Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of many forms of liver disease is largely unknown. Recent research has identified certain immunogenetic factors which may play a role in the progression of alcoholic cirrhosis as well as autoimmune forms of cirrhosis. In this study we examined the role of familial alcoholism and HLA status in determining age of liver disease onset. Patients with biopsy-proven nonalcoholic autoimmune cirrhosis and having a history of familial alcoholism experience an earlier age of onset of liver disease than patients without a family history of alcoholism. The same result was true for patients with alcoholic liver disease. This effect may be more prominent in females. Subjects with HLA B-8 also had a younger age of onset of nonalcoholic autoimmune liver disease. The presence of a family history of alcoholism in conjunction with the presence of HLA B-8 and DR-3 also was related to an earlier age of disease onset. These findings suggest that the susceptibility to develop alcoholism and nonalcoholic autoimmune liver disease may be transmitted conjointly and point to potential fruitful areas of research for identifying individuals at risk for developing cirrhosis as well as detecting genetic markers for alcoholism.
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PMID:Early onset of nonalcoholic cirrhosis in patients with familial alcoholism. 217 63

A 46-year-old female suffering from liver cirrhosis was referred to us for living-donor liver transplantation (LDLT). Pre-transplant lymphocyte cross-match tests were positive. The recipient showed immunoreactivity against donor human leukocyte antigen (HLA) Class I antigens, a finding confirmed by flow cytometry. Additional tests confirmed donor-specific lymphocyte immunoreactivity against HLA B 55. As no other suitable donor was available, we performed LDLT coupled with splenectomy, despite the positive cross-match. Tacrolimus, methylprednisolone and mycophenolate mofetil were used postoperatively for immunosuppression. The postoperative course was uneventful until Day 3 when blood tests showed disorders in liver function and the patient's condition suddenly worsened. Although intensive care (including plasma exchange) was given, her condition continued to deteriorate. Flow cytometry initially showed that immunoreactivity against Class I antigens was down-regulated immediately after LDLT, but further testing showed that it had increased again. We diagnosed humoral rejection based on clinical, immunological and histopathological findings and suggest that this was mediated by an immune response to donor-specific antigens. The patient experienced multi-organ failure and died on post-operative Day 9.
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PMID:Antibody-mediated rejection after adult living-donor liver transplantation triggered by positive lymphocyte cross-match combination. 2471 61