
can lead to some unpleasant effects. Heavy daily caffeine use — more than 500
to 600 mg a day — may cause: insomnia, nervousness, restlessness, irritability,
stomach upset, fast heartbeat, muscle tremors. 7
Drinking tea is actually better for you than drinking water. Water is
essentially replacing fluid. Tea replaces fluids and contains antioxidants, so it's
got two things going for it." Tea keeps people hydrated. A caffeinated beverage,
tea definitely contributes to the fluid needs, except when taken in a high
quantity (more than five or six cups at one time). Drinking tea may develop a
strong immune system and prevent the body against infection. Claire
Williamson of the British Nutrition Foundation said, "Studies in the laboratory
have shown potential health benefits.” 11
Drinking tea leads to certain health hazards which can't be ignored.
Researchers show that anemic people should avoid drinking tea around meal
times as it can impair the body's ability to absorb iron from food. If tea is
consumed with sugar, it my lead to health ill effects like acidity, tooth decay
and gum problems. More than three to four cups of tea a day is not considered
healthy for the body.
Drinking three to four cups of tea without any sugar and cream is a
healthy choice, offering many health benefits. The beneficial polyphenols are
derived to the maximum if tea is brewed for at least three to five minutes. The
aromatic flavor rejuvinates the mind and keeps the body fit and healthy. 6
CONCLUSION
Tea contains a large number of potentially bioactive chemicals, including
flavonoids (antioxidant), polyphenols, vitamins & mineral, theanine, caffeine,
and several polysaccharides, and a variety of health effects have been proposed
and investigated.3 Drinking three to four cups of tea is a healthy choice, offering
many health benefits. But more than three to four cups of tea a day is not
considered healthy for the body. 11
REFERENCES
1. Laura C. Martin (15 May 2007). Tea: The Drink that Changed the World.
Tuttle Publishing. p. 8. Retrieved 31 October 2012.
2. Edgar Julie. Types of Tea and Their Health Benefits. Available at:
http://www.webmd.com/diet/features/tea-types-and-their-health-benefits.
Accessed on : December 3rd 2012.
3. Brown CA, Bolton‐Smith C, Woodward M, Tunstall‐Pedoe H. Coffee
and tea consumption and the prevalence of coronary heart disease in men
and women: results from the Scottish Heart Health Survey. J Epidemiol
Com Health1993; 47:171–5.
4. Mayo Clinic Staff. Tea : Enjoy a Cup for Health and Pleasure. Available
at : http://www.mayoclinic.org/news2010-mchi/6046.html. Accessed on :
December 3rd 2012.
5. Bell Kimberly. Theanine. Available at :
http://www.webmd.com/vitamins-supplements/ingredientmono-
1053THEANINE.aspx?. Accessed on : December 3rd 2012.
6. Benefit of drinking green tea. Available at :
http://www.health.harvard.edu/press_releases/benefit_of_drinking_green
_t. Accessed on : December 3rd 2012.
7. Magee Elaine. Healthier Ways to Get Your Caffeine. Available at :
http://www.webmd.com/diet/features/healthier-ways-to-get-your-
caffeine. Accessed on : December 3rd 2012.
8. Attwood A, et al. Differential responsiveness to caffeine and perceived
effects of caffeine in moderate and high regular caffeine consumers.
Psychopharmacology. 2007;190:469.
9. Caffeine. Natural Medicines Comprehensive Database. Available on :
http://www.naturaldatabase.com. Accessed December 9th 2012.
10.Chin JM, et al. Caffeine content of brewed teas. Journal of Analytical
Toxicology. 2008;32:702.
11.Mayo clinic staff. Caffeine : How much is too much?. Available on :
http://www.mayoclinic.com/health/caffeine/AN01211 . Accessed on :
December 3rd 2012.
12. Jianyun Ruan and Ming H. Wong. "Accumulation of Fluoride and
Aluminium Related to Different Varieties of Tea Plant". Environmental
Geochemistry and Health. 2001. p.53–63.
13. Spencer, Jeremy P. E. "Flavonoids: modulators of brain function?".
British Journal of Nutrition. 2009. p.60–77.
14. Mattill, H A. "Antioxidants". Annual Review of Biochemistry. 2009. p.
77–92.
ISO Implementation in Medical Practice
Azmi Ikhsan Azhary
030.09.043
FACULTY OF MADICINE
TRISAKTI UNIVERSITY
2012
Abstract
ISO, stands for International Standardization Organization is an international standard-setting
body composed of representatives from various national standards organizations. ISO sets the
standards of many things. ISO ensure that products and services are safe, reliable and of good
quality. In medical field, they sets standards in some areas, but I will only talk about 1
standard that I think is very crucial. ISO 15189 about Medical laboratories — Particular
requirements for quality and competence.
ISO 15189is for use by medical laboratories in developing their quality management systems
and assessing their own competence, and for use by accreditation bodies in confirming or
recognising the competence of medical laboratories.1
Keywords: ISO, Quality Management System, ISO 15189
Introduction
About ISO
The International Organization for Standardization (ISO) is a worldwide federation of national
standards bodies from some 100 countries.ISO is a non-governmental organization established in
1947. The mission of ISO is to promote the development of standardization and related activities in
the world with a view to facilitating the international exchange of goods and services, and to
developing cooperation in the spheres of intellectual, scientific, technological and economic
activity.ISO's work results in international agreements are published as International Standards.2
International standardization : What does it achieve ?
Industry-wide standardization is a condition existing within a particular industrial sector when the
large majority of products or services conform to the same standards. It results from consensus
agreements reached between all economic players in that industrial sector - suppliers, users, and
often governments. They agree on specifications and criteria to be applied consistently in the choice
and classification of materials, the manufacture of products, and the provision of services. The aim is
to facilitate trade, exchange and technology transfer through :
Enhanced product quality and reliability at a reasonable price,
Improved health, safety and environmental protection, and reduction of waste,
Greater compatibility and interoperability of goods and services,
Simplification for improved usability,
Reduction in the number of models, and thus reduction in costs,
Increased distribution efficiency, and ease of maintenance.
Users have more confidence in products and services that conform to International Standards.
Assurance of conformity can be provided by manufacturers' declarations, or by audits carried out by
independent bodies.3
The ISO Standardization Process
Each member body who has an interest in the work of a committee is entitled to be a member of
that committee. Standards are reached by consensus with each member organization representing
the interests of the vendors, manufacturers, consumers, profession als, and government of it's
country.
Each standard goes through a six stage process before being published as an ISO standard.
The first stage is the proposal stage in which a need for a standard is determined and
members are identified who are willing to work on it. The standards then ent ers the
preparatory stage where a working draft of the standard is developed. When the working draft
is completed, it enters the committee stage and is sent out for comments until a consensus is
reached. The output of this stage is the Draft Internation al Standard (DIS). The DIS then
enters the enquiry stage where it is circulated among all member bodies and then voted upon.
If a DIS does not receive 75% of the vote, it returns to lower stages and work on it continues.
If it passes the enquiry stage , it becomes a Final Draft International Standard and enters the
approval stage. During this stage it will again circulate through all member bodies for a final
vote and again it must pass this stage with 75% of the vote. If the standard passes this stage, it
enters the publication stage and is sent to the ISO Central Secretariat for publication.4
ISO 15189
ISO 15189 (Medical laboratories - particular requirements for quality and competence) is a standard
which contains requirements for medical laboratories to prove their competence in providing
trustworthy service. This standard contains the competence of personnel that involved in the
examination in the medical laboratory, the facility and its equipment, reagents and supplies, factors
pre-inspection, inspection, quality assurance considerations, and factors of post-inspection.
It is an initiative that presents a global concerted approach in creating a standardized measure for
management practices in medical laboratories. An ISO 15189 certification has been seen as a critical
initiative towards harmonizing global practices in medical laboratories towards a common measure
of quality assurance and safety. The approach takes into account a lot of perspectives, including the
interpretation of test results, the method patient samples are actually collected as well as the time
required for the tests to be carried out.
The following are the basic requirements for ISO 15189 certification:
A well documented procedure analysis by the laboratories.
Training manual provided by the laboratories.
ISO 15189 requires an effective detailed analysis of medical laboratory procedures in a bid to
make sure that all weaknesses have been identified.
Detailed evaluation reports of the existing quality management system as well as other
monitoring and evaluation reports.
A detail audit of management reviews5
Discussions
According to my source, The ISO 15189 certification has a set of benefits.
The benefits are listed here below:
An ISO 15189 certification promotes development of an international reputable image for
your organization through Quality Assurance and Management Systems.
Promotes a strong degree of consistency in compliance to medical laboratory laws and
legislation both from an international and national perspective.
Fundamentally critical in promoting laboratory efficiency and responsibility for better results
and service delivery.
The certification program also has been very critical in promoting modern laboratory
practices that include professionalism and expertise in conduction of medical activities in the
labs.
Ultimately promoted the growth of customer satisfaction.6
I think ISO 15189 must be implemented to all of medical laboratory, but in some developing
countries, the implementation is still not adequately do. Example, in Indonesia there is some kind of
accreditation committee, called Komite Akreditasi Nasional (KAN) formed in 1992. Until July 2012,
KAN has accredited 21 private medical laboratories, three government health laboratories and one
government hospital laboratories. The scope of accreditation of medical laboratories that have been
accredited were include clinical chemistry, urinalysis, microbiology, immunology, hematology,
hemostasis, Drug, and anatomical pathology. For the scope of anatomic pathology laboratory, one
particular clinical pathologist was accredited. To do the medical laboratory accreditation, KAN is use
the ISO 15189 as a standard.
The number of laboratory that has been accredited is very small (according to KAN’s data, until July
2012, only about 25 laboratories that accredited). Because in Indonesia, there are so many medical
laboratories. This data indicated that the implementation of ISO 15189 in Indonesia was not done
well. 7
Conclusion
ISO 15189 is a global initiative that aims at creating a standard measure of quality in medical
laboratories. The standard has developed initiatives to promote competence and responsibility in
medical laboratory processes, equipments and outcomes. ISO 15189 was developed by the
International Standards Organizations Technical Committee and has been implemented in over 200
countries. The process involves testing of the effectiveness of laboratory equipments and the impact
those particular equipment have on the processes in the labs and their outcomes.
ISO 15189 must be implemented in any of medical laboratory, because it can promotes development
of laboratory efficiency and responsibility for better result. In the other hand, the efficiency and
better result from the lab can ultimately promoted the growth of customer satisfaction.
I think the solution to implement the ISO 15189 to other lab, is the government should point some
big lab (that has been accreditated) as a temporary model for them, until they qualified to be
accredited by KAN.
References
1. International Standardization Organization. ISO 15189:2007. Available at
http://www.iso.org/iso/catalogue_detail?csnumber=42641 Accessed December 8th
2012.
2. International Standardization Organization. About ISO. Available at
http://www.iso.org/iso/home/about.htm Accessed December 8th 2012.
3. University of Wisconsin-Madison. Introduction to ISO. Available at
http://trace.wisc.edu/docs/taacmtg_sep96/iso.htm Accessed December 8th 2012.
4. University of Pittsburgh. School of Information Sciences: The ISO Standardization
Process. Available at:
http://www.sis.pitt.edu/~mbsclass/standards/martincic/isohistr.htm Accessed
December 8th 2012.
5. Quality Systems Enhancement. ISO 15189 – Quality Management in Medical
Laboratories. Available athttp://www.enhancequality.com/iso-standards/iso-
15189-medical-laboratories-particular-requirements-for-quality-and-
competence/ Accessed December 8th 2012.
6. Quality Systems Enhancement. ISO 15189 – Quality Management in Medical Laboratories.
Available at http://www.enhancequality.com/iso-standards/iso-15189-medical-laboratories-
particular-requirements-for-quality-and-competence/ Accessed December 8th 2012.
7. Komite Akreditasi Nasional. Akreditasi Laboratorium Medik Berdasarkan SNI ISO
15189:2009. Available at http://www.kan.or.id/?p=2214&lang=id Accessed December 8th
2012.
THE AWARENESS OF OCCUPATIONAL HEALTH IN INDONESIA
BATHIN BONIA SARI
030.09.044
JAKARTA 2012
ABSTRACT
Occupational Health is the promotion and maintenance of the highest degree of physical,
mental and social well-being of workers in all occupations by preventing departures from
health, controlling risks and the adaptation of work to people, and people to their jobs.
(ILO / WHO 1950)
The health of the workers has several determinants, including risk factors at the workplace
leading to cancers, accidents, musculoskeletal diseases, respiratory diseases, hearing loss,
circulatory diseases, stress related disorders and communicable diseases and others.
What we are going to discuss are the relation of Noise-Induced, hearing loss, treatment, and
prevention that can be done.
Because there are numerous workers that experiences hearing loss after exposed to noise or
high frequency sounds from work and environment.
Keyword : occupational health, noise induce, hearing loss
CHAPTER I
INTRODUCTION
During the 1990s, Indonesia, as many other Asian countries, has undergone a period
of rapid growth until 1997 and suffered subsequently from the financial crisis. Both phases
have their own peculiarities: during the growth, the number of work-related injuries tends to
increase, whereas during the recession, unfortunately, occupational safety and health (OSH)
becomes one of the first areas to be curtailed. The ILO views that workers’ safety and health
is a basic human right and this right has to be secured no matter whether the country is in
economic growth or in recession. We should not be too preoccupied to make or save money
at the expense of human lives and health.(1)
Work is something that can not be separated from human life, especially people who are in
the productive age (20-50th). There are many risks in their work both in terms of health and
safety. Companies and workers should pay attention to it
Occupations that increases the chance of noise-induced hearing loss are agriculture,
construction, manufacture utility, transportation, and military.(2)
In each state has regulations governing occupational health and safety, including in
Indonesia.
Indonesia has a legal framework Safety Act (Act No.1, 1970). This law covers all workplaces
and emphasize primary prevention.(3)
Undang-undang Kesehatan (UU No 23, 1992) dedicates its Article 23 for occupational health
stated that all workers to work in good health without endangering themselves or their
communities, and to obtain an optimal work productivity
along with labor protection program (Departemen Kesehatan, 2002)
(Pasal 86 dan 87). The law stipulates that every worker is entitled to receive the protection of
safety and health hazards, protection against immorality and indecency, and treatment that
shows respect for human dignity and religious values. Second, states that every company
must implement OSH-MS
Based on the Employees’ Social Security Act in 1992 (UU No.3, 1992), the
Government established a public limited liability company, PT JAMSOSTEK.18 The Act
covers the benefits related to (i) employment accidents, (ii) old age, (iii) death, and (iv) health
care. The compulsory coverage applies to employers hiring 10 employees or more, or paying
a monthly wage payroll of 1 million Rupiahs or more. Workers injured at work are entitled to
benefits covering (i) the cost of transportation, (ii) the cost of medical examination, treatment,
and/or hospital care, (iii) the cost of rehabilitation, and (iv) cash payments consisting
disability or death allowances.(4)
But unfortunately the workers and firms in Indonesia are not too aware on health at work and
their safety in doing their jobs. As conveyed by KSPSI (Confederation of All Indonesian
Workers Union) that the workers have very low awareness of OSH, compared with issues
such as wages.
" People tend to think that they should get paid enough, to meet the needs of their incomes,
and improve the well-being before they are "able to" think OSH”
CHAPER II
LITERATURE REVIEW
I. Occupational health
Occupational Health is the promotion and maintenance of the highest degree of physical,
mental and social well-being of workers in all occupations by preventing departures from
health, controlling risks and the adaptation of work to people, and people to their jobs.
(ILO / WHO 1950)
Occupational health problems occur at work or because of the kind of work you do. These
problems can include
Cuts, broken bones, sprains and strains, or amputations Repetitive motion disorders
Hearing problems caused by exposure to noise
Vision problems or even blindness
Illness caused by breathing, touching or ingesting unsafe substances
Illness caused by exposure to radiation
Exposure to germs in healthcare settings
NIOSH surveyed around 30 million workers affected hearing loss from loud noises and high
frequency sounds and 9 million people from solvent and metal.(5)
44% carpenter and 48% plumbers reported that they realized to have noise-induced hearing
loss and affects real life.
49% miners will have noise-induced hearing loss at the age of 50 which is 9% to 70% at the
age of 60.
2. Noise induce hearing loss
Noise induced hearing loss is a permanent hearing impairment resulting from prolonged exposure to
high levels of noise. One in 10 man has a hearing loss that affects his or her ability to understand
normal speech. Excessive noise exposure is the most common cause of hearing loss. The National
Institute of Health reports that about 15 percent of aged 20 to 69 have high frequency hearing loss
related to occupational or leisure activities. Because of occupational risk of noise induced hearing
loss, there are government standards regulating allowable noise exposure. People working before
the mid1960s may have been exposed to higher levels of noise where there were no laws mandating
use of devices to protect hearing. (6)
CAPTER III
DISCUSION
Occupational health
Occupational Health is the promotion and maintenance of the highest degree of physical,
mental and social well-being of workers in all occupations by preventing departures from
health, controlling risks and the adaptation of work to people, and people to their jobs.
(ILO / WHO 1950)
The health of the workers has several determinants, including risk factors at the workplace
leading to cancers, accidents, musculoskeletal diseases, respiratory diseases, hearing loss,
circulatory diseases, stress related disorders and communicable diseases and others.(7)
How we hear
Hair cells in the inner ear
Hearing depends on a series of events that change sound waves in the air into electrical
signals. Our auditory nerve then carries these signals to the brain through a complex series of
steps.
Sound waves enter the outer ear and travel through a narrow passageway called the ear canal,
which leads to the eardrum.
The eardrum vibrates from the incoming sound waves and sends these vibrations to three tiny
bones in the middle ear. These bones are called the malleus, incus, and stapes.
The bones in the middle ear amplify, or increase, the sound vibrations and send them to the
inner ear—also called the cochlea—which is shaped like a snail and is filled with fluid. An
elastic membrane runs from the beginning to the end of the cochlea, splitting it into an upper
and lower part. This membrane is called the “basilar” membrane because it serves as the
base, or ground floor, on which key hearing structures sit.
The sound vibrations cause the fluid inside the cochlea to ripple, and a traveling wave forms
along the basilar membrane. Hair cells—sensory cells sitting on top of the membrane—“ride
the wave.”
As the hair cells move up and down, their bristly structures bump up against an overlying
membrane and tilt to one side. This tilting action causes pore-like channels, which are on the
surface of the bristles, to open up. When that happens, certain chemicals rush in, creating an
electrical signal.
The auditory nerve carries this electrical signal to the brain, which translates it into a “sound”
that we recognize and understand.
Hair cells near the base of the cochlea detect higher-pitched sounds, such as a cell phone
ringing. Those nearer the apex, or centermost point, detect lower-pitched sounds, such as a
large dog barking.
Hearing loss
Exposure to harmful sounds causes damage to the hair cells as well as the auditory, or
hearing, nerve (see figure). Impulse sound can result in immediate hearing loss that may be
permanent. This kind of hearing loss may be accompanied by tinnitus—a ringing, buzzing, or
roaring in the ears or head—which may subside over time. Hearing loss and tinnitus may be
experienced in one or both ears, and tinnitus may continue constantly or occasionally
throughout a lifetime.(6)
Continuous exposure to loud noise also can damage the structure of hair cells, resulting in
hearing loss and tinnitus, although the process occurs more gradually than for impulse noise.
Exposure to impulse and continuous noise may cause only a temporary hearing loss. If a
person regains hearing, the temporary hearing loss is called a temporary threshold shift. The
temporary threshold shift largely disappears 16 to 48 hours after exposure to loud noise. You
can prevent NIHL from both impulse and continuous noise by regularly using hearing
protectors such as earplugs or earmuffs.
When a person is exposed to loud noise over a long period of time, symptoms of NIHL will increase
gradually. Over time, the sounds a person hears may become distorted or muffled, and it may be
difficult for the person to understand speech. Someone with NIHL may not even be aware of the
loss, but it can be detected with a hearing test.
ONIHL is a more common cause of noise-induced hearing loss (NIHL) for the following 2 reasons: (1)
The threat of loss of employment may convince people to remain in environments with noise levels
higher than they would otherwise accept, and (2) in the workplace, high levels of noise may be
sustained on a regular basis for many hours each day over many years
ONIHL is 100 percent preventable. All individuals should understand the hazards of noise
and how to practice good hearing health in everyday life. To protect your hearing: (8)
Know which noises can cause damage (those at or above 85 decibels).
Wear earplugs or other hearing protective devices when involved in a loud activity
(special earplugs and earmuffs are available at hardware and sporting goods stores).
Be alert to hazardous noise in the environment.
Protect the ears of children who are too young to protect their own.
Make family, friends, and colleagues aware of the hazards of noise.
If you suspect hearing loss, have a medical examination by an otolaryngologist (a
physician who specializes in diseases of the ears, nose, throat, head, and neck) and a
hearing test by an audiologist (a health professional trained to measure and help
individuals deal with hearing loss).
Workers’ low OSH awareness is an indisputable concern. Nevertheless, it is
necessary to emphasize that the lack of understanding is not a case of workers alone: work
safety and health awareness is low among all. Medical doctors receive insufficient OSH
training; this results in difficulties in diagnosing illnesses and linking them to workplace
hazard exposures, thus, hindering the primary prevention at the workplace.
Besides medical doctors, mainstream engineers are frequent key players in safety and health.
Usually, these conventional engineers do not receive adequate OSH education either; for
example, only few chemical and mechanical engineers are required to demonstrate their
comprehension in toxics use reduction, safer and cleaner product design, or on industrial
hygiene. Nevertheless, “engineering controls” are on the top of the hazard control hierarchy
to eliminate and minimize work safety and health risks.
More often than not, most business school graduates have studied hardly any work safety and
health subjects. Any entrepreneur who considers
starting a business needs at least basic knowledge and skills in the workplace risk
identification, exposure assessment, existing OSH regulatory requirements, etc to implement
preventive measures against accident and health hazards successfully.
Furthermore, when one describes working conditions in developing and even in
developed countries, the first, the most frequently-heard, and unfortunately often the only
narrative is: “workers do not use respirators or masks”. Sadly, these workers-don’t-use-masks
attitudes indicate how poorly hazard prevention principles have been instilled in societies. It
is not that only workers’ OSH awareness is low – the global OSH awareness is low.
NIOSH recommends that all workers' exposure to noise must be controlled under a level
equivalent to 85 dBA for eight hours of work to minimize noise-induced hearing loss.
NIOSH also recommends 3 dBA exchange rate so that each increase of 3 dBA doubles the
amount of noise and halves the recommended amount of exposure time.(9)
Prevention hearing loss in occupational health
To prevent noise-induced hearing loss there are 6 steps which are(10) :
Identification and assessment of the risks from health hazards in the workplace. This involves
surveillance of the factors in the working environment and working practices which may
affect workers' health. It also requires a systematic approach to the analysis of occupational
"accidents", and occupational diseases.
Advising on planning and organisation of work and working practices, including the design
of work-places, and on the evaluation, choice and maintenance of equipment and on
substances used at work. In so doing, the adaptation of work to the worker is promoted.
Providing advice, information, training and education, on occupational health, safety and
hygiene and on ergonomics and protective equipment.
Surveillance of workers' health in relation to work.
Contributing to occupational rehabilitation and maintaining in employment people of
working age, or assisting in the return to employment of those who are unemployed for
reasons of ill health or disability.
Organising first aid and emergency treatment.
CHAPTER IV
CONCLUTION
Danger of noise can cause hearing loss and irreversible reversible.
Therefore we must do a better prevention and treatment of hearing loss that occurs is not
getting worse.
Besides it takes the awareness and cooperation of the company nor the workers themselves
about the benefits and occupational health procedures.
Early awareness would prevent damage which will ultimately affect the quality of life.
BIBLIOGRAPHY
1. History of Occupational Safety and Health in Indonesia ; by Safe Design, 2000;
available at http://safe.gq.nu/safstory.html
2. Myers M; Chapter on Agriculture and Natural Resource Based Industries; in ILO
Encyclopaedia of Occupational Health and Safety ; Fourth Edition; Stellman JM
(Ed); Vol. III; the ILO; Geneva; 1998
3. National Safety Council of Indonesia, K3; Keselamatan dan Kesehatan Kerja di
Indonesia 1900-2000 ; Dewan Keselamatan dan Kesehatan Kerja National; 2000
4. Social Security and Coverage for all: Restructuring the Social Security System in
Indonesia – Issues and options , ILO, Jakarta 2002.
5. ASEAN OSHNET Occupational Safety and Health Network ; 2003; available at
http://www.asean-osh.net/
6. Daniel E. 2007. Noise and hearing loss: a review. The Journal of school health 77: 225-31
7. Warta Kesehatan Kerja ; Media Komunikasi Kesehatan Kerja; No. 1, 2002. Newsletter A published by the Occupational
8. The Department of Health, Indonesia; Strategic Planning of Occupational Health
Programme 2002 – 2004 ; 2002
9. Strategy for the Improvement of OSH and Working Conditions ; Report of an ILO
Advisory Mission and Proceedings of a National Workshop, Jakarta 16-17, May 1995
10. The ILO-IPEC Footwear Programme Team; Markkanen P; Improving Safety, Health,
and Productivity in the Informal Footwear Sector ; the ILO-IPEC; 2002
Hypogonadism and Diabetes Mellitus in Adult Male
BRILLI BAGUS DIPO
030.09.0049
JAKARTA 2012
ABSTRACT
In recent years concepts are developing whether male hypogonadism and testosterone
deficiency are the factors for developing insulin resistance and subsequent development of
type 2 diabetes mellitus. This hypothesis developed from the observations that, testosterone
deficiency in adult male is associated with type 2 diabetes mellitus, coronary artery disease
and heart failure. Replacement of testosterone hormone to this subset of patients results in
improvement of the condition. Recent studies have shown that male hypogonadism is more
prevalent than thought earlier, is strongly associated with metabolic syndrome and may be a
risk factor for the development of type 2 diabetes mellitus and coronary artery disease. Long-
term studies are required to establish the relation with these diseases, the effect of
testosterone replacement and its long-term safety profile with the exception of increase in
haematocrit, which already we know.
The prevalence of both hypogonadism and type 2 diabetes mellitusincreases with age.
But it is not proved beyond doubt, whether male hypogonadism contributes to the
development of type 2 diabetes mellitus or type 2 diabetes mellitus leads to the development
of hypogonadism or both are the presentations of some age related condition like increased
fat mass. This concept, if it is supported by large multicentric studies, a new arena of
understanding, treating and preventing diabetes mellitus in men will be opened.
Keywords : Hypogonadism, type 2 diabetes mellitus
INTRODUCTION
Testosterone is the key male hormone. It regulates a man's libido (sex drive) and the
development of secondary male sex characteristics, such as facial and body hair, the testes
and the penis. Testosterone also protects the health of bone and muscle tissues. Testosterone
deficiency is associated with many chronic health conditions, including type 2 diabetes
mellitus and other metabolic disorders.
Testosterone deficiency has been estimated to affect about 1 in 200 Australian men,
although this may under-represent the true number due to not all cases being diagnosed. In
men from Boston, USA, testosterone deficiency was found to affect about 1 in 18 men aged
30–79 years, but in men aged 60–79 this increased to about 1 in 8. Significantly, there is also
a strong association between testosterone deficiency and diabetes. A study in the United
Kingdom found that 42% of men with type 2 diabetes also had low or borderline levels of
testosterone..
DISCUSSION
Hypogonadism
Definition
Male hypogonadism is a condition in which the body doesn't produce enough
testosterone, the hormone that plays a key role in masculine growth and development during
puberty. You may be born with male hypogonadism, or it can develop later in life from injury
or infection. The effects depend on the cause and at what point in your life male
hypogonadism occurs. Some types of male hypogonadism can be treated with testosterone
replacement therapy.
Symptoms
In adult males, hypogonadism may alter certain masculine physical characteristics and
impair normal reproductive function. Signs and symptoms may include:
Erectile dysfunction
Infertility
Decrease in beard and body hair growth
Decrease in muscle mass
Development of breast tissue (gynecomastia)
Loss of bone mass (osteoporosis)
Hypogonadism can also cause mental and emotional changes. As testosterone decreases,
some men may experience symptoms similar to those of menopause in women. These may
include:
Fatigue
Decreased sex drive
Difficulty concentrating
Hot flashes
Ethiology and Pathogenesis
Male hypogonadism means the testicles don't produce enough of the male sex
hormone testosterone. There are two basic types of hypogonadism:
Primary
This type of hypogonadism — also known as primary testicular failure — originates
from a problem in the testicles.
Secondary
This type of hypogonadism indicates a problem in the hypothalamus or the pituitary
gland — parts of the brain that signal the testicles to produce testosterone. The
hypothalamus produces gonadotropin-releasing hormone, which signals the
pituitarygland to make follicle-stimulating hormone (FSH) and luteinizing hormone.
Luteinizing hormone then signals the testes to produce testosterone.
Either type of hypogonadism may be caused by an inherited (congenital) trait or something
that happens later in life (acquired), such as an injury or an infection.
Primary hypogonadism
Common causes of primary hypogonadism include:
Klinefelter syndrome
This condition results from a congenital abnormality of the sex chromosomes, X and Y. A
male normally has one X and one Y chromosome. In Klinefelter syndrome, two or more X
chromosomes are present in addition to one Y chromosome. The Y chromosome contains the
genetic material that determines the sex of a child and related development. The extra X
chromosome that occurs in Klinefelter syndrome causes abnormal development of the
testicles, which in turn results in underproduction of testosterone.
Undescended testicles
Before birth, the testicles develop inside the abdomen and normally move down into their
permanent place in the scrotum. Sometimes one or both of the testicles may not be descended
at birth. This condition often corrects itself within the first few years of life without
treatment. If not corrected in early childhood, it may lead to malfunction of the testicles and
reduced production of testosterone.
Mumps orchitis
If a mumps infection involving the testicles in addition to the salivary glands (mumps
orchitis) occurs during adolescence or adulthood, long-term testicular damage may occur.
This may affect normal testicular function and testosterone production.
Hemochromatosis
Too much iron in the blood can cause testicular failure or pituitary gland dysfunction
affecting testosterone production.
Injury to the testicles
Because they're situated outside the abdomen, the testicles are prone to injury. Damage to
normally developed testicles can cause hypogonadism. Damage to one testicle may not
impair total testosterone production.
Cancer treatment
Chemotherapy or radiation therapy for the treatment of cancer can interfere with
testosterone and sperm production. The effects of both treatments often are temporary, but
permanent infertility may occur. Although many men regain their fertility within a few
months after treatment ends, preserving sperm before starting cancer therapy is an option that
many men consider.
Secondary hypogonadism
In secondary hypogonadism, the testicles are normal but function improperly due to a
problem with the pituitary or hypothalamus. A number of conditions can cause secondary
hypogonadism, including:
Kallmann syndroms
Abnormal development of the hypothalamus — the area of the brain that controls the
secretion of pituitary hormones — can cause hypogonadism. This abnormality is also
associated with impaired development of the ability to smell (anosmia) and red-green color
blindness.
Pituitary disorders
An abnormality in the pituitary gland can impair the release of hormones from the
pituitary gland to the testicles, affecting normal testosterone production. A pituitary tumor or
other type of brain tumor located near the pituitary gland may cause testosterone or other
hormone deficiencies. Also, the treatment for a brain tumor, such as surgery or radiation
therapy, may impair pituitary function and cause hypogonadism.
Inflammatory disease
Certain inflammatory diseases, such as sarcoidosis, histiocytosis and tuberculosis, involve
the hypothalamus and pituitary gland and can affect testosterone production, causing
hypogonadism.
HIV/AIDS
HIV/AIDS can cause low levels of testosterone by affecting the hypothalamus, the
pituitary and the testes.
Medications
The use of certain drugs, such as opiate pain medications and some hormones, can affect
testosterone production.
Obesity
Being significantly overweight at any age may be linked to hypogonadism.
Normal aging
Older men generally have lower testosterone levels than younger men do. As men age,
there's a slow and continuous decrease in testosterone production. The rate at which
testosterone declines varies greatly among men. As many as 30 percent of men older than 75
have a testosterone level that's below normal, according to the American Association of
Clinical Endocrinologists.
Hypogonadism and Aging
Several studies have established the proportionate fall of testosterone with age. Total
testosterone (TT) in circulation consist of:
Sex Hormone Binding Globulin (SHBG) bound testosterone (SHBG-TE) = 58%
Albumin bound testosterone (ABT) = 40%
Free testosterone (FT) = 2%
Age related fall in total testosterone with increase in SHBG level and decrease in
bioavailable free testosterone has been observed even if Body Mass Index (BMI) does not
exceed 26 kg/m2 Feldmaen, observed a decline of total testosterone by 0.8% per year of age,
whereas both free and albumin bound testosterone declines at about 2% per year. SHBG
levels increased at 1.6% per year. But luteinizing hormone (LH) and follicle stimulating
hormone (FSH) levels tend to rise with age.
Observed the fact that the major age related changes in testosterone levels are caused
by changes at testicular function and not due to hypothalamic pituitary axis pathway, which is
not altered with age. They noted that treatment of aging men with clomiphene citrate, an anti-
estrogen agent, could not increase the level of bioavailable testosterone as is seen in younger
men even though LH pulse characteristics and bioavailable LH levels were similar in two
groups.
Diagnosis
Because symptoms are nonspecific in nature, a complete history, physical
examination, and laboratory analysis must accompany the clinical presentation for diagnosis.
A history that focuses on developmental milestones will help the clinician determine the
onset of the disorder. Possible causes must also be ruled out during a patient history, such as
exposure to environmental toxins, medications that have been associated with the disorder, or
evidence of a congenital cause such as Klinefelter's syndrome or pituitary gland hormone
deficiency. In addition, patients should be asked about recreational drug use, eating disorders,
and excessive exercise, as all of these can transiently alter testosterone levels.
If clinical symptoms are present, serum testosterone levels should be measured. The
total testosterone level should be the first measurement taken to determine hypogonadic state.
It should be drawn between the hours of 8 am and 11 am to ensure that a peak level is
captured (diurnal fluctuations can occur throughout the day, especially in younger men). If
an abnormal laboratory value is identified, a confirmatory measurement should be performed
to ensure that the diagnosis is appropriate. It has been reported that up to 30% of patients with
a low testosterone level upon initial laboratory measurement have a normal level upon repeat
measurement. Numerous factors can transiently alter testosterone levels, including time of
measurement (day and year), medications, and acute illness.
In most references, a total testosterone level <300 ng/mL is considered low; however,
some controversy surrounds the inconsistency with measurement assays in determining this
reference range. Free testosterone should be measured if it is suspected that the patient may
have alterations in his sex hormone–binding globu lin (SHBG). Testosterone is highly bound
to SHBG and albumin; thus, when SHBG concentrations are significantly affected,
circulating testosterone levels can be as well. Many things can cause alterations in SHBG
concentrations, some of which include obesity, nephrotic syndrome, hypothyroidism, and use
of glucocorticoids, progestins, and androgenic steroids. Conditions associated with increased
levels of SHBG include aging, hepatic cirrhosis, hyperthyroidism, HIV, and use of
anticonvulsants or estrogens. The lower limit of normal when discussing free testosterone is
typically 50 pg/mL.
Other laboratory measurements that should be completed if testosterone levels return
low include measurement of LH and FSH. These stimulatory hormones help clinicians
determine whether the identified hypogonadism is of primary or secondary nature. As
described previously, primary or hypergonadotropic hypogonadism would demonstrate an
elevation in these hormones, signifying adequate pituitary function. On the other hand, if LH
and FSH levels are low, a suspected pituitary cause must be considered, with further imaging
necessary to rule out structural abnormalities.
Type 2 Diabetes Mellitus
Definition
Type 2 diabetes, once known as adult-onset or noninsulin-dependent diabetes, is
caused by the body’s ineffective use of insulin. It often results from excess body weight and
physical inactivity.With type 2 diabetes, your body either resists the effects of insulin — a
hormone that regulates the movement of sugar into your cells — or doesn't produce enough
insulin to maintain a normal glucose level. Untreated, type 2 diabetes can be life-threatening.
There's no cure for type 2 diabetes, but you can manage — or even prevent — the condition.
Start by eating well, exercising and maintaining a healthy weight. If diet and exercise aren't
enough to control your type 2 diabetes, you may need diabetes medications or insulin therapy
to manage your blood sugar.
Symptoms
Type 2 diabetes symptoms may develop very slowly. In fact, you can have type 2
diabetes for years and not even know it. Look for:
Increased thirst and frequent urination.
As excess sugar builds up in your bloodstream, fluid is pulled from the tissues. This
may leave you thirsty. As a result, you may drink — and urinate — more than usual.
Increased hunger.
Without enough insulin to move sugar into your cells, your muscles and organs
become depleted of energy. This triggers intense hunger.
Weight loss.
Despite eating more than usual to relieve hunger, you may lose weight. Without the
ability to metabolize glucose, the body uses alternative fuels stored in muscle and fat.
Calories are lost as excess glucose is released in the urine.
Fatigue.
If your cells are deprived of sugar, you may become tired and irritable.
Blurred vision.
If your blood sugar is too high, fluid may be pulled from the lenses of your eyes. This
may affect your ability to focus clearly.
Slow-healing sores or frequent infections.
Type 2 diabetes affects your ability to heal and resist infections.
Areas of darkened skin.
Some people with type 2 diabetes have patches of dark, velvety skin in the folds and
creases of their bodies — usually in the armpits. This condition, called acanthosis
nigricans, may be a sign of insulin resistance.
Causes
Type 2 diabetes develops when the body becomes resistant to insulin or when the
pancreas stops producing enough insulin. Exactly why this happens is unknown, although
excess weight and inactivity seem to be contributing factors.
Insulin is a hormone that comes from the pancreas, a gland situated just behind and
below the stomach. When you eat, the pancreas secretes insulin into the bloodstream. As
insulin circulates, it acts like a key by unlocking microscopic doors that allow sugar to enter
your cells. Insulin lowers the amount of sugar in your bloodstream. As your blood sugar level
drops, so does the secretion of insulin from your pancreas.
Glucose — a sugar — is a main source of energy for the cells that make up muscles
and other tissues. Glucose comes from two major sources: the food you eat and your liver.
After intestinal digestion and absorption, sugar is absorbed into the bloodstream. Normally,
sugar then enters cells with the help of insulin.
The liver acts as a glucose storage and manufacturing center. When your insulin
levels are low — when you haven't eaten in a while, for example — the liver metabolizes
stored glycogen into glucose to keep your glucose level within a normal range.
In type 2 diabetes, this process works improperly. Instead of moving into your cells,
sugar builds up in your bloodstream. This occurs when your pancreas doesn't make enough
insulin or your cells become resistant to the action of insulin.
Pathophysiology
Type 2 diabetes is characterized by a combination of peripheral insulin resistance and
inadequate insulin secretion by pancreatic beta cells. Insulin resistance, which has been
attributed to elevated levels of free fatty acids and proinflammatory cytokines in plasma,
leads to decreased glucose transport into muscle cells, elevated hepatic glucose production,
and increased breakdown of fat.
A role for excess glucagon cannot be underestimated; indeed, type 2 diabetes is an
islet paracrinopathy in which the reciprocal relationship between the glucagon-secreting
alpha cell and the insulin-secreting beta cell is lost, leading to hyperglucagonemia and hence
the consequent hyperglycemia.
For type 2 diabetes mellitus to occur, both insulin resistance and inadequate insulin
secretion must exist. For example, all overweight individuals have insulin resistance, but
diabetes develops only in those who cannot increase insulin secretion sufficiently to
compensate for their insulin resistance. Their insulin concentrations may be high, yet
inappropriately low for the level of glycemia.
A simplified scheme for the pathophysiology of abnormal glucose metabolism in type 2
diabetes mellitus is depicted in the image below.
With prolonged diabetes, atrophy of the pancreas may occur. A study by Philippe et al
used computed tomography (CT) scan findings, glucagon stimulation test results, and fecal
elastase-1 measurements to confirm reduced pancreatic volume in individuals with a median
15-year history of diabetes mellitus (range, 5-26 years). This may also explain the associated
exocrine deficiency seen in prolonged diabetes.
How does insulin resistance affect testosterone levels?
Testosterone production is affected in diabetic men because they have higher than
normal concentrations of glucose in their blood. When blood glucose levels are high, the
pituitary gland produces less LH than it normally would. As testosterone is only produced
whenLH is secreted from the pituitary, this reduces the amount of testosterone produced by a
man's body.
The association between diabetes and hypogonadism are interdependent – that is, they
work both ways. Low testosterone is a risk factor for diabetes and the metabolic syndrome
because testosterone levels affect body fat composition, glucose transport and the ways in
which the body's cells use testosterone. Diabetes is also a risk factor for hypogonadism
because it is associated with increased body mass and altered hormone profiles (e.g. reduced
LH as a result of high blood glucose levels, which in turn reduces testosterone levels).
Diagnosis
Diagnostic criteria by the American Diabetes Association (ADA) includes the following:
A fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or higher, or
A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher during a 75-g
oral glucose tolerance test (OGTT), or
A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a patient with
classic symptoms of hyperglycemia or hyperglycemic crisis
Whether a hemoglobin A1c (HbA1c) level of 6.5% or higher should be a primary
diagnostic criterion or an optional criterion remains a point of controversy.
Indications for diabetes screening in asymptomatic adults includes the following:
Sustained blood pressure >135/80 mm Hg
Overweight and 1 or more other risk factors for diabetes (eg, first-degree relative with
diabetes, BP >140/90 mm Hg, and HDL < 35 mg/dL and/or triglyceride level >250
mg/dL)
ADA recommends screening at age 45 years in the absence of the above criteria
The Correlation between Hypogonadism and Type 2 Diabetes Mellitus
The association between low levels of testosterone (a condition known as
hypogonadism) and type 2 diabetes mellitus are well recognised, but it also appears that
testosterone deficiency is common in men with diabetes regardless of type. Metabolic
syndrome is a condition characterised by several co-occurring metabolic imbalances (e.g.
impaired insulin metabolism, obesity, high blood pressure); it often procedes type 2 diabetes
mellitus, and is also associated with testosterone deficiency. There is considerable evidence
that men with metabolic syndrome are more likely to develop hypogonadism. Testosterone
replacement therapy has been shown to improve insulin metabolism.
Testosterone and testosterone metabolism
In men, testosterone is primarily produced by the Leydig cells of the testes.
Testosterone production in the testes is stimulated when a man's pituitary gland produces a
hormone called luteinising hormone (LH). If either the pituitary gland or the testes are
dysfunctional, testosterone production may decline or stop, leading to testosterone deficiency
or hypogonadism.
Insulin and insulin metabolism
Insulin is a hormone produced by the pancreas and functions to lower levels of
glucose in the blood. If the body does not produce enough insulin, or if the insulin produced
does not function properly to reduce blood glucose, levels of blood glucose rise and lead to
health conditions such as metabolic syndrome and type 1 and type 2 diabetes mellitus.
Evidence of the associations between diabetes, metabolic syndrome and testosterone
deficiency
Studies have reported that 20–64% of men with testosterone
deficiency/hypogonadism also have type 2 diabetes. The proportion of men who have both
type 2 diabetes mellitus and hypogonadism increases in older groups of men.
Men who have slightly reduced testosterone concentrations (but not low enough to be
considered testosterone deficient) are also more likely to have low insulin (and high blood
glucose) levels. Therapies that reduce testosterone levels (e.g. androgen deprivation therapy,
which is used by men with prostate cancer because testosterone stimulates the growth of
prostate cancer) have also been shown to lower insulin levels.
Men with low testosterone concentrations, in addition to having lower insulin levels,
are more likely to develop the metabolic syndrome or one of the metabolic imbalances that
characterise it (e.g. impaired insulin metabolism, obesity, high blood pressure). Scientists
have even suggested that hypogonadism should be considered one of the imbalances that
characterise metabolic syndrome.
Evidence shows that approximately one third of type 2 diabetics are testosterone
deficient. An even greater proportion of men who are both diabetic and obese experience
testosterone deficiency, and the likelihood of testosterone deficiency increases as type 2
diabetes progresses or worsens.
There is also evidence of an association between insulin resistance, glucose levels,
abdominal obesity and free testosterone levels in type 1 diabetic men. Abdominal obesity
appears to play a particularly important role in these relationships. Abdominal obesity causes
insulin resistance, which in turn reduces testosterone levels because it increases the amount of
testosterone converted to estradiol.
Increasing knowledge about the associations between testosterone deficiency and
diabetes have lead to trialling testosterone replacement therapy (TRT) as a treatment for
insulin resistance in diabetic men. Evidence to date shows that TRT improves insulin
metabolism in hypogonadal diabetic men.
Assessing and managing lifestyle risk factors
In addition to starting TRT, it is important for hypogonadal men with metabolic
conditions to manage modifiable lifestyle factors, as an unhealthy lifestyle may make their
metabolic conditions worse and also reduce the effectiveness of their treatment. Lifestyle
factors play an important role in the development of type 2 diabetes mellitus, metabolic
syndrome and testosterone deficiency. In particular, low levels of physical activity, unhealthy
eating habits (e.g. eating too much, consuming too much fat and sugar), smoking and obesity
increase the risk of each of these conditions. The risk of testosterone deficiency in men with
diabetes increases further if they are also obese. Men with diabetes who maintain a healthy
lifestyle may prevent the onset of testosterone deficiency.
CONCLUSION
Multiple studies have shown that testosterone deficiency in men is associated with
Type 2 diabetes and metabolic syndrome, coronary artery disease and heart failure.
Testosterone replacement has also shown to improve the above conditions. But in absence of
large long duration multicentric studies, we cannot allow hypogonadism to join as a family
member of metabolic syndrome at present, and cannot also allow routine recommendation of
testosterone replacement to treat or prevent metabolic syndrome or diabetes mellitus. But
physicians should be mindful to screen for metabolic syndrome and diabetes mellitus in all
cases of hypogonadism. As an isolated case, they can try testosterone replacement after
discussing with the patient regarding advantages and disadvantages more so, in cases of
sexual dysfunction and develop a novel approach. But watch for complications like
erythrocytosis and prostatic carcinoma should always guide these approaches. This new
concept also indulges us to think whether female sex hormone has got any equivalent role in
women or not.
REFERENCES
1. Kalyani RR, Dobs AS. Androgen deficiency, diabetes and the metabolic syndrome in
men. Curr Opin Endocrinol Diabetes Obes. 2007;14(3):226-34.
2. American Association of Clinical Endocrinologists Hypogonadism Task Force.
American Association of Clinical Endocrinologists medical guidelines for clinical
practice for the evaluation and treatment of hypogonadism in adult male patients—
2002 update. Endocr Pract 2002;8:439-56.
3. Miner MM, Seftel AD. Testosterone and Ageing: what have we learned since the
institute if medicine report and what lies ahead? Int J Clin Pract. 2007;61(4):622-32.
4. Tan RS, Pu SJ. Impact of obesity on hypogonadism in the andropause. Int J Androl
2002;25:195-201.
5. Kapoor D, Malkin CJ. Channer KS, Jones TH. Androgens, insulin resistance and
vascular disease in men. Clinical Endocrinology 2005:239-50.
6. Simon D, Charles MA, Lahlou N, et al. Androgen therapy improves insulin sensitivity
and decreases leptin level in healthy adult men with low plasma total testosterone: a
3-month randomized placebo-controlled trial [letter]. Diabetes Care 2001.
7. Zitzmann M. Testosterone deficiency, insulin resistance and the metabolic
syndrome. Nat Rev Endocrinol. 2009;5(12):673-81.
8. Diabetes statistics. American Diabetes Association. http://www.diabetes.org/diabetes-
basics/diabetes-statistics. Accessed Dec. 10, 2012.
9. Allan CA, McLachlan RI. Testosterone deficiency in men: Diagnosis and
management. Aust Fam Physician. 2003;32(6):422-7.
10. Traish AM, Guay A, Feeley R, Saad F. The dark side of testosterone deficiency:
Metabolic syndrome and erectile dysfunction. J Androl. 2009;30(1):10-22.
11. McCulloch DK. Initial management of blood glucose in type 2 diabetes mellitus.
http://www.uptodate.com/home/index.html. Accessed Dec. 18, 2012.
12. Miner MM, Sadovsky R. Evolving issues in male hypogonadism: Evaluation,
management and comorbidities. Cleve Clin J Med. 2007;74(Suppl 3):S38-46.
13. Grossman M, Thomas MC, Panagiotopoulos S, et al. Low testosterone levels are
common and associated with insulin resistance in men with diabetes. J Clin
Endocrinol Metab. 2008;93(5):1834-40.
14. Shabsigh R, Arver S, Channer KS, et al. The triad of erectile dysfunction,
hypogonadism and the metabolic syndrome. Int J Clin Pract. 2008;62(5):791-8.
The Management of Asthma in Diabetes
Written by:
Christopher Roswell P. Siagian
030. 09. 053
FACULTY OF MEDICINE
TRISAKTI UNIVERSITY
JAKARTA, DECEMBER 2012
ABSTRACT
Asthma is a syndrome characterized by airflow obstruction that varies markedly,
both spontaneously and with treatment, and is one of the three chronic obstructive pulmonary
diseases besides chronic bronchitis and emphysema. The process involves in asthma is an
inflammation that leads to three events: bronchoconstriction, hypersecretion of mucus, and
swollen of bronchi. Diabetes is a disease in which blood glucose, or sugar, levels are too
high. Glucose comes from the foods. Insulin is a hormone that helps the glucose get into the
cells to give them energy. With type 1 diabetes, the body does not make insulin. With type 2
diabetes, the more common type, the body does not make or use insulin well. Without enough
insulin, the glucose stays in the blood. In diabetes, the patient becomes vulnerable to
microorganisms infections because the reduced of immunity. One of the treatments
commonly used in asthma is corticosteroid, either oral or inhaled. These drugs which are
classified in steroid class have an effect in suppressing the immune system, thus increasing
the risk of infection and also increase blood sugar. The issue in managing asthma in diabetes
is how to relieve the asthma symptoms in patient without worsening the pre-existing diabetes.
Keywords: asthma, diabetes, corticosteroid, blood glucose
CHAPTER I
INTRODUCTION
Asthma affects 5-10% of the population or an estimated 23.4 million persons,
including 7 million children. The overall prevalence rate of exercise-induced bronchospasm
is 3-10% of the general population if persons who do not have asthma or allergy are
excluded, but the rate increases to 12-15% of the general population if patients with
underlying asthma are included. Asthma affects an estimated 300 million individuals
worldwide. Annually, the World Health Organization (WHO) has estimated that 15 million
disability-adjusted life-years are lost and 250,000 asthma deaths are reported worldwide. (1)
The management of asthma differs according to the classification of severity.
Corticosteroids may be used from mild to severe – persistent asthma, ranging from low dose
with alternative medicines to high dose and its combinations.Although use of systemic
corticosteroids is recommended early in the course of acute exacerbations in patients with an
incomplete response to beta agonists, oral administration is equivalent in efficacy to
intravenous administration. Corticosteroids speed the resolution of airway obstruction and
prevent a late-phase response.(1,2)
Diabetes is a chronic disease, which occurs when the pancreas does not produce
enough insulin, or when the body cannot effectively use the insulin it produces. This leads to
an increased concentration of glucose in the blood (hyperglycaemia).Type 1 diabetes
(previously known as insulin-dependent or childhood-onset diabetes) is characterized by a
lack of insulin production.Type 2 diabetes (formerly called non-insulin-dependent or adult-
onset diabetes) is caused by the body’s ineffective use of insulin. It often results from excess
body weight and physical inactivity.(3)
Rates of diabetes are increasing worldwide. The International Diabetes Federation
predicts that the number of people living with diabetes will to rise from 366 million in 2011
to 552 million by 2030.The top 10 countries in number of people with diabetes are currently
India, China, the United States, Indonesia, Japan, Pakistan, Russia, Brazil, Italy, and
Bangladesh.(4)
Patient with diabetes has impaired immunity which leads to high risk from
infections. In the following chapter we will be talking about the necessity of using
corticosteroids for asthma in diabetes.
CHAPTER II
LITERATURE REVIEW
I. Asthma
Asthma is best described as a chronic disease that involves inflammation of the
pulmonary airways and bronchial hyperresponsiveness that results in the clinical expression
of a lower airway obstruction that usually is reversible. Asthma is characterised by a specific
pattern of inflammation that is largely driven viaimmunoglobulin (Ig)E-dependent
mechanisms. Genetic factors have an importantinfluence on whether atopy develops and
several genes have now been identified.Mostof the genetic linkages reported for asthma are
common to all allergic diseases.However, environmental factors appear to be more important
in determining whether anatopic individual develops asthma, although genetic factors may
exert an influence onhow severely the disease is expressed and the amplification of the
inflammatory response.(5,6)
I. A. Etiology
Genetics
Genome-wide linkage studies and case–control studies have identified 18 genomic
regions and more than 100 genes associated with allergy and asthma in 11 different
populations. In particular, there are consistently replicated regions on the long arms of
chromosomes 2, 5, 6, 12 and 13. Association studies of unrelated individuals have also
identified more than 100 genes associated with allergy and asthma, 79 of which have been
replicated in at least one further study.A recent genome-wide association study identified a
new gene, ORMDL3, that exhibited a highly significantly association with asthma (p < 10−12)
(for single nucleotide polymorphism rs8067378, odds ratio 1.84, 95% confidence interval
1.43–2.42) a finding that has now been replicated in several populations. (7,8,9,10)
Stress
A number of animal models have suggested that prenatal maternal stress acts
through regulation of the offspring’s hypothalamic–pituitary–adrenal axis to decrease cortisol
levels, which may affect the development of an allergic phenotype. Although there is a
correlation between caregiver stress early in the infant’s life and higher levels of
immunoglobulin E in the infant and early wheezing, no studies to date have shown an
association with asthma.(11.12)
Obesity
A study by Cottrell et al explored the relationship between asthma, obesity, and
abnormal lipid and glucose metabolism. The study found that community-based data linked
asthma, body mass, and metabolic variables in children. Specifically, these findings described
a statistically significant association between asthma and abnormal lipid and glucose
metabolism beyond body mass association.Accelerated weight gain in early infancy is
associated with increased risks of asthma symptoms according to one study of preschool
children. (1)
Other etiologies include environmental allergens, viral respiratory tract infections,
exercise, hyperventilation, gastroesophageal reflux disease, chronic sinusitis or rhinitis,
aspirin or nonsteroideal anti-inflammatory drug (NSAID) hypersensitivity, sulfite sensitivity,
use of beta-adrenergic receptor blockers, environmental pollutants, tobacco smoke,
occupational exposure, irritants and perinatal factors. (1)
I. B. Pathophysiology
The pathophysiology of asthma can be divided into four events: bronchoconstriction,
airway edema, airway hyperresponsiveness and airway remodeling. (13)
Bronchoconstriction
In asthma, the dominant physiological event leading to clinical symptoms is airway
narrowing and a subsequent interference with airflow. In acute exacerbations of asthma,
bronchial smooth muscle contraction (bronchoconstriction) occurs quickly to narrow the
airways in response to exposure to a variety of stimuli including allergens or irritants.
Allergen-induced acute bronchoconstriction results from an IgE-dependent release of
mediators from mast cells that includes histamine, tryptase, leukotrienes, and prostaglandins
that directly contract airway smooth muscle.(13)
Airway edema
As the disease becomes more persistent and inflammation more progressive, other
factors further limit airflow. These include edema, inflammation, mucus hypersecretion and
the formation of inspissated mucus plugs, as well as structural changes including hypertrophy
and hyperplasia of the airway smooth muscle.(13)
Airway hyperresponsiveness
Airway hyperresponsiveness—an exaggerated bronchoconstrictor response to a wide
variety of stimuli—is a major, but not necessarily unique, feature of asthma. The degree to
which airway hyperresponsiveness can be defined by contractile responses to challenges with
methacholine correlates with the clinical severity of asthma. The mechanisms influencing
airway hyperresponsiveness are multiple and include inflammation, dysfunctional
neuroregulation, and structural changes; inflammation appears to be a major factor in
determining the degree of airway hyperresponsiveness. Treatment directed toward reducing
inflammation can reduce airway hyperresponsiveness and improve asthma control.(13)
Airway remodeling
In some persons who have asthma, airflow limitation may be only partially
reversible. Permanent structural changes can occur in the airway; these are associated with a
progressive loss of lung function that is not prevented by or fully reversible by current
therapy. Airway remodeling involves an activation of many of the structural cells, with
consequent permanent changes in the airway that increase airflow obstruction and airway
responsiveness and render the patient less responsive to therapy. These structural changes can
include thickening of the sub-basement membrane, subepithelial fibrosis, airway smooth
muscle hypertrophy and hyperplasia, blood vessel proliferation and dilation, and mucous
gland hyperplasia and hypersecretion.(13)
I. C. Treatment
The goal of asthma treatment is to achieve and maintainclinical control. Medications
to treat asthma can beclassified as controllers or relievers.The following will discussed only
about the role of glucocorticosteroids in treating asthma. (14)
I. C. 1. Controllers
Inhaled glucocorticosteroids
Inhaled glucocorticosteroids are currentlythe most effective anti-inflammatory
medications for thetreatment of persistent asthma. Studies have demonstratedtheir efficacy in
reducing asthma symptoms, improvingquality of life, improving lung function, decreasing
airwayhyperresponsiveness,controlling airway inflammation,reducing frequency and severity
of exacerbations, andreducing asthma mortality. However, they do not cureasthma, and when
they are discontinued deterioration ofclinical control follows within weeks to months in
aproportion of patients.(14)
Systemic glucocorticosteroids
Long-term oral glucocorticosteroidtherapy (that is, for periods longer than two
weeks as aglucocorticosteroid “burst”) may be required for severelyuncontrolled asthma, but
its use is limited by the risk ofsignificant adverse effects. The therapeutic index(effect/side
effect) of long-term inhaled glucocorticosteroidsis always more favorable than long-term
systemicglucocorticosteroids in asthma. If oral glucocorticosteroidshave to be administered
on a long-term basis,attention must be paid to measures that minimize thesystemic side
effects. Oral preparations are preferred overparenteral (intramuscular or intravenous) for
long-termtherapy because of their lower mineralocorticoid effect,relatively short half-life,
and lesser effects on striatedmuscle, as well as the greater flexibility of dosing that
permitstitration to the lowest acceptable dose that maintains control.(14)
Other controllers are leukotriene modifiers, theophylline, long-acting inhaled and
oral β2 agonists, anti Ig-E, allergen-specific immunotherapy and oral anti-allergic compounds.
I. C. 2. Relievers
Systemic glucocorticosteroid
Although systemic glucocorticosteroidsare not usually thought of as reliever
medications, they areimportant in the treatment of severe acute exacerbationsbecause they
prevent progression of the asthmaexacerbation, reduce the need for referral to
emergencydepartments and hospitalization, prevent early relapseafter emergency treatment,
and reduce the morbidity of theillness. The main effects of systemic glucocorticosteroidsin
acute asthma are only evident after 4 to 6 hours. Oraltherapy is preferred and is as effective as
intravenoushydrocortisone. A typical short course of oral glucocorticosterodsfor an
exacerbation is 40-50 mgprednisolone given daily for 5 to 10 days depending on theseverity
of the exacerbation. When symptoms havesubsided and lung function has approached the
patientʼspersonal best value, the oral glucocorticosteroids can bestopped or tapered, provided
that treatment with inhaledglucocorticosteroids continues. Intramuscular injectionof
glucocorticosteroids has no advantage over a shortcourse of oral glucocorticosteroids in
preventing relapse.(14)
II. Diabetes
Diabetes is a chronic disease, which occurs when the pancreas does not produce
enough insulin, or when the body cannot effectively use the insulin it produces. This leads to
an increased concentration of glucose in the blood (hyperglycaemia).(3)
II. A. Type 1 Diabetes Mellitus
Type 1 diabetes mellitus (DM) is a multisystem disease with both biochemical and
anatomic/structural consequences. It is a chronic disease of carbohydrate, fat, and protein
metabolism caused by the lack of insulin, which results from the marked and progressive
inability of the pancreas to secrete insulin because of autoimmune destruction of the beta
cells.(3)
Pathophysiology
Type 1 diabetes usually develops as a result of autoimmune pancreatic beta-cell
destruction in genetically susceptible individuals. Up to 90% of patients will have
autoantibodies to at least one of 3 antigens: glutamic acid decarboxylase (GAD); insulin; and
a tyrosine-phosphatase-like molecule, islet auto-antigen-2 (IA-2).Beta-cell destruction
proceeds sub-clinically for months to years as insulitis (inflammation of the beta cell). When
80% to 90% of beta cells have been destroyed, hyperglycaemia develops. Insulin resistance
has no role in the pathophysiology of type 1 diabetes. However, with increasing prevalence of
obesity, some type 1 diabetic patients may be insulin resistant in addition to being insulin
deficient.(15)
II. B. Type 2 Diabetes Mellitus
Type 2 diabetes mellitus is a progressive disorder defined by deficits in insulin secretion
and action that lead to abnormal glucose metabolism and related metabolic
derangements. Although the aetiologies of type 1 and type 2 diabetes differ dramatically,
both lead to hyperglycaemic states, and both share common macrovascular (coronary heart,
cerebrovascular, and peripheral vascular disease) and microvascular (retinopathy,
nephropathy, and neuropathy) complications. Type 2 diabetes is usually diagnosed based on
screening. It is preceded by a state of pre-diabetes, which may be clinically detected by a
fasting plasma glucose of 5.6 mmol/L to 6.9 mmol/L (100 to 125 mg/dL). Diabetes diagnosis
is based on 2 confirmed values of: fasting plasma glucose >6.9 mmol/L (125 mg/dL); HbA1c
of 48 mmol/mol (6.5%) or greater; or (less commonly) abnormal glucose tolerance test
results, or a random plasma glucose of ≥200 mg/dL plus symptoms of hyperglycaemia.(16)
Pathophysiology
The precise mechanism by which the diabetic metabolic state leads to microvascular
and macrovascular complications is only partly understood but likely involves both
uncontrolled BP and uncontrolled glucose, increasing the risk of microvascular complications
such as retinopathy and nephropathy. Mechanisms may involve defects in aldose reductase
and other metabolic pathways, damage to tissues from accumulation of glycated end
products, and other mechanisms. With respect to macrovascular complications, high BP and
glucose raise risk, but so do lipid abnormalities and tobacco use. One unifying theory
postulates the existence of a metabolic syndrome that includes diabetes mellitus,
hypertension, dyslipidaemias, and obesity, and predisposes to coronary heart disease, stroke,
and peripheral artery disease. However, this theory is not universally accepted as more
clinically useful than assessing individual cardiovascular risk factors.(16)
\
Source: Taylor SI, Olefsky JM. Diabetes mellitus: a fundamental and clinical text. 3 rded. Philadelphia: Lippincott Williams & Wilkins; 2004.
Source: http://www.caninsulin.com/Pathophysiology-algorithm.htm
CHAPTER III
DISCUSSION
As seen in previous chapter, asthma can be determined in any of the following ways:
the underlying cause of asthma symptoms, severity of symptoms, and the way it’s controlled.
Source: .New York State Department of Health.Clinical guideline for the diagnosis, evaluation and management
of adults and children with asthma. Available at: http://www.nyhealth.gov. accessed on : December 1st 2012.
Type 1 diabetes mellitus (T1DM) is an autoimmune disease that involves the
progressive destruction of the insulin-producing beta cells in the islets of langerhans. It is a
complex process that results from the loss of tolerance to insulin and other beta-cell-specific
antigens. Various genetic and environmental factors have been studied so far, but precise
causation has yet to be established. Numerous studies in rodents and human subjects have
been performed in order to elucidate the role of B and T cells, which determine the risk of
development and progression of diabetes. These studies have demonstrated that while T1DM
is fundamentally a T-cell-mediated autoimmune response, the development of this disease
results from complex interactions between the adaptive and innate immune systems, with
numerous cell types thought to contribute to pathogenesis. Like any complex disease, the
variation in severity and incidence of T1DM can be attributed to a combination of genetic
and environmental factors.(17)
Source: Ting C, Bansal V, Batal I, Mounayar M, et al. Impairment of immune systems in diabetes. In: Diabetes:
an old disease, a new insight. Ahmad SI, editor. Texas: LANDES Bioscience; 2012.
Infectious diseases are common and serious complication of diabetes mellitus (DM)
and hyperglycemia. The increase of infections in patients with DM is known to depend upon
an immunosuppressive condition which is brought about by impaired innate immunity and
acquired immunity. For instance, functions of neutrophils such as phagocyte, chemotaxis and
cytokine-production are decreased in DM model mouse and hyperglycemia and a Th2-axis
shift which reduces Th1-dependent immunity are observed in DM patients. However, the
majority of results concerning interaction of hyperglycemia and immune function are
controversial and relevance of hyperglycemia and/or hyperinsulinemia to immunosuppressive
mechanisms remains unclear.(18)
High glucose levels lead to shunting through the polyol pathway, an increase in
diacylglycerol which activates protein kinase C, an increase in the release of electrons that
react with oxygen molecules to form superoxides, and the non-enzymatic glycosylation of
proteins that result in greater formation of advanced glycation end products. Each of these
can lead to aberrant cell signalling that affects innate immunity for example, by activating the
MAP kinase pathway or inducing activation of transcription factors such as NF-kappaB. This
may be a common feature of several complications including periodontal disease,
atherosclerosis, nephropathy, impaired healing and retinopathy. These complications are
frequently associated with increased expression of inflammatory cytokines such as TNF-
alpha, IL-1beta and IL-6 and enhanced generation of reactive oxygen species.(19)
Source: Graves DT, Kayal RA. Diabetic complications and dysregulated innate immunity. Front
Biosci2008;13:1227-1239.
In the management of asthma, inhaled corticosteroids (ICS) can be prescribed in low
dose in mild persistent to high dose ICS in severe persistent asthma. Whilst oral
corticosteroid is used to maintain control in severe persistent after the initiating treatment is
done. Most of the benefit from ICS is achieved in adults at low doses, equivalent to 400 ug of
budenoside per day. Increasing to higher doses provides little further benefit in terms of
asthma control but increases the risk of side effects. Current evidence suggest that in adults,
systemic effects of ICS are not a problem at doses of 400 ug or less budesonide or equivalent
daily. In long-term high doses however, side effects can occur such as cataract and
osteoporosis. It does not mention the correlation between ICS and blood glucose serum.(14)
In a study by Slatore CG, et all in side effect of inhaled corticosteroid in diabetic
subjects however; there is evidence in increasing blood glucose concentration by 1.82 mg/dL
in every additional 100 ug of ICS dose. On the other hand, oral corticosteroid has greater
impact in increasing blood glucose serum.(20)
Other study shows that moderately high dose ICS for treatment of asthma and
COPD is associated with small disturbances in glucose control after a relatively brief period
of therapy in diabetic subjects relative to oral montelukast therapy. The changes are
detectable but smaller than those that would be considered clinically significant, therefore
changing or stopping therapy is not necessary. Careful monitoring of blood glucose is
required when ICS therapy is initiated. In diabetics use of steroids may warrant adjusting or
increasing dose of anti-diabetic therapy. (21)
The systemic side effects of long-term oralor parenteral corticosteroidtreatment
includeosteoporosis, arterial hypertension, diabetes, hypothalamicpituitary-adrenal axis
suppression, obesity, cataracts,glaucoma, skin thinning leading to cutaneous striae andeasy
bruising, and muscle weakness. Patients with asthmawho are on long-term systemic
glucocorticosteroids in anyform should receive preventive treatment for osteoporosis.Caution
and close medical supervision are recommendedwhen considering the use of systemic
glucocorticosteroidsin patients with asthma who also have tuberculosis,parasitic infections,
osteoporosis, glaucoma, diabetes,severe depression, or peptic ulcers.(14)
CHAPTER IV
CONCLUSION
The pathophysiology of asthma involves four events: bronchoconstriction, airway
edema, airway hyperresponsiveness and airway remodeling. Management of asthma includes
prescription of inhaled corticosteroid or oral corticosteroid, ranging from low doses to high
doses depends on the severity of asthma. These medicines have effects in endocrine,
metabolic and immune system. Diabetes is characterized in increased blood glucose
concentration (hyperglycemia). Diabetic patient with asthma should be monitored carefully
because the side effects of corticosteroids medicine.
In conclusion, there are some important points:
Careful monitoring of blood glucose is required when ICS therapy is
initiated.
In diabetics use of steroids may warrant adjusting or increasing dose of anti-
diabetic therapy.
Caution and close medical supervision are recommendedwhen considering
the use of systemic glucocorticosteroidsin patients with asthma who also
have diabetes.
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2. New York State Department of Health.Clinical guideline for the diagnosis, evaluation and management of adults and children with asthma. Available at: http://www.nyhealth.gov. accessed on : December 1st 2012.
3. World Health Organization. Diabetes. Available at:http://www.who.int/topics/diabetes_mellitus/en/. Accessed on : December 1st 2012.
4. Khardori R. Type 2 Diabetes Mellitus. Available at: httP://emedicine.medscape.com/article/117853-overview#a0156. accessed on : December 1st 2012.
5. Fireman P. Understanding asthma pathophysiology. Allergy Asthma Proc 2003:24;79-83.
6. Barnes PJ. Pathophysiology of asthma. Available at:
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7. Ober C, Hoffjan S. Asthma genetics 2006: the long and winding road to gene discovery.
Genes Immun 2006;7:95-100.
8. Moffat MF, Kabesch M, Liang L, et al. Genetic variants regulating ORMDL3 expression
contribute to the risk of childhood asthma. Nature 2007;448:470-3.
9. Galanter J, Choudhry S, Eng C, et al. ORMDL3 gene is associated with asthma in three
ethnically diverse populations. Am J RespirCrit Care Med 2008:177:1194-1200.
10. Tavendale R, Macgregor DF, Mukhopadhay, et al. A polymorphism controlling ORMDL3
expression is associated with asthma that is poorly controlled by current medications. J
Allergy ClinImmunol 2008;121:860-3.
11. Wright RJ, Finn P, Contreras JP, et al. Chronic caregiver stress and IgE expression,
allergen-induced proliferation, and cytokine profiles in a birth cohort predisposed to atopy. J
Allergy ClinImmunol 2004;113:1051-7.
12. Lin YC, Wen HJ, Lee YL, et al. Are maternal psychological factors associated with cord
immunoglobulin E in addition to family atopic history and mother immunoglobulin E?
ClinExp Allergy 2004;34:548-554.
13. National Asthma Education and Prevention Program, Third Expert Panel on the
Diagnosis and Management of Asthma. Expert Panel Report 3: Guidelines for the Diagnosis
and Management of Asthma. Available at: http://www.ncbi.nlm.nih.gov/books/NBK7223/.
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16. Best Practice. Type 2 Diabetes. Available at:
http://bestpractice.bmj.com/best-practice/monograph/24/basics.html. accessed on : December
2nd 2012.
17. Ting C, Bansal V, Batal I, Mounayar M, et al. Impairment of immune systems in
diabetes. In: Diabetes: an old disease, a new insight. Ahmad SI, editor. Texas: LANDES
Bioscience; 2012.
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2008;66:2233-7.
19. Graves DT, Kayal RA. Diabetic complications and dysregulated innate immunity. Front
Biosci 2008;13:1227-1239.
20. Slatore CG, Bryson CL, Au DH. The association of inhaled corticosteroid use with serum
glucose concentration in a large cohort. Am J Med 2009;122:472-8.
21. Faul JL, Wilson SR, Chu JW, Canfield J, Kuschner WG.The effect of an inhaled
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Yth, dr. suweino Ini kumpulan makalah azmi, ayunda afdal, bathin bonia, brili, dan
Christopher.
Kira2 kapan sebaiknya kami mempresentasikan inggris 3 ini ??