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 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

Prior to offering the hepatitis B (HB) vaccine, a prescreen for hepatitis B virus (HBV) antibodies was conducted in a 565 bed hospital in Pasadena, California. Antibodies to the hepatitis B virus were detected in 14.5% of 1,745 employees tested. There was a significantly higher prevalence in those with a previous history of hepatitis, blood transfusions, exposure to needlesticks, number of years in the same occupation, and in the same hospital work area. Employees of Asian extraction (33.3%) and blacks (23.1%) had a higher prevalence of antibodies to the hepatitis B virus than Hispanics (13.7%) and whites (10.2%). Anti-HBs was detected in 92.6% of 865 employees who received three doses of the hepatitis B vaccine. Only 28.6% of nonresponders receiving a fourth dose of hepatitis B vaccine produced anti-HBs. The nonresponders to the HB vaccine were older (average age 64.9 years) when compared to the responders (average age 37.5 years), and more males failed to produce anti-HBs after vaccination than females. Hepatitis B vaccination of the majority of individuals with either "low level" anti-HBs alone or anti-HBc alone did not elicit an anamnestic response after one dose of vaccine, implying that these "low level" antibodies are nonspecific and do not represent antiviral antibodies. Adverse reactions to the hepatitis B vaccine were minor and included a flu-like syndrome, sore arm, and rash and swelling at the injection site. The reasons for nonparticipation were obtained from 179 individuals, and the main issue was concern about safety of the hepatitis B vaccine.
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PMID:A hepatitis B vaccination program in a community teaching hospital. 295 17

We report our experience with 29 symptomatic herpesvirus infections occurring during the course of 87 pediatric transplant procedures performed over the 10-year period, 1973 to 1982. The yearly attack rate ranged from 0.05 to 0.40 case per cumulative patient years at risk. A greater proportion (9 of 14) of children who received more than 10 units of whole blood or packed red blood cells prior to transplantation developed a viral infection compared with those given 10 transfusions or fewer (8 of 25) (P = 0.10). Fever occurred in 22 (76%) children, pulmonary disease in 8 (28%), hepatitis in 11 (35%), leukopenia in 7 (24%), thrombocytopenia in 9 (31%) and central nervous system disease in 3 (10%). Herpesvirus infections were responsible for allograft loss in 7 (24%) patients. However, no differences in the actuarial graft survival curves were noted for transplants performed since 1979 in children with and without viral infection. The etiologic viral agents were cytomegalovirus in 19 (65%) episodes, herpes simplex virus in 8 (28%), Epstein-Barr virus in 2 (7%) and varicella-zoster virus in 2 (7%). Cytomegalovirus-infected patients were younger and more commonly developed primary infection compared with children with herpes simplex virus disease who were more likely to have secondary infection and to manifest a mucocutaneous vesicular rash. We conclude that the etiologic agents and clinical features of herpesvirus infections are similar in pediatric and adult renal allograft recipients. Moreover except for distinctive syndromes such as mucocutaneous vesicular eruption or a central nervous system lymphoma, the various herpes-viruses cause clinically indistinguishable illnesses in pediatric transplant patients with similar end organ involvement and untoward renal consequences.
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PMID:Clinical manifestations of herpesvirus infections in pediatric renal transplant recipients. 299 34

Papular acrodermatitis (Gianotti-Crosti syndrome) was seen in a six-year-old girl. The disease was marked by the characteristic triad of a papular-vesicular rash, lymphadenopathy and liver damage. Serological findings suggest an infection with Epstein-Barr virus as the causative factor. In such cases hepatitis-B induced papular eruptive acrodermatitis should be considered in differential diagnosis.
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PMID:[Infantile acro-localized papulovesicular syndrome]. 301 24

Adverse drug reactions may mimic almost any kind of liver disease. Acute hepatitis is often due to the formation of reactive metabolites in the liver. Despite several protective mechanisms (epoxide hydrolases, conjugation with glutathione), this formation may lead to predictable toxic hepatitis after hugh overdoses (e.g. paracetamol), or to idiosyncratic toxic hepatitis after therapeutic doses (e.g. isoniazid). Both genetic factors (e.g. constitutive levels of cytochrome P-450 isoenzymes, or defects in protective mechanisms) and acquired factors (e.g. malnutrition, or chronic intake of alcohol or other microsomal enzyme inducers) may explain the unique susceptibility of some patients. Formation of chemically reactive metabolites may also lead to allergic hepatitis, probably through immunization against plasma membrane protein epitopes modified by the covalent binding of the reactive metabolites. This may be the mechanism for acute hepatitis produced by many drugs (e.g. amineptine, erythromycin derivatives, halothane, imipramine, isaxonine, alpha-methyldopa, tienilic acid, etc.). Genetic defects in several protective mechanisms (e.g. epoxide hydrolase, acetylation) may explain the unique susceptibility of some patients, possibly by increasing exposure to allergenic, metabolite-altered plasma membrane protein epitopes. Like toxic idiosyncratic hepatitis, allergic hepatitis occurs in a few patients only. Unlike toxic hepatitis, allergic hepatitis is frequently associated with fever, rash or other hypersensitivity manifestations; it may be hepatocellular, mixed or cholestatic; it promptly recurs after inadvertent drug rechallenge. Lysosomal phospholipidosis occurs frequently with three antianginal drugs (diethylaminoethoxyhexestrol, amiodarone and perhexiline). These cationic, amphiphilic drugs may form phospholipid-drug complexes within lysosomes. Such complexes resist phospholipases and accumulate within enlarged lysosomes, forming myeloid figures. This phospholipidosis has little clinical importance. In a few patients, however, it is associated with alcoholic-like liver lesions leading to overt liver disease and, at times, cirrhosis. Subjects with a deficiency in a particular isoenzyme of cytochrome P-450 poorly metabolize perhexiline and are at higher risk of developing liver lesions. Prolonged, drug-induced liver-cell necrosis may also lead to subacute hepatitis, chronic hepatitis or even cirrhosis. This usually occurs when the drug administration is continued, either because the liver disease remains undetected or because its drug aetiology is overlooked. Several autoantibodies may be present.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute and chronic drug-induced hepatitis. 304 68

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

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

Arene oxide metabolites of aromatic anticonvulsants (phenytoin, phenobarbital, and carbamazepine) may be involved in the pathogenesis of hypersensitivity reactions. We investigated 53 patients with clinical sensitivity to anticonvulsants by exposing their lymphocytes in vitro to drug metabolites generated by a murine hepatic microsomal system. The diagnosis of a hypersensitivity reaction was corroborated by in vitro rechallenge for each drug (phenytoin, n = 34; phenobarbital, n = 22; carbamazepine, n = 25) when cytotoxicity (% dead cells) exceeded 3 SD above the mean result for controls. Cross-reactivity among the drugs was noted. 7 out of 10 patients who had received all three anticonvulsants had adverse reactions to each. 40 out of 50 patients tested to all three drugs in vitro were positive to each. Adverse reactions were indistinguishable among anti-convulsants. Skin rash (87%), fever (94%), hepatitis (51%), and hematologic abnormalities (51%) were common clinical features of each drug. 62% of reactions involved more than two organs. Cells from patients' parents exhibited in vitro toxicity that was intermediate between values for controls and patients. In vitro testing can help diagnose hypersensitivity to anticonvulsants. Cells from patients may also be used for prospective individualization of therapy to decrease risk of adverse reaction. Cross-reactivity among the major anticonvulsants is common and should be considered before deciding on alternative therapy.
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PMID:Anticonvulsant hypersensitivity syndrome. In vitro assessment of risk. 319 57

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

History of diagnosed illnesses, medical symptoms, and reproductive outcomes and their relation to combat intensity and herbicide exposure were studied, via a mailed questionnaire, among 6810 American Legionnaires who served during the Vietnam War (42% in Southeast Asia, 58% elsewhere). Heart disease, venereal disease, and benign fatty tumors were reported significantly more often by Vietnam veterans than by controls. Combat intensity was significantly dosage-related to history of high blood pressure, ulcers, arthritis and rheumatism, genito-urinary problems, nervous system disease, major injury, hepatitis, and benign fatty tumors. Agent Orange exposure was significantly dosage-related to history of benign fatty tumors, adult acne, skin rash with blisters, and increased sensitivity of eyes to light. Rates of the latter two conditions and of change in skin color were especially elevated in men whose military occupations involved direct handling of herbicides. Five "symptom complex" scales were constructed via factor analysis to measure degrees of feeling faint, fatigue or physical depression, body aches, colds, and skin irritation. Means of all five scales were significantly higher in Vietnam veterans compared to controls, and in herbicide handlers compared to nonhandlers. Both combat and Agent Orange exposure were significant, independent predictors of each of the five scales. Neither combat nor Agent Orange exposure was associated with difficulty in conception, time to conception of first child, or to birthweight or sex ratio of offspring, but maternal smoking was strongly related to reduced birthweight. The percentage of spouses' pregnancies which resulted in miscarriages was significantly higher for Vietnam veterans than controls (7.6% vs 5.5%, P less than 0.001). Logistic regression analysis showed that Agent Orange exposure and maternal smoking were both independently and significantly associated with miscarriage rates in a dose-related manner.
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PMID:Health and reproductive outcomes among American Legionnaires in relation to combat and herbicide exposure in Vietnam. 326 69


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