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artikel ilmiah #2 17.01 Practical Preventive Therapy for Tuberculosis? Every new episode of tuberculosis — there were 9 million in 2010 — follows a period of asymptomatic infection lasting from weeks to decades. These subclinical infections, which are detectable with a tuberculin skin test or interferon- release assay, offer a target for prophylactic treatment either with drugs or, potentially, a vaccine. Vaccination after infection is not yet an option, but drug treatment has been available for 60 years in the form of 6 to 12 months of isoniazid preventive therapy (IPT), which protects up to 90% of infected persons from active tuberculosis. And yet very few tuberculosis-control programs have successfully carried out IPT on a large scale or even as a targeted treatment for persons at especially high risk for tuberculosis, such as children, contacts of persons with infectious cases, patients with human immunodeficiency virus (HIV) infection, or migrants from countries in which tuberculosis is highly endemic.
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The limited success of IPT is due to a combination of the patients' choice and public-health priorities. Infected but asymptomatic persons who have a small chance of progressing to active tuberculosis are often resistant to taking a drug every day for up to 12 months, risking hepatitis and other side effects. Operationally, program managers know that it would be hard to ensure adherence to the lengthy treatment regimen. Furthermore, IPT is less cost-effective than treating patients with active tuberculosis. The reason is that although isoniazid is cheap, hundreds of infected persons must be treated to prevent one case of tuberculosis. Chemotherapy for active tuberculosis, the principal control strategy today, is comparatively cost-effective but far from ideal. At the patient level, we wait for infections to progress to a potentially fatal, infectious illness for which treatment is not always successful. At the population level, the rate of reduction in the incidence of tuberculosis under chemotherapy is constrained by long periods of latency. Even in the best control programs, in which infection is diagnosed early and with high cure rates, it is not feasible to cut the incidence of tuberculosis by more than about 10% per year. Present evidence suggests that the control programs now operating in most high-burden countries, despite successes in elevating cure rates and reducing mortality, are achieving much less than 10% per year. To compound the problem, as the incidence of tuberculosis falls, the rate of decline slows because growing numbers of cases are developing from old infections. The upshot is that a direct attack on latent infection will be needed before we can think about the elimination of tuberculosis. The latest in a series of investigations of shorter preventive regimens is presented in this issue of the Journal. Sterling et al. carried out a randomized trial of the efficacy of 3 months of isoniazid plus rifapentine combination therapy, given once a week under supervision, as compared with 9 months of daily, self-administered isoniazid alone. This was a noninferiority trial because the efficacy of isoniazid alone in preventing active tuberculosis is already high; the main question was whether efficacy and effectiveness would be at least as good with the shorter, more easily supervised regimen. Because the study evaluated high-efficacy treatments in four low-incidence countries (Brazil, Canada, Spain, and the United States), there were few cases in either of the two well-matched groups in the trial. During 33 months of follow-up in 7731 subjects, an intention-to-treat effectiveness analysis counted 7 cases of tuberculosis in the combination-therapy group and 15 in the isoniazid-only group, for cumulative incidence rates of 0.19% and 0.43%, respectively, and a hazard ratio of 0.38 (95% confidence interval, 0.15 to 0.99). Because intention-to-treat analysis confounds adherence with therapeutic efficacy (better adherence was expected and observed in the shorter, supervised combination-therapy group), Sterling et al. rightly present a per-protocol efficacy analysis, inevitably yielding a smaller difference between the two study groups. However, both analyses showed that combination therapy tended to be superior to isoniazid alone and was clearly not inferior. In the combination-therapy group, fewer patients had hepatotoxicity, as expected from the lower total dose of isoniazid, but hypersensitivity was more commonly associated with the combination of isoniazid plus rifapentine. The findings of this trial, performed in low-incidence countries, suggest that isoniazid plus rifapentine is as good as the principal competing regimens — notably, 3 months of isoniazid plus rifampin or 4 months of rifampin monotherapy in places where the use of isoniazid is not recommended. However, a head-to-head comparison of these three options remains to be performed. Preventive therapy has the potential to deliver greater health benefits in high-incidence countries. In this context, a critical question for the isoniazid-plus-rifapentine regimen is whether 3 months of treatment will provide protection for longer than 2 to 3 years. Evidence from other studies has suggested that it might be adequate for HIV-negative persons but not for those with HIV infection. In a population of Alaskan Inuit living under intense transmission of tuberculosis (before the HIV era), a course of IPT was strongly protective for at least a decade. In contrast, recent studies of HIV-positive patients in Botswana and South Africa have reinforced the earlier finding that the incidence of tuberculosis increases soon after the discontinuation of IPT. In Botswana, the incidence of tuberculosis was more than 10% per year soon after the discontinuation of IPT, presumably because of the reactivation of residual infection, supplemented by reinfection. Would combination therapy with isoniazid plus rifapentine have to be given continuously and under supervision to protect HIV-positive or HIV-negative persons from reactivation or reinfection? A long-term study in a high-incidence setting is needed to find out.
R EF ER EN C ES 1. Global tuberculosis control: WHO report 2011. Geneva: World Health Organization, 2011. 2. Dye C, Floyd K. Tuberculosis. In: Jamison DT, Alleyne GAO, Breman JG, et al., eds. Disease control priorities in developing countries. 2nd ed. Washington, DC: Oxford University Press, 2006:289309. 3. Dye C, Williams BG. Eliminating human tuberculosis in the 21st century. J R Soc Interface 2008;5:653-662 4. Leung CC, Rieder HL, Lange C, Yew WW. Treatment of latent infection with Mycobacterium tuberculosis: update 2010. Eur Respir J 2011;37:690-711 5. Martinson NA, Barnes GL, Moulton LH, et al. New regimens to prevent tuberculosis in adults with HIV infection. N Engl J Med 2011;365:11-20 6. Sterling TR, Villarino ME, Borisov AS, et al. Three months of rifapentine and isoniazid for latent tuberculosis infection. N Engl J Med 2011;365:2155-2166 7. Kaplan GJ, Fraser RI, Comstock GW. Tuberculosis in Alaska, 1970: the continued decline of the tuberculosis epidemic. Am Rev Respir Dis 1972;105:920-926 8. Samandari T, Agizew TB, Nyirenda S, et al. 6-Month versus 36-month isoniazid preventive treatment for tuberculosis in adults with HIV infection in Botswana: a randomised, double-blind, placebocontrolled trial. Lancet 2011;377:1588-1598
artikel ilmiah #1 16.49 Aortic Stenosis The aorta is the main artery carrying blood out of the heart. When blood leaves the heart, it flows through the aortic valve, into the aorta. In aortic stenosis, the aortic valve does not open fully. This decreases blood flow from the heart.
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Causes
As the aortic valve becomes more narrow, the left ventricle has to increase pressure to pump blood out through the valve. To do this extra work, the muscles in the ventricle walls become thicker, which can lead to chest pain. As the pressure continues to rise, blood may back up into the lungs. Severe forms of aortic stenosis prevent enough blood from reaching the brain and the rest of the body. Aortic stenosis may be present from birth (congenital), but usually it develops later in life (is acquired). Children with aortic stenosis may have other congenital conditions. In adults, aortic stenosis usually occurs due to calcium deposits that narrow the valve. This is called calcific aortic stenosis, and it generally affects older people. The other common cause is rheumatic fever, a condition that may develop after strep throat or scarlet fever. Valve problems do not develop for 5 - 10 years or longer after rheumatic fever occurs. Rheumatic fever is increasingly rare in the United States. Calcification of the valve happens sooner in patients who are born with abnormal aortic or bicuspid valves. In rare cases, calcification can also occur more quickly in patients who have received radiation treatment to the chest. Aortic stenosis is not very common. It occurs more often in men than in women. Symptoms
People with aortic stenosis may have no symptoms until late in the course of the disease. The diagnosis may have been made when the health care provider heard a heart murmur and performed tests. Symptoms of aortic stenosis include: Breathlessness with activity Chest pain, angina-type Crushing, squeezing, pressure, tightness Pain increases with exercise, is relieved with rest Pain is felt under the chest bone but may move to other areas, most often the left side of the chest Fainting, weakness, or dizziness with activity Sensation of feeling the heart beat (palpitations) In infants and children, symptoms include: Becoming easily tired with exertion (in mild cases) Failure to gain weight Poor feeding Serious breathing problems that develop within days or weeks of birth (in severe cases) Children with mild or moderate aortic stenosis may get worse as they get older. They also run the risk of developing a heart infection (bacterial endocarditis). Exams and Tests
The health care provider will be able to feel a vibration or movement when placing a hand over the heart. A heart murmur, click, or other abnormal sound is almost always heard through a stethoscope. There may be a faintpulse or changes in the quality of the pulse in the neck (this is called pulsus parvus et tardus). Blood pressure may be low. The following tests may be performed: Chest x-ray Doppler echocardiography ECG Exercise stress testing Left cardiac catheterization MRI of the heart Transesophageal echocardiogram (TEE) Treatment
If there are no symptoms or symptoms are mild, you may only need to be monitored by a health care provider. Anyone with aortic stenosis should be monitored with a health history, physical exam, and an echocardiogram (heart ultrasound). People with severe aortic stenosis are usually told not to play competitive sports, even if they don't have symptoms. If symptoms do occur, strenuous activity must be limited. Medications are used to treat symptoms of heart failure or abnormal heart rhythms (most commonly atrial fibrillation). These include diuretics (water pills), nitrates, and beta-blockers. High blood pressure should also be treated. If aortic stenosis is severe, this treatment must be done carefully so blood pressure does not drop to dangerously low levels. In the past, most patients with heart valve problems were given antibiotics before dental work or an invasive procedure such as colonoscopy. The antibiotics were given to prevent an infection of the damaged heart. However, antibiotics are now used much less often before dental work and other procedures. Check with your health care provider to find out whether you need antibiotics. Patients should stop smoking and be treated for high cholesterol. Surgery to repair or replace the valve is the preferred treatment for adults or children who develop symptoms. Even if symptoms are not very bad, the doctor may recommend surgery based on test results. A less invasive procedure called balloon valvuloplasty may be done instead of surgery. A balloon is placed into an artery in the groin, threaded to the heart, placed across the valve, and inflated. However, narrowing often occurs again after this procedure. A newer procedure done at the same time as valvuloplasty can implant an artificial (prosthetic) valve. This procedure is usually done only in patients who cannot have surgery. Some children may need aortic valve repair or replacement. Children with mild aortic stenosis may be able to participate in most activities and sports. Outlook (Prognosis)
Without surgery, a person with aortic stenosis who has angina, fainting (syncope), or signs of heart failure will usually do poorly. Aortic stenosis can be cured with surgery. After surgery there is a risk for irregular heart rhythms, which can cause sudden death, and blood clots, which can cause a stroke. There is also a risk that the new valve will develop problems (become narrowed or leaky) and will need to be replaced. Possible Complications
Angina (chest pain) Arrhythmias Endocarditis Fainting (syncope) Left-sided heart failure Left ventricular hypertrophy (heart wall thickening) caused by the extra work of pushing blood through the narrowed valve When to Contact a Medical Professional
Call your health care provider if you or your child has symptoms of aortic stenosis. For example, call if you or your child has a sensation of feeling the heart beat (palpitations) for more than a short period of time. Also contact your doctor immediately if you have been diagnosed with this condition and your symptoms get worse or new symptoms develop. Alternative Names
Aortic valve stenosis; Left ventricular outflow tract obstruction; Rheumatic aortic stenosis; Calcium aortic stenosis References
Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr., Faxon DP, Freed MD, et al; 2006 Writing Committee Members; American College of Cardiology/American Heart Association Task Force. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients with Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118:e523-e661. Carabello BA. Valvular heart disease. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 75. Nishimura RA, Carabello BA, Faxon DP, et al. ACC/AHA 2008 guideline update on valvular heart disease: focused update on infective endocarditis: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;52(8):676-685. Otto CM, Bonow RO. Valvular heart disease. In: Bonow RO, Mann DL, Zipes Dp, Libby P, Braunwald E, eds.Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. St. Louis, Mo: WB Saunders; 2011:chap 66.
artikel kuliah #2 16.41 MODUL 8 IMUN DAN KULIT LBM 3: Immunodeficiency
STEP 7 1. Definisi Kelainan atau kondisi di mana respon kekebalan tubuh berkurang atau tidak ada, sehingga infeksi lebih sering terjadi, lebih sering berulang, luar biasa berat dan berlangsung lebih lama dari biasanya. Imunodefisiensi ini hasil dari masalah perkembangan organ maupun jaringan limfoid, infeksi virus yang menekan fungsi kekebalan tubuh, dan paparan/pengobatan melalui agen imunosupresif. ( S U M B E R : H T T P : / / W W W .U T O R O N T O .C A / K I D S / I M M U N O D E F I C I E N C Y .H T M A R T I K E L O L E H D R . S A U L G R E E N B E R G , U N I V E R S I T A S T O R O N T O .)
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2. Etiologi § Genetik § Defisiensi metabolisme dan biokimia § Defisiensi vitamin dan mineral § Gangguan embriogenesis § Penyakit autoimun § Defisiensi imun didapat
( SUMBER: ARTIKEL OLEH REBECCA H. BUCKLEY, MD.)
3. Klasifikasi § Imunodefisiensi Primer Terjadi pada manusia, sangat jarang ditemukan, dan mempengaruhi setiap tahap diferensiasi dalam sistem imun. o Defisiensi sel B ü IgA deficiency & Common Variable Immunodeficiency (CVID) IgA merupakan imunoglobulin utama dalam sekresi mukosa sehingga terlibat dalam pertahanan saluran pernapasan dan pencernaan. Melemahnya pertahanan mukosa memudahkan seseorang mengalami infeksi sinopulmonal dan diare yang berulang. Meskipun dasar molekular kelainan ini belum dimengerti, yang diduga sebagai penyebabnya adalah defek sel B/perubahan produksi sitokin sel T yang mengendalikan respon IgA. ü Transient hypo-g-globulinemia Biasanya terjadi pada bayi, di mana maternal IgG menurun, dan terjadi masalah serius pada bayi prematur. Terjadi infeksi saluran napas yang berulang, terkait dengan kadar IgG yang rendah yang tiba-tiba sering normal kembali pada umur 4 tahun. o Defisiensi sel T ü Rentan terhadap infeksi opportunistik ü Berdampak negatif pada imunitas humoral ü Memungkinkan munculnya alergi, keganasan limfoid, serta autoimun sindrom. Dikarenakan seleksi negatif pada timus tidak efisien atau kegagalan untuk menghasilkan regulatory cells. o Severe Combined Immunodeficiency Atau Imunodefisiensi Kombinasi Berat mewakili sekumpulan sindrom yang berbeda secara genetik yang semuanya menunjukkan adanya defek, baik dalam respon imun humoral maupun imun selular. Janin yang terserang mudah mengalami infeksi berulang yang berat oleh berbagai macam patogen dan infeksi opportunistik. § Imunodefisiensi Sekunder Dapat ditemukan pada pasien malnutrisi, infeksi, kanker, penyakit ginjal. Penyakit ini juga terjdi pada pasien yang menerima kemoterapi atau terapi radiasi untuk keganasan atau menerima obat imunosupresif untuk mencegah penolakan graft atau mengobati penyakit autoimun. Beberapa keadaan imunodefisiensi sekunder ini dapat disebabkan oleh hilangnya imunosintesis imunoglobulin yang tidak memadai (malnutrisi), atau deplesi limfosit (karena obat atau infeksi yang berat). Sebagai suatu kelompok, imunodefisiensi sekunder lebih umum terjadi daripada gangguan primer yang bersifat genetik.
(SUMBER : BUKU AJ AR PATOLOGI EDISI 7 VOL. 1 , ROBBINS KUMAR COTRAN, EGC )
4. Contoh penyakit · AIDS
Syndrom Chdiak-higasi :netrofil tidak bisa melisiskan antigen, mekanisme fagosit masih bisa, gangguan lisosom.
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5. Mekanisme · Penularan melalui cairan (saliva = cairan tubuh yang dapat menularkan penyebaran virus HIV), melalui hub sexual. HIV masuk melalui mukosa vaginaà makrofag beredar di kulit (denditrik) à di permukaan mukosa, makrofag mengikat virus à membawa virus ke limfonodi (byk mengandung sel Th/ CD4+ ) à menyerang àreplikasi à melekat di permukaan sel Th à mengeluarkan reseptor à HIV tidak berkapsul dan melakukan penetrasi ke sel à bertranskrip genom à masuk ke DNA manusia à berubah menjadi rantai protein àkeluar dari membran à menyerang . · Karena DNA virus bergabung dengan DNA manusia, terjadilah deficiency à virus menyebar ke seluruh jaringan limfoid à ke jaringan sekitarnyaà sel kelelahan à terjadi deficiency.
Dasar utama patogenesis HIV adalah kurangnya jenis Lymfosit T helper/inducer yang mengandung marker CD4 (sel T4) . Lymfosit merupakan pusat dan sel utama yang terlibat secara langsung maupun tidak langsung dalam menginduksi fungsi - fungsi imunologik. Kelainan selektif pada satu, jenis sel menyebabkan kelainan selektif pada satu jenis sel. Human Immunodeficiency Virus mempunyai tropisme selektif terhadap sel T4,karena molekul CD4 yang terdapat pada dindingnya adalah reseptor dengan affinitas yang tinggi untuk virus ini. Setelah HIV mengikat diri pada molekul CD4, virus masuk kedalam target dan ia melepas bungkusnya kemudian dengan enzym reverse transcryptase ia merubah bentuk RNAnya menjadi DNA agar dapat bergabung menyatakan diri dengan DNA sel target. Selanjutnya sel yang berkembang biak akan mengundang bahan genetik virus. Infeksi oleh HIV dengan demikian menjadi irreversibel dan berlangsung seumur hidup. Berbeda dengan virus lain, virus HIV menyerang sel target dalam jangka lama. Jarak dari masuknya virus ke tubuh sampai terjadinya AIDS sangat lama yakni 5 tahun atau lebih. Infeksi oleh virus HIV menyebabkan fungsi sistem kekebalan tubuh rusak yang mengakibatkan daya tahan tubuh berkurang atau hilang, akibatnya mudah terkena penyakit-penyakit lain seperti penyakit infeksi yang disebabkan oleh bakteri protozoa dan jamur dan juga mudah terkena penyakit kanker seperti sarkoma kaposi. HIV mungkin juga secara lansung menginfeksi sel-sel syaraf menyebabkan kerusakan neurologis.
(SUMBER: HTTP://LIBRARY.USU.AC.ID/DOWNLOAD/FKM/FKMFAZIDAH5 .PDF)
6. Gejala à Tanda-tanda gejala-gejala (symptom) secara klinis pada seseorang penderita AIDS adalah diidentifikasi sulit karena symptomasi yang ditujukan pada umumnya adalah bermula dari gejala-gejala umum yang lazim didapati pada berbagai penderita penyakit lain, namun secara umum dapat kiranya dikemukakan sebagai berikut : • Rasa lelah dan lesu • Berat badan menurun secara drastis • Demam yang sering dan berkeringat diwaktu malam • Mencret dan kurang nafsu makan • Bercak-bercak putih di lidah dan di dalam mulut • Pembengkakan leher dan lipatan paha • Radang paru-paru • Kanker kulit à Manifestasi klinik utama dari penderita AIDS pada umumnya ada 2 hal antara lain tumor dan infeksi oportunistik : § Manifestasi tumor di antaranya: ü Sarkoma kaposi ; kanker pada semua bagian kulit dan organ tubuh. Frekuensi kejadiannya 36-50% biasanya terjadi pada kelompok homoseksual, dan jarang terjadi pada heteroseksual serta jarang menjadi sebab kematian primer. ü Limfoma ganas ; terjadi setelah sarkoma kaposi dan menyerang syaraf, dan bertahan kurang lebih 1 tahun. § Manifestasi Oportunistik diantaranya ü Manifestasi pada Paru-paru o Pneumonia Pneumocystis (PCP) Pada umumnya 85% infeksi oportunistik pada AIDS merupakan infeksi paru-paru PCP dengan gejala sesak nafas, batuk kering, sakit bernafas dalam dan demam. o Cytomegalo Virus (CMV) Pada manusia virus ini 50% hidup sebagai komensial pada paru-paru tetapi dapat menyebabkan pneumocystis. CMV merupakan penyebab kematian pada 30% penderita AIDS. o Mycobacterium Avilum Menimbulkan pneumoni difus, timbul pada stadium akhir dan sulit disembuhkan. o Mycobacterium Tuberculosis Biasanya timbul lebih dini, penyakit cepat menjadi miliar dan cepat menyebar ke organ lain di luar paru. ü Manifestasi pada Gastroitestinal Tidak ada nafsu makan, diare khronis, berat badan turun lebih 10% per bulan. § Manifestasi Neurologis Sekitar 10% kasus AIDS nenunjukkan manifestasi Neurologis, yang biasanya timbul pada fase akhir penyakit. Kelainan syaraf yang umum adalah ensefalitis, meningitis, demensia, mielopati dan neuropari perifer. (SU M BER : H T T P : / / R E P O S I T O R Y .U S U .A C .I D / B I T S T R E A M / 1 2 3 4 5 6 7 8 9 / 3 6 8 4 / 1 / F K M F A Z I D A H 4 .P D F )
artikel kuliah #1 Selasa, 12 Februari 201310.14 MODUL 8 IMUN DAN KULIT LBM 2: SLE
STEP 7 1. Definisi autoimun? Respon imun terhadap antigen jaringan sendiri yang disebabkan kegagalan mekanisme normal yang berperan untuk mempertahankan self-tolerance sel B, sel T, atau keduanya. ( S U M B E R : I M U N O L O G I D A S A R O L E H K A R N E N G A R N A B A R A T A W I D J A J A F K U I .) 2. Apa faktor yang memperberat autoimun? § Family or Personal History of Autoimmune Disease Many, if not most autoimmune diseases, have a genetic or hereditary basis. This means that if you have a family member with an autoimmune disease, you are at an increased risk of developing an autoimmune condition as well. And it does not have to be the same disease - one relative may have autoimmune thyroid disease, another multiple sclerosis, and another inflammatory bowel disease. § Gender or Hormonal Status Seventy-five percent of autoimmune diseases occur in women, and most frequently during the childbearing years. Higher estrogen levels seem to stimulate the immune system, which may explain why men are less affected. § Bacterial and Viral Infections and Illnesses Viruses, bacteria and mycoplasma, a type of small-cell bacteria, are implicated in autoimmune diseases. Often a bout of illness with a virus such as the Epstein- Barr virus triggers the onset of an autoimmune disease. § Toxic Metal Exposure An estimated twenty-five percent of us have some form of heavy metal poisoning. Studies have shown that exposure to toxic metals such as mercury, cadmium, lead, arsenic, aluminum, nickel and other heavy metals can be linked to the autoimmune process: The heavy metals induce autoantibodies, which then create autoimmune diseases. § Toxic Chemical Exposure Toxins such as pesticides, solvents, industrial chemicals, even household cleaners and hair dyes are being implicated in autoimmune diseases. These toxins are are everywhere, and they greatly increase the risk of all diseases in general. § Vaccinations/Immunizations Scientists have found a connection between some autoimmune diseases and vaccinations. In the February 2000 issue of Autoimmunity, ten research articles evaluate the causal link between vaccinations and autoimmune disease. For instance, the controversial anthrax vaccine has been causally linked to the development of autoimmune diseases. § Stress and Trauma Many people have noticed a direct link between a major stressful life event and the development of an autoimmune disease six to twelve months later. Unmanaged stress is a risk factor for the developemnt of all major diseases, including heart disease and cancer. I myself noticed that I always got much worse symptom-wise during any stressful situations. Our thoughts and feelings have a direct impact on our immune system. Loneliness is now recognized as the number one predictor of disease due to its immune suppressing action. Laughter and feelings of happiness, on the other hand, increase and enhance the actions of our immune cells. § Smoking Smoking increases the risk of several autoimmune diseases, primarily because of the chemicals in cigarettes. § Nutritional Deficiencies Poor diet is an important factor in autoimmunity because poor nutrition compromises the immune system. Processed foods are loaded with chemicals, hormones, steroids, trans-fats and sugars, which promote the creation of free radicals in the body, which in turn damage the cells. ( S U M B E R : A U T O I M M U N E – T H E C A U S E A N D T H E C U R E O L E H A N N E S S B R O C K L E Y D A N K R I S T I N U R D I A L E S .) 3. Klasifikasi (macam – macam) autoimun? Jelaskan patogenesis, gejala, tanda, pemeriksaan penunjang! § Organ spesific Adalah respon imun yang menyerang dari antigen ke organ atau kelenjar tertentu. Selsel organ dapat langsung dipengaruhi oleh humoral atau sel efektor, dan kadang antibodi lebih menstimulus/menghambat fungsi normal dari organ target. Beberapa penyakit autoimun melibatkan kerusakan sel langsung dan dengan demikian terjadi ketika limfosit atau antibodi mengikat pada antigen sel membran, menyebabkan sel lisis. Secara bertahap kinerja organ menurun akibat kerusakan sel. § Systemic/Non-organ spesific Adalah respon imun yang menyerang berbagai antigen target dan melibatkan sejumlah organ dan jaringan. Ini mempengaruhi sistem kekebalan tubuh secara keseluruhan, yang pada gilirannya mengaktifkan sel T dan sel B. Kerusakan jaringan tersebar luas. ( S U M B E R : H T T P : / / W W W .B I O T E C H A R T I C L E S .C O M / B I O T E C H R ESEA R C H-A R TI C LE/ A U TOI M M U N I TY -OV ER V I EW-A N D C L A S S I F I C A T I O N - O F - A U T O I M M U N E - D I S E A S E S - 7 7 1 .H T M L ART I KEL AU T O I MMU N I T Y - O VERVI EW AN D CL ASSI FI CAT I O N O F A U T O I M M U N E D I S E A S E O L E H P R E E T H I V E N K A T E S W A R A N .) (SU M BER : I M M U N OBI OLOGY : THE I M M U N E SY STEM I N HEA LTH A N D D I S E A S E . 5 T H E D I T I O N . J A N E W A Y C A J R , T R A V E R S P , W A L P O R T M , E T A L . N E W Y O R K : G A R L A N D S C I E N C E; 2 0 0 1 .) 6. Apa yang dimaksud self tolerance? · Imunosupresi hanya terhadap satu antigen dan tidak disertai oleh gangguan terhadap respon antigen yang lain. · Keadaan tidak adanya respon sel limfoid yang aktif terhadap antigen tertentu. · Mekanisme homeostasis pada keadaan normal tubuh yang melindunginya terhadap rangsangan jaringan tubuh sendiri yang tidak dikehendaki. ( S U M B E R : I M U N O L O G I D A S A R O L E H K A R N E N G A R N A B A R A T A W I D J A J A F K U I .) Ada empat mekanisme utama yang bertanggung jawab untuk self-tolerance: § Clonal deletion Atau disebut juga apoptosis. Reseptor antigen dengan antibodi di dalam tubuh bereaksi dan mengirimkan sinyal bahwa ada sel yang harus terprogram untuk mati. § Clonal anergy Mengacu pada keadaan fungsional yang tidak responsif. Berbeda dengan clonal deletion, clonal anergy ini tidak menyebabkan apoptosis, tapi menghasilkan disfungsi sementara reaktivitas terhadap antigen. § Clonal ignorance Mengacu pada keadaan di mana antigen tertentu muncul dan tidak terdeteksi oleh sistem imun di dalam keadaan normal sehingga clonal ignorance terbentuk pada keadaan ini. § Active regulation Makrofag sangat penting dalam mekanisme ini. (SU M BER : H T T P : / / I M M U N E W E B .X X M U .E D U .C N / R E A D I N G / C L I N I C / 9 .P D F A R TI KEL A U TOI M M U N E D I SEA SE OLEH R OBER T V OLP E, U N I V E R S I T Y O F T O R O N T O .)
M H C (Major Histocompatibility Complex) Merupakan suatu daerah kromosom yang terdiri dari satu seri gen yang memberi kode untuk ekspresi permukaan sel antigen-antigen transplantasi. Antigen-antigen transplantasi ini umumnya adalah glikoprotein yang berada pada permukaan kebanyakan sel berinti. MHC tidak hanya mengendalikan sintesis antigen transplantasi dan penolakan cangkok, tetapi juga mempengaruhi respon imun terhadap tantangan infeksi dan kerentanan terhadap perkembangan penyakit yang ditengahi imunologik. Misal: Sel B mengenal epitop pada molekul utuh, sedangkan sel T mengenal epitop pada fragmen antigen yang diikat oleh molekul pada permukaan APC. H L A (Human Leucocyte Antigens) Adalah MHC pada manusia. Antigen HLA terdiri atas berbagai golongan, yang mampu menyandi molekul MHC-I, MHC-II, dan protein lain. ( S U M B E R : I M U N O L O G I D A S A R O L E H K A R N E N G A R N A B A R A T A W I D J A J A F K U I .) 8. Dari skenario, gambaran bercak menyerupai kupu-kupu itu tanda-tanda penyakit SLE (sistemik lupus eritremartosus). Jadi definisi SLE? è SLE merupakan penyakit autoimun yang ditandai oleh produksi antibodi terhadap komponen-komponen inti sel yang berhubungan dengan manifestasi klinis yang luas. Penyakit ini multi-sistem dengan etiologi dan patogenesis yang belum jelas. è Diduga terbentuknya kompleks imun merupakan ciri imunopatologis lupus. Antibodi yang mengikat nukleosum dapat terjadi di ginjal dan membentuk kompleks imun in situ. Baik kompleks imun yang dibentuk dalam sirkulasi atau insitu berperan dalam terjadinya kerusakan ginjal, kulit, plexus koroid di otak, dan jaringan lainnya. ( S U M B E R : H T T P : / / E J O U R N A L .U N U D .A C .I D / A B S T R A K / 7 _ E D I T E D .P D F TI N J A U A N P U STA KA A SP EK I M U N OLOGI SLE OLEH Y U R I A W A N T I N I D A N K E T U T S U R Y A N A , F K U N U D .)
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