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)

A multicenter prospective randomized trial of four versus six weeks of amphotericin B, 0.3 mg/kg per day, plus flucytosine, 150 mg/kg per day, was performed with 194 patients with cryptococcal meningitis. One or more toxic drug reactions developed in 103 patients: azotemia (51), renal tubular acidosis (two), leukopenia (30), thrombocytopenia (22), diarrhea (26), nausea/vomiting (10), and hepatitis (13). The four- and six-week regimens were complicated by toxicity in 44 percent and 43 percent of cases, respectively. Toxicity appeared during the first two weeks of therapy in 56 percent and during the first four weeks in 87 percent. Azotemia did not occur more frequently in renal transplant recipients or diabetic patients. Cytopenias did not appear more often in patients with hematologic malignancies or those receiving immunosuppressive therapies. Toxic reactions that contributed to death developed in five patients (two with azotemia, one with pancytopenia, one with hepatitis, one with ileus). Amphotericin B-induced azotemia was not a significant risk factor for the subsequent development of bone marrow, gastrointestinal, or hepatic toxicity attributable to flucytosine. Flucytosine toxicity was associated with peak serum flucytosine levels of 100 micrograms/ml or more during two or more weeks of therapy (p = 0.005). Peak 5-fluorouracil levels were not predictive of toxicity. An initial dose of flucytosine is recommended based on the creatinine clearance: 150 mg/kg per day at a creatinine clearance above 50 ml/minute, 75 mg/kg per day at a creatinine clearance of 26 to 50 ml/minute, and 37 mg/kg per day at a creatinine clearance of 13 to 25 ml/minute. The serum creatinine level should be monitored twice weekly and the creatinine clearance weekly during therapy in order to anticipate changes in serum flucytosine concentration. In addition, it is recommended that the serum flucytosine level be determined two hours after an oral dose once a week, and that the dose be adjusted to maintain a level of 50 to 100 micrograms/ml.
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PMID:Toxicity of amphotericin B plus flucytosine in 194 patients with cryptococcal meningitis. 330 26

The toxicities of antimalarial drugs vary because of the differences in the chemical structures of these compounds. Quinine, the oldest antimalarial, has been used for 300 years. Of the 200 to 300 compounds synthesised since the first synthetic antimalarial, primaquine in 1926, 15 to 20 are currently used for malaria treatment, most of which are quinoline derivatives. Quinoline derivatives, particularly quinine and chloroquine, are highly toxic in overdose. The toxic effects are related to their quinidine-like actions on the heart and include circulatory arrest, cardiogenic shock, conduction disturbances and ventricular arrhythmias. Additional clinical features are obnubilation, coma, convulsions, respiratory depression. Blindness is a frequent complication in quinine overdose. Hypokalaemia is consistently present, although apparently self-correcting, in severe chloroquine poisoning and is a good index of severity. Recent toxicokinetic studies of quinine and chloroquine showed good correlations between dose ingested, serum concentrations and clinical features, and confirmed the inefficacy of haemodialysis, haemoperfusion and peritoneal dialysis for enhancing drug removal. The other quinoline derivatives appear to be less toxic. Amodiaquine may induce side effects such as gastrointestinal symptoms, agranulocytosis and hepatitis. The main feature of primaquine overdose is methaemoglobinaemia. No cases of mefloquine and piperaquine overdose have been reported. Overdose with quinacrine, an acridine derivative, may result in nausea, vomiting, confusion, convulsion and acute psychosis. The dehydrofolate reductase inhibitors used in malaria treatment are sulfadoxine, dapsone, proguanil (chloroguanide), trimethoprim and pyrimethamine. Most of these drugs are given in combination. Proguanil is one of the safest antimalarials. Convulsion, coma and blindness have been reported in pyrimethamine overdose. Sulfadoxine can induce Lyell and Stevens-Johnson syndromes. The main feature of dapsone poisoning is severe methaemoglobinaemia which is related to dapsone and to its metabolites. Recent toxicokinetic studies confirmed the efficacy of oral activated charcoal, haemodialysis and haemoperfusion in enhancing removal of dapsone and its metabolites. No overdose has been reported with artemesinine, a new antimalarial tested in the People's Republic of China. The general management of antimalarial overdose include gastric lavage and symptomatic treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Clinical features and management of poisoning due to antimalarial drugs. 330 66

The authors present eight cases of hepatitis probably due to amodiaquine taken at a prophylactic dose. Seven cases were minor forms with vomiting, nausea and 3 to 8 fold rise in transaminases. One case had jaundice. The symptoms regressed when amodiaquine was replaced by chloroquine. An in vitro test done once was positive.
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PMID:[Minor hepatitis probably caused by amodiaquine]. 360 9

A 31-year-old male patient with lepromatous leprosy developed fever, malaise, nausea, anorexia, lymphadenopathy, hepatitis, exfoliative dermatitis and ainhum like lesions while on multidrug therapy comprised of dapsone, clofazimine and rifampicin. The provocation tests confirmed the dapsone to be cause of this event.
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PMID:Dapsone syndrome--a case report. 361 56

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71

The authors report the case of a 63 year-old woman who developed high-grade fever with chills, nausea, diarrhea, severe pain in the right hypochondrium, and jaundice after one month's treatment with 300 mg of hydroquinidine hydrochloride daily. Serum bilirubin and aminotransferases were slightly increased, while alkaline phosphatases and gamma-glutamyl-transpeptidase serum activities were markedly raised. Histological examination of a liver specimen obtained by the transvenous route showed numerous epithelioid granulomas with giant cell formation and eosinophils in hepatic lobules and portal tracts. Symptoms disappeared three days after withdrawal of the drug, but hepatomegaly and a mild increase in serum gamma-glutamyl-transpeptidase persisted more than eighteen months. Quinidine-induced hepatitis is almost always associated with fever, and, in one-third of the cases, with a pseudo-cholangitis picture. Extrahepatic hypersensitivity manifestations are often present. Histological examination of the liver shows granulomatous or cytolytic hepatitis. Withdrawal of the drug is rapidly followed by a favorable outcome; readministration causes immediate relapse; progression to chronic liver disease has never been reported previously.
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PMID:[Hepatitis caused by quinidine. Study of a case and review of the literature]. 373 35

An epidemic outbreak of non-A, non-B hepatitis occurred in 1977/78 involving 30 donors at a plasmapheresis center. Of 27 hospitalized patients with peak ALT values between 334 and 1736 (mean 831) IU/l, only 16 had subjective symptoms like fatigue and lack of appetite, 11 had nausea, 11 were jaundiced and one developed transient arthritis. Patients with jaundice became chronically ill significantly less frequently than those without jaundice. Nineteen of 26 patients followed up had elevated ALT values after 12 months (73%) and 11 after 46 months (42%). Needle liver biopsies performed in 18 of the 19 patients with elevated ALT after 12 months revealed chronic persistent hepatitis in 14 and chronic active hepatitis in three. Follow-up biopsies always showed improvement (nine patients) or complete recovery (eight patients).
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PMID:Epidemic outbreak of non-A, non-B hepatitis in a plasmapheresis center. II: Clinical observations and a four-year follow-up of patients. 392 97

We report the cases of 2 female patients aged 69 and 61 yr, suffering from fulminant hepatitis induced by pirprofen, a new nonsteroidal antiinflammatory drug. The duration of pirprofen administration before the onset of hepatitis was long, 7 and 9 mo, respectively. Hepatitis was not preceded or accompanied by hypersensitivity manifestations. The liver lesion consisted of massive, predominantly centrilobular hepatic cell necrosis and microvesicular steatosis. One patient died of liver failure. Although the risk of fulminant hepatitis is very low, we recommend that, in patients taking pirprofen for more than 2 mo and complaining of asthenia, nausea, or vomiting, serum aminotransferase levels should be measured and administration of the drug should be interrupted as soon as an increased level is noted.
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PMID:Pirprofen-induced fulminant hepatitis. 400 6

In an ongoing study patients with severe rheumatoid arthritis (RA) who had previously failed conventional therapy including gold salts and penicillamine were randomly assigned on an open basis to a plasma exchange or fractionated total lymphoid irradiation protocol. Nine patients (eight female, one male) with erosive RA of long duration exchanged 40 ml/kg of plasma over a period of two to four weeks. Nine patients (eight female, one male) with similar characteristics, received 2,000 rads to lymphoid tissues in fractionated doses (200 rads each) over 4 to 5 weeks. Treatment was completed in all patients and follow-up ranged from two to twelve months for plasma exchange and eight to sixteen months for radiation. Results of the study showed subjective and objective improvement including morning stiffness, joint score, and pertinent laboratory evaluation in six patients admitted to plasmapheresis with duration of remission lasting as long as seven weeks. Three patients failed to show any improvement in the activity of the disease. Eight patients on the radiation protocol showed a marked decrease in disease activity which has been maintained until the present time. Side effects for the plasma exchange group included mild febrile reactions during the exchange and one non-A non-B Hepatitis. In the radiation group occipital alopecia, loss of appetite and nausea was seen in all patients and severe leucopenia in one (WBC 500/mm3). The present results suggest that both procedures can reduce disease activity in severe RA. Plasma exchange efficacy appears to be short-lived when compared to total lymphoid radiation. The latter was poorly tolerated by all patients submitted to the program.
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PMID:Plasmapheresis vs total lymphoid irradiation in the treatment of severe rheumatoid arthritis. 401 9

This report describes five cases of hepatocellular injury following halothane anesthesia. Four patients had multiple exposures to the anesthetic. Three of the five died from submassive to massive liver cell necrosis. The two survivors developed jaundice and/or dark urine following each exposure to halothane; liver biopsy in one showed centrilobular and linear areas of necrosis. Fever, anorexia, nausea, vomiting, abdominal pain and jaundice were present in all cases. In the two survivors the prothrombin time was less than 20 seconds throughout the course of the disease, whereas in the three who died the prothrombin time was more than 20 seconds from the onset. The English literature to the end of 1971 is reviewed. Approximately 600 cases of halothane-related hepatitis have been reported
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PMID:Halothane hepatitis. 468 24


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