Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of primary biliary cirrhosis (PBC)-autoimmune hepatitis (AIH) overlap syndrome with concurrent idiopathic thrombocytopenic purpura (ITP) and Hashimoto's disease with positivity for anticentromere antibody. The patient was a 64-year-old woman with symptoms of jaundice and general fatigue. About 30 years earlier, she had been diagnosed as having ITP and had undergone splenectomy. As part of her present history, she had exhibited liver dysfunction in 1995, during the follow-up of Hashimoto's disease, and a liver biopsy led to the diagnosis of PBC. In March 2000, she was admitted to hospital because of general fatigue and jaundice. Blood tests revealed: total protein (TP), 6.6 g/dl; gamma-globulin (glb), 35.9%; total bilirubin (T-bil), 9.41 mg/dl; direct bilirubin (D-bil), 7.52 mg/dl; aspartate aminotransferase (AST), 957 U/l; alanine aminotransferase (ALT), 651 U/l; alkaline phosphatase (ALP), 595 U/l; gamma-guanosine triphosphate (GTP), 129 U/l; IgG, 2620 mg/dl; IgM, 223 mg/dl; hepatitis B surface antigen (HBsAg), negative; anti-hepatitis C virus (HCV), negative; antinuclear antibody, positive; antimitchondrial antibody (AMA), negative (by the immunofluorescence [IF] method); and anti-pyruvate dehydrogenase complex (PDC)-E2 antibody, positive (by Western blotting). Anticentromere antibody (ACA), which is an alternative diagnostic marker for PBC, was detected in this patient. Prednisolone was administered after admission and liver function test results improved markedly. The liver biopsy in 1995 had revealed infiltration of lymphocytes and plasma cells in the portal areas with fibrous expansion and periportal necrosis. Destructive cholangitis was observed, as well as scattered epitheloid cell granulomas in some portal areas. Liver biopsy after the steroid treatment revealed alleviated necrotic inflammatory responses of hepatocytes, while the destructive cholangitis persisted. This is a very rare case of PBC-AIH overlap syndrome accompanied by ITP and Hashimoto's disease which provides a possible insight into the mechanisms and interplay of autoimmune diseases.
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PMID:PBC-AIH overlap syndrome with concomitant ITP and Hashimoto's disease with positivity for anti-centromere antibody. 1517 50

The objective was to investigate the clinical features, glycoprotein B (gB) genotype and therapy of the human cytomegalovirus (CMV)-associated idiopathic thrombocytopenic purpura (ITP) in Chinese children. Clinical features and laboratory data of 25 CMV-associated ITP, including 18 males and 7 females with a median age of 0.3 y, were analysed and compared with 116 CMV-negative ITP. The CMV gB of 17 cases was genotyped. Apart from dermatorrhagia, jaundice was noted in 6 cases. Cough, diarrhoea, fever, splenohepatomegaly, alimentary tract haemorrhage and raised ALT were also found. Compared with CMV-negative ITP, CMV-associated ITP has a younger median age, raised ALT and AST, and longer hospitalization (p<0.05, respectively). The most prevalent genotype was gB1 (15/17), followed by coinfection and gB3. Compared with congenitally CMV-infected children in our previous study, more prevalence of gB1 was noted (40/79 vs 15/17, p=0.004). Most of these cases were receiving the therapy of immunoglobulin, corticoid and/or gancyclovir with good therapeutic effect except for 2 cases. In conclusion, CMV infection, especially gB1 genotype, is an important cause of ITP and careful examination of markers of CMV in all cases of apparent 'idiopathic' ITP is required. Combination therapy of immunoglobulin, corticoid and gancyclovir is effective.
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PMID:Cytomegalovirus-associated idiopathic thrombocytopenic purpura in Chinese children. 1861 35

We describe a case of a 64-year-old man with a history of ITP which had required several treatments including splenectomy, and with chronic hepatitis C virus (HCV) infection untreated due to severe thrombocytopenia. In March 2011, platelet count was 14,000/mmc and a thrombopoietic therapy with romiplostim was initiated at the dose of 2 mcg/kg/week that was increased to 8 mcg/kg/week. At week 32, platelet count was 65,000/mmc and an anti-HCV therapy with peginterferon and ribavirin was then started. At baseline laboratory tests indicated AST 99IU/l, ALT 125UI/l, HCV_RNA 3,220 UI/ml and HCV genotype 2a/2c. An early virological response (EVR) with normalization of transaminases in the course of antiviral therapy, such as a sustained virological response (SVR) after its interruption were recorded. Therefore a satisfactory platelet count (range 54.000-179.000/mmc) at the dose of 4 mcg/week during antiviral therapy, such as at the dose of 2 mcg/kg/week after antiviral interruption (range 65.000-292.000/mmc) was recorded. Romiplostim proved effective and safe in the course of antiviral treatment. Therefore it permitted the start of anti-HCV therapy despite severe thrombocytopenia and also avoided any peg-interferon dosage modification or discontinuation. Further prospective studies in larger patient cohort should be encouraged to validate this strategy.
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PMID:Romiplostim for severe thrombocytopenia in the treatment of chronic hepatitis C virus infection: a new option for clinicians? 2453 Nov 77