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 complications of D-penicillamine are rare. It generally consists of reversible cholestatic hepatitis which may, however, be fatal. The authors report a typical case with a benign outcome and with concomitant signs of cutaneous intolerance with eosinophilia. The definite role of D-penicillamine was confirmed by the re-introduction of the drug.
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PMID:[Liver complications caused by D-penicillamine. Apropos of a case]. 370 7

The clinical features and laboratory findings of 78 cases of methyldopa fever are reported. This drug reaction masqueraded as a variety of acute infectious diseases including septicaemia, meningitis, hepatitis and gastroenteritis, occurred within five weeks of starting the drug and appeared to be unrelated to its dosage. Eosinophilia and skin rashes were conspicuous by their absence. In the majority of patients, symptoms were relieved within 48 hours of the withdrawal of the drug. Sixty-one per cent of patients had biochemical evidence of liver damage but jaundice was uncommon. This pattern of mild hepatotoxicity in patients with early febrile reactions to methyldopa contrasts with the later more serious viral hepatitis-like illness due to the drug.
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PMID:Methyldopa: an often overlooked cause of fever and transient hepatocellular dysfunction. 371 91

After the suggestion was made that the "Palm Island mystery disease" might have been an epidemic of visceral larva migrans that was caused by the flying fox parasite, Toxocara pteropodis, work was undertaken to elucidate this nematode's life-cycle and pathogenicity. Studies of infections in various laboratory animals have shown unexpectedly variable susceptibility patterns, with mice harbouring most larvae for the longest time period. However, in all susceptible animals (which include mice, guinea-pigs and suckling rats), the larvae demonstrated marked hepatotropism. Experimental infections in monkeys demonstrated that primates are susceptible to this infection, but large doses of 20,000 infective eggs produced blood eosinophilia and focal granulomatous hepatitis without clinical disease or biochemical abnormalities in the blood. It is concluded that humans are susceptible to larval infections with this nematode, but that clinical manifestations would be unlikely to develop.
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PMID:Toxocariasis--an unlikely cause of Palm Island mystery disease. 372 21

When adverse reactions occur, it is important to identify the etiologic drug. We describe a case of hepatitis associated with allopurinol. A 66-year-old female was admitted for rehabilitation of a cerebral hemorrhage on September 11, 1981. Allopurinol, clofibrate, and baclofen were administered. Severe hepatitis developed on November 13. The clinical laboratory data returned to normal on November 30. Challenge tests were conducted on clofibrate, allopurinol, and baclofen. The challenge test was positive after the administration of allopurinol. Allopurinol hepatitis is most likely a hypersensitivity reaction, as is suggested by the symptoms of eosinophilia and rash. Renal dysfunction may predispose one to develop hepatitis associated with allopurinol.
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PMID:Hepatitis associated with allopurinol. 400 38

We report the cases of two adult patients in whom fulminant hepatitis developed after 17 and 103 days of ketoconazole administration. Histologic administration showed massive, predominantly centrilobular necrosis. Clinical manifestations of hypersensitivity and eosinophilia were absent in both patients, which suggests that ketoconazole hepatotoxicity is not mediated through an immunoallergic mechanism.
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PMID:Ketoconazole-induced fulminant hepatitis. 400 5

An association of granulocytopenia, eosinophilia, skin reaction and hepatitis during propylthiouracil (PTU) therapy for thyrotoxicosis in a 47 year old black female is reported. Clinical and biochemical abnormalities disappeared soon after discontinuation of PTU. That the drug was directly responsible for the observed complications is suggested by the clinical course and by in vitro lymphocyte transformation studies. The latter revealed sensitization to PTU during the acute phase of the disease, which was greatly reduced 5 weeks after discontinuation of the drug and was completely absent after 5 months.
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PMID:Multiple complications of propylthiouracil treatment: granulocytopenia, eosinophilia, skin reaction and hepatitis with lymphocyte sensitization. 622 Oct 46

Ketoconazole has only recently been recognized as a cause of hepatic injury, with most reports coming from outside the United States. In order to characterize more fully the U.S. experience, we undertook an analysis of 54 reports of alleged ketoconazole-induced liver injury submitted to the Food and Drug Administration from the time of initial marketing in 1980. Thirty-three reports were considered likely instances of ketoconazole-induced hepatitis. The majority of these cases occurred in women more than 40 yr of age. Jaundice was recorded in 27 individuals after therapy of 11-168 days with an average daily dose of 200 mg. Anorexia, malaise, nausea, and vomiting accompanied liver injury in one-third of cases. No instances of rash or eosinophilia were recorded. Serum transaminase and alkaline phosphatase values were consistent with acute hepatocellular injury in 18 patients, with primarily cholestatic injury in 5 patients, and with a mixed pattern in 9 individuals. Only one death seemed attributable to ketoconazole. In that patient, the drug was continued after the appearance of clinical and biochemical evidence of hepatic injury and massive hepatocellular necrosis was present at autopsy. The incidence of symptomatic, potentially serious hepatic injury appears to be very low, perhaps 1 in 15,000 exposed individuals. The presumed mechanism of injury is metabolic idiosyncrasy, although hypersensitivity has not been completely dismissed in some cases reported in the literature. The incidence of mild, asymptomatic, reversible elevations in serum transaminases occurring in ketoconazole recipients has been estimated to be 5%-10%. Periodic biochemical testing and monitoring for symptoms of hepatitis during ketoconazole therapy is recommended to help prevent the development of serious or fatal hepatic injury.
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PMID:Hepatic injury associated with ketoconazole therapy. Analysis of 33 cases. 631 20

A middle-aged diabetic woman after four weeks of chlorpropamide treatment developed cholestatic hepatitis with systemic manifestations of idiosyncratic reaction. After recovery, unintended rechallenge with the same drug induced a brisk exacerbation of the symptoms and signs that reversed completely following chlorpropamide withdrawal. Tolbutamide medication was subsequently well tolerated for several weeks, followed by another flare of cholestatic liver lesion and cutaneous eruption with eosinophilia (after each reaction the patient was treated with insulin). Eventually glibenclamide (glyburide) was instituted resulting in very satisfactory control of diabetes, with no untoward reaction.
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PMID:Favorable effects of glibenclamide in a patient exhibiting idiosyncratic hepatotoxic reactions to both chlorpropamide and tolbutamide. 644 88

Carbamazepine is one of the drugs most widely prescribed for the treatment of trigeminal neuralgia and psychomotor seizures. Coincidentally with its use, hypersensitivity reactions to this agent have ben reported with increasing frequency. This report documents our recent encounter with 2 patients who developed hepatitis within one month of beginning carbamazepine therapy for temporal-lobe epilepsy. The occurrence of fever, skin rash and arthralgias suggest immunologic hypersensitivity as does eosinophilia and raised level of IgE, as seen in our patients. After withdrawal of the drug, symptoms and signs disappeared rapidly. We also describe a patient with psychomotor seizures who had ingested carbamazepine for less than 2 months before presenting with a febrile illness characterized by rash, arthritis, lymphadenopathy, epatosplenomegaly and diffuse pulmonary infiltrates with eosinophilia. The reaction cleared on cessation of the drug. Besides showing antinuclear antibody without DNA-precipitating antibody, this patient had an increased helper-T-cell count as well as a decreased number of T lymphocytes with suppressor activity. Taken together, these observations make it reasonable to speculate that carbamazepine may have interfered with lymphocyte triggering, thereby favouring the emergence of B cells with autoimmune propensities.
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PMID:[Immuno-allergic side effects induced by the administration of carbamazepine. Case contribution]. 646 8

A life-threatening toxicity syndrome consisting of an erythematous, desquamative skin rash, fever, hepatitis, eosinophilia, and worsening renal function in 78 patients receiving allopurinol is described. In a majority of cases, the development of this syndrome was associated with the use of standard (200 to 400 mg per day) doses of allopurinol in patients with renal insufficiency. In pharmacologic studies, it was demonstrated that the renal clearance of the major metabolite of allopurinol, oxipurinol, is directly proportional to the renal clearance of creatinine (oxipurinol clearance = 0.22 X creatinine clearance -2.87). An inverse linear relation was noted between the serum oxipurinol half-life and the renal creatinine clearance [( serum oxipurinol half-life in hours]-1 = 0.00034 X creatinine clearance in milliliters per minute + 0.0045). Long-term use of 300 mg per day of allopurinol was found to result in elevated steady-state serum oxipurinol concentrations in patients with renal insufficiency (serum oxipurinol concentration in micromoles per liter = -2.5 X creatinine clearance in milliliters per minute + 326). Avoidance of allopurinol or use of reduced doses in patients with renal insufficiency according to proposed guidelines should be adequate to inhibit uric acid production in most patients and may reduce the incidence of life-threatening allopurinol toxicity.
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PMID:Severe allopurinol toxicity. Description and guidelines for prevention in patients with renal insufficiency. 669 61


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