Multiple Sclerosis (MS) is an autoimmune disease that causes myelin destruction in the Central Nervous System (CNS). Characteristics of this disease are perivascular infiltration by inflammatory cells, demyelination and loss of axons, accompanied by multiple plaque formation in the brain and spinal cord. According to the National Multiple Sclerosis Society, 400,000 people suffer from MS in the United States and about 2.5 million people worldwide. The disease is usually diagnosed in patients aged 20-45 years and more often found in females than males with a ratio of 2: 1. Nevertheless, the etiology of MS is still unknown, but it is suspected that genetic and environmental factors may induce a response to central nervous system autoantigen, such as Epstein-Barr Virus (EBV) infection. It then causes edema, demyelination, axon destruction and loss of oligodendrosites, resulting in neurological deficits, plaque formation, scarring and reduced brain volume. Multiple sclerosis symptoms and signs actually vary greatly depending on the location of the lesions and the course of the various diseases. Multiple sclerosis, moreover, can be divided into four clinical categories, namely Clinically Isolated Syndrome (CIS), Relapsing Remitting Multiple Sclerosis (RRMS), Secondary Progressive Multiple Sclerosis (SPMS) and Primary Progressive Multiple Sclerosis (PPMS). Diagnosis of Multiple sclerosis is established based on clinical symptoms and supporting investigations, such as MRI, CSF and neurological examination. In CSF examination, oligoclonal bands are found in over 90% of patients, considered as one of the laboratory criteria supporting the diagnosis of MS. There are four kinds of drugs that have been approved by the FDA as disease modifying therapy for the initial treatment of MS patients, namely interferon beta-1a, subcutaneous (SC) interferon beta-1a, interferon beta-1b and glatiramer acetate In conclusion, life expectancy in MS patients is only slightly reduced and survival is related to the disability occurred.
by The American College of Rheumatology published in 1982 and revised in 1997. Diagnosis of SLE is made if a patient satisfied 4 of 11 the criteria. 5 The criteria are malar rash, discoid rash, photosensitivity, oral ulcers, nonerosive arthritis, pleuritis or pericarditis, renal disorder, neurologic disorder, hematologic disorder, immunologic disorder, positive antinuclear antibody. DiscussionThis autoimmune disease characterized by the aberrant production of a broad and heterogenous group of autoantibodies. Autoantibodies directed to nuclear (ANAs), cytoplasmic, and cellular membrane antigens are considered the serological hallmark in SLE. ANAs consist of various types of autoantibodies characterized by different antigen specificities. These nuclear antigens include single strand (ss) and double strand (ds) DNA (deoxyribonucleic acid), histone proteins, nucleosome (histone-DNA complex), centromere proteins, and extractable nuclear antigens (ENA) (Smith antigen (Sm), Ro, La, ribonucleoprotein), etc. Common autoantibody -mediated mechanisms of damage in SLE include immune complex mediate damage, cell surface binding and cytotoxicity, reactivity with autoantigens expressed on apoptotic or activated cell surface, penetration into living cells, and binding to cross reactive extracellular molecules. Even though the presence of autoantibodies in SLE has been known, for more than 60 years, still nowadays a great effort is being made to understand the pathogenetic, diagnostic, and prognostic meaning of such Autoantibodies. 7,8The traditional methods for detecting ANA are indirect immunofluorescence (IIF) and enzyme immunoassay (ELISA).9 In general, if a patient presents clinical manifestations of an autoimmune disease, the first test to be requested is ANA detection using indirect immunofluorescence using HEp-2cells, due to its great sensitivity. The different possible patterns, the intensity, and the titers obtained by consecutive dilutions must be carefully examined, The usefulness of this testing has been evaluated in retro-spective studies of patients with systemic rheumatic disease (SRD), and it has been proven that its positive predictive value is low due to the relatively large amount of false positive results.10 ANA pattern is reffered to the pattern of nuclear fluorescence observed under fluorescence microscopy. Certain patterns of fluorescence are associated with certain nuclear antigens and specific disease. Patterns of staining provide a clue to the category of nuclear antigen involved and are dependent upon the type of substrate used, and to a certain extent, the experience of the technician. Reliance on ANA patterns has largely been replaced by identification of specific antinuclear antibodies through the ANA profile. 11ANA profile with immunoblotting or ELISA methods can detect some antibodies such as seen in Table 1. 9,12,13 Double stranded DNA antibodies (anti-dsDNA) have been considered useful and valuable in the diagnosis of SLE.1 Anti-Sm antibodies are a highly specific marker for SLE and Anti-Sm re...
Systemic Lupus Erythematosus (SLE) adalah penyakit autoimun dan bersifat multi organ. Kelainan hematologi sering ditemukandi penyakit ini, begitu juga dengan kelainan ginjal yang merupakan salah satu faktor yang sangat berpengaruh. Uji ANA profile dapatmengetahui subtipe antibodi antinuklear yang khas. Autoantibodi tersebut diduga berhubungan dengan manifestasi klinis. Penelitian inimerupakan penelitian analitik retrospektif di Laboratorium Patologi Klinik dan Instalasi Rekam Medik RSUP. Dr. Wahidin SudirohusodoMakassar dengan mengambil data hasil ANA profile, darah rutin dan urinalisis pasien terduga SLE masa waktu Januari 2014–Juli 2016.Data dikelompokkan menjadi SLE dan nonSLE. Analisis statitik dengan uji Chi Kuadrat dan Fisher. Dari 72 sampel, 39 dengan diagnosaakhir SLE. Terdapat hubungan bermakna antara anti RNP/Sm, Sm, SS-A, Ro-52, dsDNA, Nucleosome, Histone, Ribosomal P denganSLE (p<0,05). Terdapat hubungan bermakna antara anti dsDNA (p=0,029) dan anti nucleosome (p=0,037) dengan anemia serta antidsDNA (p=0,013) dan anti nucleosome (p=0,036) dengan gangguan ginjal. Tidak ditemukan hubungan bermakna antara autoantibodidalam penelitian ini dengan leukopenia, limfopenia dan trombositopenia. Anti RNP/Sm, Sm, SS-A, Ro-52, dsDNA, nucleosome, Histones,Ribosomal P berhubungan dengan SLE. Anti dsDNA dan anti nucleosome berhubungan dengan anemia dan gangguan ginjal padaSLE, sehingga mungkin dapat digunakan untuk meramalkan kejadian tersebut, walaupun dibutuhkan penelitian lanjutan untukmembuktikannya. Tidak ditemukan autoantibodi yang dapat dihubungkan dengan leukopenia, limfopenia dan trombositopenia.
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