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)

We report a case of cholestatic hepatitis accompanied by peripheral and hepatic eosinophilia in a patient taking acetohexamide for a period of 1.5 yr. Jaundice developed acutely and was accompanied by fever. After discontinuation of the drug, there was no evidence of further damage, with prompt normalization of liver enzymes, bilirubin, and eosinophil count.
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PMID:Reversible cholestatic hepatitis caused by acetohexamide. 271 85

The authors present an account on 60 patients where, based on the clinical picture, parasitological examination and laboratory parameters, the diagnosis of giardiasis was established. Among these patients a rise of one or several indicators of liver metabolism was found in 31%. The authors discuss whether the above conditions can be considered hepatitis within the framework of the basic parasitic disease. They eliminated non-parasitic causes (obstruction, HBsAg positive hepatitis, drug hepatitis, toxic hepatopathies) of elevated transaminase and bilirubin levels. For collection of duodenal juice or faeces for parasitological examination they used a gastrofibroscope or rectoscope. After treatment normalization of transaminase and bilirubin serum levels was recorded as well as regression of clinical symptoms and of eosinophilia.
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PMID:[Elevated indicators of liver metabolism in patients with giardiasis]. 276 82

To test the hypothesis that allopurinol-associated granulomatous hepatitis may present itself with fibrin-ring granulomas, we requested details of such cases, as reported to the World Health Organization, from 13 national adverse reaction monitoring centers, and as reported in the literature. Details and histology of 6 cases were obtained and reviewed. All consisted of acute hypersensitivity signs with fever, rash, arthralgia, or eosinophilia as hallmarks, starting within 6 wk of commencing treatment with allopurinol. In all cases there were either epithelioid granulomas or granulomalike lesions, but none of these contained fibrin rings. It is concluded that, if fibrin-ring granulomas are a manifestation of allopurinol-induced granulomatous hepatitis, this feature is probably uncommon.
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PMID:Fibrin ring granulomas and allopurinol. 292 64

We present a detailed case report of an idiosyncratic reaction to phenytoin and review the manifestations in 16 additional pediatric patients (2.5-21 years of age) described in the literature. These cases illustrate the frequency of fever (82%), rash (94%), lymphadenopathy (94%), hepatitis (94%), and eosinophilia (76%). This constellation of signs and symptoms will frequently mimic common pediatric illnesses so the pediatrician responsible for the care of the seizure patient being treated with phenytoin should be aware of the possibility of an idiosyncratic reaction. Delay in discontinuation of the drug may be life-threatening.
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PMID:Idiosyncratic reactions to phenytoin. 294 5

The ability to induce granulomatous hepatitis has been attributed to numerous drugs; some sixty causative drugs have been culled from the literature for this review. Additionally, granulomas or granulomatoid lesions have resulted from occupational exposure to toxic substances (e.g. silica, copper sulphate, beryllium compounds), and particulate material from various therapeutic or diagnostic procedures (e.g. reactions to starch, talc, suture material, polyvinyl pyrrolidone, silicone, barium sulphate, thorium dioxide) or from intravenous drug abuse (e.g. talc). Clinically, patients with drug-induced or toxic granulomatous hepatitis may be asymptomatic. More frequently, the presentation is that of an acute febrile illness, with or without a rash and eosinophilia, followed by jaundice and biochemical evidence of hepatic dysfunction. The diagnosis of drug-induced granulomatous hepatitis is based largely on ruling out other aetiologies. Liver biopsy plays a key role in diagnosis. Recovery is the rule following withdrawal of the drug. Morphologically, drug-induced granulomas may be impossible to distinguish from those due to other causes. Associated lesions suggesting a drug aetiology include significant tissue eosinophilia, unicellular hepatocytic degeneration and necrosis, cholestasis and acute cholangitis or vasculitis. Special stains, polarizing and phase contrast microscopy, transmission and scanning electron microscopy and energy dispersive X-ray microanalysis all play a role in the aetiologic diagnosis of some types of granulomas.
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PMID:Drug-induced and toxic granulomatous hepatitis. 304 71

A 37 year old female with rheumatoid arthritis developed clinical and biochemical evidence of hepatitis after receiving 80 mg of sodium aurothiomalate. Inadvertent rechallenge with sodium aurothiomalate led to recurrence of the biochemical abnormalities and a profound neutropenia and eosinophilia.
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PMID:Hepatitis and neutropenia secondary to gold thiomalate therapy for rheumatoid arthritis. 308 48

Ketoconazole was introduced in the United Kingdom in 1981. By November 1984 the Committee on Safety of Medicines had received 82 reports of possible hepatotoxicity associated with the drug, including five deaths. An analysis of the 75 cases that had been adequately followed up suggested that 16, including three deaths, were probably related to treatment with the drug. Of the remainder, 48 were possibly related to treatment, five were unlikely to be so, and six were unclassifiable. The mean age of patients in the 16 probable cases was 57.9, with hepatotoxicity being more common in women. The average duration of treatment before the onset of jaundice was 61 days. None of these well validated cases occurred within the first 10 days after treatment. The results of serum liver function tests suggested hepatocellular injury in 10 (63%); the rest showed a mixed pattern. In contrast, the results of histological examination of the liver often showed evidence of cholestasis. The characteristics of the 48 patients in the possible cases were similar. Allergic manifestations such as rash and eosinophilia were rare. Hepatitis was usually reversible when treatment was stopped, with the results of liver function tests returning to normal after an average of 3.1 months. In two of the three deaths probably associated with ketoconazole treatment the drug had been continued after the onset of jaundice and other symptoms of hepatitis. Clinical and biochemical monitoring at regular intervals for evidence of hepatitis is advised during long term treatment with ketoconazole to prevent possible serious hepatic injury.
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PMID:Hepatic reactions associated with ketoconazole in the United Kingdom. 310 6

A 10-year-old black girl had an episode of diphenylhydantoin(DPH)-induced exfoliative dermatitis, lymphadenopathy, hepatitis, peripheral eosinophilia, and transient renal failure. The findings of specific lymphocyte sensitization of DPH, a clinically typical delayed hypersensitivity reaction, multinucleated histiocytes in the renal interstitium, and negative renal immunofluorescence studies for immune reactants indicate that the child's renal injury was at least partially cell-mediated.
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PMID:Diphenylhydantoin-induced hypersensitivity reaction with interstitial nephritis. 315 84

Skin rash, fever, and eosinophilia developed in a previously healthy 35-year-old woman three weeks after starting carbamazepine. Fulminant respiratory and renal failure ensued. Autopsy showed pneumonitis, nephritis, serositis, pancreatitis, hepatitis, and carditis, characterized by an infiltrate of eosinophils and lymphocytes. The severity, duration, and extensive organ involvement of the reaction make this case unique.
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PMID:Carbamazepine-induced severe systemic hypersensitivity reaction with eosinophilia. 322 45

Trimethoprim-sulfamethoxazole (co-trimoxazole) is used extensively for treatment of pulmonary and urinary tract infections. Side effects may affect skin, blood, bone marrow, kidney and the liver. Although a number of sulfonamides have been reported to have produced hepatic lesions, hepatitis following therapy with trimethoprim-sulfamethoxazole is a rather rare event. While trimethoprim has not yet been reported as a cause of hepatic disorders, sulfamethoxazole has occasionally been described as inducing hepatic injury. In some cases, these reactions are accompanied by symptoms indicative for allergic reactions such as fever, rash and eosinophilia. Seven well documented cases are analyzed and discussed with respect to the nature of side effects caused by co-trimoxazole.
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PMID:Co-trimoxazole-induced hepatic injury--an analysis of cases with hypersensitivity-like reactions. 350 74


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