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)

The authors report the cases of 3 patients who died from fulminant hepatitis after receiving iproclozide, a hydrazine-containing monoamine oxidase inhibitor. Fulminant hepatitis in these patients resembled that reported in patients receiving other hydrazine-containing monoamine oxidase inhibitors: (1) the 3 patients were women; (2) the monoamine oxidase inhibitor has been ingested for 1 month or more; (3) the main clinical manifestations were jaundice and disorders of consciousness; (4) hypersensitivity manifestations were absent; (5) the predominant liver lesion was necrosis; (6) all 3 patients died. In our 3 patients, jaundice occurred 7 to 10 days after the adjunction to iproclozide of a microsomal enzyme inducer. These observations suggest that concomitant administration of iproclozide and of microsomal enzyme inducers may produce fulminant hepatitis in man. It is speculated that iproclozide could be, like iproniazid, transformed into a hepatotoxic metabolite, the production of which would be increased by microsomal enzyme induction.
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PMID:Iproclozide fulminant hepatitis. Possible role of enzyme induction. 68 May 6

We report two cases of fulminant hepatitis which might be due to toloxatone, a new type-A monoamine oxidase inhibitor. Hepatitis occurred 20 days after the beginning of toloxatone administration in the first case and 138 days after the reintroduction of treatment in the second case. Clinical features included vomiting and jaundice, followed by asterixis and coma. Histologically, hepatic cell necrosis was predominant in the centrilobular area in the first case, and affected the entire lobule in the second case. Both patients died despite emergency liver transplantation.
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PMID:[Fatal fulminant hepatitis in 2 women taking toloxatone (Humoryl)]. 236 78

Serum monoamine oxidase (MAO) was separated electrophoretically into three bands. These bands were termed as Fraction I, II and III in that order from anode to cathode. Elevation of serum MAO activity in Fraction I was observed in patients with organ fibrosis particularly in liver cirrhosis and acromegaly. On the other hand, elevation of MAO activity in Fraction II was observed in patients with massive hepatic necrosis. MAO activities partially purified from aortic vessel and from rat liver mitochondria had electrophoretically in the same position as Fraction I and II respectively. Both of Fraction I and aortic extract were inhibited by aminoacetonitrile but not by pargyline. On the contrary, both of Fraction II and mitochondria were inhibited by pargyline but not by aminoacetonitrile. These findings suggested that the elevation of serum MAO in patients with organ fibrosis correlates with the enhancement of connective tissue metabolism and the increment of serum MAO in fulminant hepatitis correlates with the breakaway of MAO from damaged liver mitochondria.
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PMID:[Monamine oxidase (MAO)]. 760 74

Anti-mitochondria (anti-M6) autoantibodies have been found in the serum of patients with immunoallergic iproniazid (Marsilid)-induced hepatitis, but to date the identity of the protein antigen has not been determined. Here we show, using immunoprecipitation of pargyline-labelled proteins, that among the mitochondrial proteins, liver MAO-B is specifically recognized by the sera containing anti-M6 antibodies. Moreover the enzymatic activity of MAO-B towards phenylethylamine and tyramine is also suppressed after this immunoprecipitation, contrary to the MAO-A activity towards 5-hydroxy-tryptamine. As MAO is irreversibly inhibited by iproniazid, these results suggest that the mechanism of iproniazid-induced appearance of anti-M6 antibodies could be another example of the reactive metabolite/enzyme haptenization mechanism already proposed in the case of tienilic acid for the appearance of anti-organelle antibodies in a drug-induced hepatitis.
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PMID:Human anti-mitochondria autoantibodies appearing in iproniazid-induced immunoallergic hepatitis recognize human liver monoamine oxidase B. 857 15

We report a new case of subfulminant hepatitis due to iproniazid, a MAO-inhibitor antidepressant, in a 27-year-old man. An auxiliary liver transplantation was performed. Liver function returned to normal and the patient was discharged from the hospital. However, the patient's native liver did not regenerate, and immunosuppressive therapy had to be maintained. Iproniazid hepatotoxicity is characterized by jaundice in 1% of cases, with a fulminant or subfulminant course in 20% of icteric patients. Although iproniazid is no longer sold in most countries, it is still commercialized in France. Because of the frequency and severity of hepatic injury, commercialization of iproniazid in France should no longer be authorized.
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PMID:[Auxiliary hepatic transplantation in iproniazid-induced subfulminant hepatitis. Should iproniazid still be sold in France?]. 1059 80

Thirty-eight cases clinically diagnosed as advanced schistosomiaisis were subject to splenectomy in Dongzhi County Special Hospital for Schistosomiasis because of portal hypertension, splenomegaly and/or hypersplenism. Liver biopsy was undertaken in all cases during surgical intervention. Before operation, ultrasonography on the liver and spleen was carried out. Also done was biochemical assay on several indices related to liver damage and fibrosis. Among the 38 cases, 24 were diagnosed as schistosomiasis by the finding of eggs in feces, 13 were diagnosed by positive serological test with IHA or COPT, and only in one case, the diagnosis of schistosomiasis was doubtful before operation. However, the eggs were found in the liver section upon histological examination. All the 38 cases had symptoms and signs of portal hypertension and most of them had general symptoms. Histories of hematemesis and melena were recorded in three cases. The causes of hospitalization were mainly splenomegaly and abdominal distension, and two were suffering from upper gastrointestinal bleeding. Upon histopathological examination, schistosome eggs were found in 33 out of 38 cases. Advanced schistosomaiasis was shown in 18 cases and schistosomiasis associated with hepatitis or cirrhosis was seen in other 20 patients. The main pathological changes were egg granulomas with different degrees of fibrosis and some differences in the pathological changes between schistosomal liver fibrosis (SLF) and mixed liver cirrhosis (both schistosome and hepatitis in origin) were seen. Compared with normal ultrasonography, in all the 38 cases, the length of the left and right liver, and the spleen, and the thickness of the left liver, the width of portal trunk, were all out of normal ranges. The differences between the patients and normal records were significant. However, there were no statistically significant differences in terms of above-mentioned indices as well as liver parenchyma changes on ultrasound between advanced schistosomaiasis and schistosomiasis complicated with hepatitis or cirrhosis (all P>0.5). According to WHO classification criteria on ultrasonography for schistosomiasis, among 20 cases combined with hepatitis or cirrhosis, 11 cases fell in Grade II, and nine cases in Grade III hepatic fibrosis, whereas among 18 cases with schistosomiasis fibrosis, 12 and six were in Grade II and III, respectively. The mean value of serum MAO, PIIIP, IVC and HA in the 38 cases were all significantly higher than normal range. However, no significant differences (all P>0.1) were seen between advanced schistosomiasis and those complicated with hepatitis or cirrhosis in terms of the levels of the four indices. The results showed that ultrasonography has its importance in the diagnosis and evaluation of liver fibrosis. However, in differentiation of the two types of liver damage, ultrasound does not provide important information. Histopathological examination, on the other hand, can provide useful information to identify the hepatic diseases.
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PMID:Study on histopathology, ultrasonography and some special serum enzymes and collagens for 38 advanced patients of schistosomiasis japonica. 1202 Aug 97