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)

Long-term administration of quinidine was associated with persistent elevation of serum concentrations of SGOT, lactic acid dehydrogenase, and alkaline phosphatase. Liver biopsy showed active hepatitis. Discontinuance of quinidine therapy led to normalization of liver function tests. A challenge dose of quinidine caused clinical symptoms and abrupt elevation of SGOT, alkaline phosphatase, and lactic acid dehydrogenase values. We concluded that this patient had quinidine hepatotoxicity and believe that this is the first case reported with liver biopsy documentation. This report also suggests that, even after long-term administration, the hepatic toxicity is reversible.
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PMID:Quinidine hepatitis. 4 62

The hepatoprotective antioxidant bioflavonoid cianidanol has beneficial therapeutic and immunomodulatory effects in chronic hepatitis. Its action on natural killer (NK) cell activity has not yet been studied in hepatitis B virus (HBV) infection. In the present study, the in vitro and in vivo effects of the drug on NK cell activity have been determined in six patients with chronic HBV hepatitis and in ten healthy control subjects. Two methods were used: an enzyme release assay and a cytotoxicity test based on the assessment of endogenous alkaline phosphatase activity of the target cells. The in vitro effect of the drug was assessed using cianidanol at 10(-6), 10(-5) and 10(-4) M concentrations. For in vivo studies, HBV hepatitis patients were treated with cianidanol at a daily dose of 3.0 g cianidanol for seven days and were investigated before and after the treatment. Chronic HBV hepatitis patients showed a moderate decrease in NK cell activity compared to the controls, but after the cianidanol therapy their NK cell activity significantly rose to 68.0% +/- 9.5% (p less than 0.01). Cianidanol in vitro inhibited the NK cell activity both in hepatitis and healthy groups when using K-562 target cells and the lactic acid dehydrogenase enzyme release assay, but did not influence or even slightly enhance the NK activity when human embryonic fibroblast cells and alkaline phosphatase assay were used for the test. After the 7-day in vivo treatment, the in vitro inhibitory action of the drug was diminished or absent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cianidanol on natural killer cell activity in patients with chronic B virus hepatitis. 359 73

A 53-year-old woman developed fever and fatigue after eating raw oysters, and consulted a local clinic. She exhibited liver dysfunction and jaundice, and was therefore referred and admitted to our hospital. Hepatitis A was diagnosed based on virus markers, and palliative therapy was administered. After admission, the increased levels of transaminases and lactic acid dehydrogenase (LDH) normalized rapidly. However, marked thrombocytopenia was observed, and steroid pulse therapy was administered. Thereafter, idiopathic anemia developed, and a bone marrow puncture was performed. Bone marrow smears showed marked depletion of cells of the erythroblastic and megakaryocytic series. Parvovirus B19 infection was ruled out, and an additional steroid was administered. However, the patient's anemia and thrombocytopenia persisted. She suffered a prolonged period of cholestasis and died of acute renal failure. At autopsy, the bone marrow revealed severe erythroblastopenia. A diagnosis of thrombocytopenia due to an autoimmune mechanism was made on the basis of elevated levels of platelet-associated immunoglobulin G (PAIgG) and immune complex. Furthermore, the advanced anemia was complicated by concurrent hemolysis. This case may provide information useful for clarifying the pathogenesis of hematopoietic disorders complicated by hepatitis.
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PMID:[Autoimmune thrombocytopenia and erythroid hypoplasia associated with hepatitis A]. 1107 Sep 36

The rhizome of Phragmites australis has long been used for the treatment of hepatitis in traditional Chinese medicine. In this study, the hepatoprotective and antioxidant activities of an aqueous extract from the rhizome of P. australis (AE-PA) were evaluated. The acute toxicity test in mice showed that AE-PA was nontoxic since a dose of 2000 mg/kg body weight (b.w.) did not cause toxic symptoms or mortality. The prolongation of hexobarbital-induced sleeping time by carbon tetrachloride (CCl4) administration to mice was significantly reduced after pretreatment with AE-PA at 500 mg/kg b.w., proving the protective effect of the extract on microsomal drug-metabolizing enzyme. The oral administration of AE-PA to rats for 5 days before CCl4 intoxication caused a significant decrease in the CCl4-induced elevation of hepatic enzymes activities in serum, such as aspartate aminotransferase, alanine aminotransferase, and lactic acid dehydrogenase. This suggested that AE-PA had good hepatoprotective activity against CCl4-induced liver injury, which was confirmed by pathomorphological examination of the liver. Through evaluation of hydroxyl radical and superoxide anion radical scavenging activities, respectively, it was demonstrated that AE-PA had good antioxidant activity, which possibly contributed to its hepatoprotective activity. More research is needed to study the bio-active compounds in P. australis and to identify the potential hepatoprotective and antioxidant agents.
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PMID:Hepatoprotective and antioxidant activities of the aqueous extract from the rhizome of Phragmites australis. 2460 Oct 81