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)

Microchimerism may be involved in the etiopathogenesis of autoimmune diseases such as scleroderma. Primary biliary cirrhosis (PBC) shares some features with scleroderma, including a female predominance and a histologic picture reminiscent of chronic graft-versus-host disease. Our aim was to detect Y-chromosome-specific sequences as a marker for microchimerism in liver tissue of female patients with PBC. Liver biopsies of 105 female patients were investigated (28 patients with primary biliary cirrhosis, 25 patients with chronic hepatitis C, 6 patients with chronic hepatitis B, 9 with autoimmune hepatitis, and 37 patients with other liver diseases) by a sensitive Y-chromosome-specific polymerase chain reaction and/or fluorescence in situ hybridization (FISH) technique for the detection of the Y chromosome on a single cell level. In the liver of 9 (8.6%) female patients Y-chromosome-specific sequences were detected by PCR. Five of the patients had PBC as underlying disease, 2 had chronic hepatitis C, and 2 other liver diseases. No significant difference in the positivity rate for Y-specific sequences in females with PBC and patients with other liver diseases was found (P > 0.05). By FISH, single cells with one Y chromosome were detected in liver specimens from 3 of 21 patients suffering from PBC and from 1 of 13 patients with other liver diseases. In summary, microchimerism can be detected in livers of patients with hepatic diseases. However, in our study we found no evidence for an increased prevalence of microchimerism in the livers of patients with primary biliary cirrhosis. Our data suggest that microchimerism does not play a significant role in the development of PBC.
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PMID:Lack of evidence for involvement of fetal microchimerism in pathogenesis of primary biliary cirrhosis. 1235 28

Male microchimerism is frequent in the adult female liver and is attributed to fetal cells originating from previous male offspring. It has never been studied in pregnant women, female children, or fetuses. We examined its frequency and cellular nature in normal and diseased female livers from fetal life to adulthood. Forty-six liver samples from 29 women, 6 female children, and 11 female fetuses were screened for the Y chromosome via polymerase chain reaction (PCR) assay and fluorescent in situ hybridization (FISH). The X chromosome was used as an internal control. A third PCR assay was used for Y genotyping. The Y chromosome was detected in 5 of 6 children, 7 of 11 fetuses, 3 of 9 women with normal liver, 7 of 10 women with chronic hepatitis C, 5 of 6 women with acute liver disease during pregnancy with male offspring, and 2 of 4 nonpregnant women with fulminant hepatitis. In positive samples, the mean XY/XX ratio was 0.012 (+/-0.004). In women, male microchimerism was correlated with previous male offspring. Male hepatocytes, detected via FISH combined with anti-hepatocyte immunohistochemistry, were observed only in fetuses (4/9) and in postpartem women (4/6). Y genotypes were different from each other in 4 of 5 female livers. In conclusion, male liver microchimerism is frequent in normal and diseased female livers. The presence of male cells in the liver of female children and fetuses is probably due to the transplacental transmission of fetal cells preexisting in the mother and acquired either from previous pregnancy with male offspring or during the mother's own fetal life.
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PMID:Male cell microchimerism in normal and diseased female livers from fetal life to adulthood. 1596 17

Since first being described in 1998, de novo autoimmune hepatitis (AIH) after liver transplantation has been reported in several cases suffering from non-autoimmune liver diseases and primary biliary cirrhosis (PBC). Glutathione S-transferase (GST) T1 genotype mismatches between donor and recipient have also been suggested to constitute a risk factor for de novo AIH. Here, we report a 33-yr-old woman who presented complaining of marked fatigue and jaundice four yr after living-donor liver transplantation for PBC. On examination, transaminase levels were highly elevated and ANA and antimitochondrial antibody M2 were positive. Histological findings showed zonal necrosis with lymphoplasmacytic infiltration closely resembling AIH. She had pretreatment AIH score of 16 and 19 points after relapse of de novo AIH. Two color fluorescence in situ hybridization with X and Y chromosome-specific probes clearly revealed that the hepatocytes were of donor origin and lymphocytes were of patient origin. The GSTT1 genotype of the patient and the donor were the same null type, suggesting that mechanisms other than GSTT1 mismatches may exist in de novo AIH development. In conclusion, recipient immune cells attacked the allogeneic transplanted liver of the patient via de novo AIH, although the exact participation of autoimmune mechanisms is unclear.
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PMID:De novo autoimmune hepatitis following living-donor liver transplantation for primary biliary cirrhosis. 1819 May 52

Alpha-fetoprotein (AFP) computational secreted network construction and analysis of human hepatocellular carcinoma (HCC) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer and the database for annotation, visualization, and integrated discovery, we identified and constructed significant molecule AFP secreted network from 25 no-tumor hepatitis/cirrhotic liver tissues and 25 HCC patients in the same GEO Dataset GSE10140-10141. Our result verified AFP secreted module in the upstream of no-tumor hepatitis/cirrhotic liver tissues (AMELY, LCN2, and REG3A activation; DKK1, SFRP4, and SPINK1 inhibition) and its downstream (PRSS1, REG3A, and TSHB activation; AMELY and DKK1 inhibition), and also in the upstream of HCC (LCN2, REG3A, and SFRP4 activation; AMELY and DKK1 inhibition) and its downstream (AMELY activation; DKK1, LCN2, PRSS1, SEMA3B, and SPINK1 inhibition). Importantly, we data-mined that AFP secreted cluster of HCC is involved in disease mutation (only in HCC terms) without cell surface receptor linked signal transduction, neuroactive ligand-receptor interaction, cell-cell signaling, and pancreas (only in no-tumor hepatitis/cirrhotic liver tissues terms), the condition which is vital to invasion of HCC. Our result demonstrated that common terms in both no-tumor hepatitis/cirrhotic liver tissues and HCC include secreted extracellular region, extracellular region part, extracellular space, signal peptide, signal, disulfide bond, glycosylation site N-linked (GlcNAc...), and glycoprotein, and these terms are less relative to invasion; therefore, we deduced the weaker AFP secreted network in HCC consistent with our number computation. We predicted AFP high expression localization within cells of HCC and without secretion to extracellular matrix. It would be necessary of AFP secreted function to decrease invasion of HCC.
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PMID:AFP computational secreted network construction and analysis between human hepatocellular carcinoma (HCC) and no-tumor hepatitis/cirrhotic liver tissues. 2053 28