Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eighty eight patients of glomerulonephropathies (HBsAg positive 67; HBsAg negative 21) and 88 matched and healthy controls were screened for non-organ specific autoantibodies-ANA, AMA, ASMA and APCA by indirect immunofluorescent technique. The 2.3 per cent positivity in the test group and the 8 per cent positivity in the control group did not suggest the involvement of hepatitis-B virus (HBV), as an influencing or associated agent. When 48 patients with glomerulonephropathies and 23 controls were screened for liver cell membrane (LMA) and renal cell membrane antibodies (RMA) by indirect immunofluorescent technique using isolated rat hepatocytes and renal cells, 79.2 per cent LMA positivity was seen in the HBsAg positive group and 41.7 per cent in the negative group and RMA positivity was 58 per cent in the positive group and 25 per cent in the negative group. Simultaneous positivity for both LMA and RMA was recorded in 50 per cent of the HBsAg positive patients and 15.7 per cent of the negative ones. The results suggest the possibility of an organ specific autoimmune trigger more frequently in HBV associated glomerulonephropathy.
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PMID:Non-organ specific & organ-specific auto-antibodies in hepatitis-B virus associated glomerulonephropathies. 280 26

To verify the possible effect of IFN-beta treatment on auto antibodies development in multiple sclerosis (MS) we studied 69 MS patients before and during the treatment with IFN-beta 1b (n=35) and IFN-beta 1a (n=20) for 27 and 12 months respectively, and, as controls, 14 untreated MS patients. The serum, collected every 3 months from all the patients, was investigated for the presence of antinuclear (ANA), anti-smooth muscle (ASMA), anti-mitochondrial (AMA), anti-native DNA (nDNA) anti-cardiolipin (aCL), anti-parietal cells (APCA), anti-microsomal (AMC) and anti-tireoglobulin (ATG) antibodies. Among the IFN-beta 1b-treated MS patients an increase of the frequency and of the level of ANA, AMC and ATG was observed. ASMA and ANA antibodies were already present in about 45% of the MS patients before the treatment and fluctuated over the time. In one patient the treatment was interrupted after 6 months because of the occurrence of high ASMA level and of an autoimmune hepatitis. The data obtained in the smaller number of MS patients treated with IFN-beta 1a were very similar. No increase in aCL level was observed during both the IFN treatments. Our results indicate that the treatment with IFN-beta induces an increase of AMC and ATG antibodies in MS patients and confirm that, although rare, autoimmune diseases could be observed. The possible effect of these auto antibodies on the treatment efficacy and on MS clinical course need to be further investigated.
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PMID:Serum auto antibodies presence in multiple sclerosis patients treated with beta-interferon 1a and 1b. 1087 87