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)

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 on a patient suffering from early secondary syphilis associated with hepatitis and generalized papular rash which clinically and histologically appeared as non-Hodgkin lymphoma of the centrocytic-centroblastic type. The benign course and the response of the papular rash to penicillin therapy as well as repeated histological examination of many plasma cells and epithelioid cells, however, revealed pseudolymphoma.
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PMID:[Non-Hodgkin's lymphoma-like pseudolymphoma in syphilis II]. 401 59

In a prospective study 43 consecutive children in hospital, aged between 6 months and 7 years and displaying at least one of the clinical signs of infectious mononucleosis (IM), were investigated for Epstein-Barr (EB) virus-specific IgM antibodies by an indirect immunofluorescence test. On this basis EB virus infection was considered confirmed in 8 patients, each of whom had IgM antibodies in the initial serum sample. In one additional patient, IgM antibodies were only detected in a second sample. The IgM antibodies disappeared with 3-11 weeks. Assessment of IgG antibodies had no diagnostic value in the acute phase of IM. Clinically the 3 youngest children, about 1 year of age, were diagnosed as having pneumonia or hepatitis, the 5 other consecutive patients as having IM. Hepatosplenomegaly was fairly frequently associated with IM, while sore throat, lymphadenopathy, and rash were often signs of other diseases. Only the oldest child had heterophil antibodies. Atypical lymphocytes (greater than 10%) were present in 4 of the 9 IM cases and were seen in children with other diseases as well. Our data stress the importance of measuring EB virus-specific IgM antibodies in order to diagnose IM in early childhood.
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PMID:Primary Epstein-Barr virus infection in early childhood. 625 87

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

The autopsies of seven patients with disseminated varicella were reviewed. Six patients had acute lymphoblastic leukemia (ALL) and the seventh had Hodgkin's disease. All the patients were on chemotherapy at the time of commencement of their varicella rash, and at autopsy only the patient with Hodgkin's disease had residual tumor. The typical anatomic lesion of varicella was one of focal necrosis (often hemorrhagic) with eosinophilic intranuclear (Cowdry type-A) inclusions. In fatal disseminated varicella the complications most commonly encountered at autopsy were interstitial pneumonitis, hepatitis, necrotizing splenitis and lymphadenitis, esophagitis, enteritis, colitis, and pancreatitis. The most significant of these complications appears to be the interstitial pneumonitis, as the major cause of death is respiratory failure.
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PMID:Disseminated varicella at autopsy in children with cancer. 632 Oct 8

We treated a patient in whom acute non-A, non-B hepatitis was complicated by a serum sickness-like syndrome (rash, arthralgias). Serum from this patient demonstrated a fall in C3, C4, and total hemolytic complement levels during the syndrome, in association with circulating IgM immune complexes. Fatal aplastic anemia developed later in the patient. This case illustrates that non-A, non-B hepatitis may be complicated by immune complex features that have previously been emphasized to occur with acute hepatitis B. Additional evidence supporting the occurrence of this clinical picture in non-B forms off viral hepatitis is presented.
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PMID:Acute non-A, non-B hepatitis with serum sickness-like syndrome and aplastic anemia. 645 Feb 90

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 56-year-old woman had rash, arthralgia, and lymphadenopathy. Prednisone therapy caused the symptoms to abate but not disappear. Medication was continued for almost eight weeks, during which time the symptoms persisted. While the patient was receiving therapy, serologic evidence of hepatitis B infection was noted. When prednisone therapy was stopped, the patient rapidly passed from the prodrome to typical, acute, icteric hepatitis. Prednisone may have suppressed normal immunologic responses to the hepatitis virus, resulting in persistence of the serum sickness-like state. Corticosteroids are not indicated in the treatment of the prodrome to hepatitis B infection.
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PMID:Prolongation of the prodrome to acute hepatitis B infection by corticosteroids. 661 7

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

Reports of cases of primary and secondary syphilis are increasing in the United States, particularly in urban areas and among homosexual men. While primary syphilis poses little diagnostic difficulty, many physicians are unfamiliar with the multisystem nature of secondary lues. Patients who have secondary syphilis commonly present with systemic signs, skin rash, mucous membrane lesions and generalized adenopathy. Less commonly, secondary syphilis may occur as acute meningitis, sensorineural hearing loss, iritis, anterior uveitis, optic neuritis, Bell's palsy, gastropathy, proctitis, hepatitis, pulmonary infiltration, nephrotic syndrome, glomerulonephritis, periostitis, tenosynovitis and polyarthritis. The diagnosis of secondary syphilis is easily confirmed. Its various manifestations are readily treated with penicillin and, if treated early, are entirely reversible. Two recent cases of secondary syphilis, one presenting as nephrotic syndrome and one as chorioretinitis and ptosis, illustrate the usual and unusual features of this common infection.
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PMID:Secondary syphilis: uncommon manifestations of a common disease. 670 90


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