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)

Ninety-six patients with recurrent, drug-refractory tachyarrhythmias were treated with amiodarone for 8.0 +/- 7.5 months (range 1 day to 27 months): 77 for recurrent ventricular tachycardia or ventricular fibrillation (VT/VF), two for complex ventricular ectopy, and 17 for supraventricular tachyarrhythmias. The actuarial incidence of successful amiodarone therapy was 52 +/- 7% at 12 months and 28 +/- 9% at 24 months for patients with VT/VF. Neither patient with complex ventricular ectopy was successfully treated. Among the patients with supraventricular tachyarrhythmias, 64.7% were successfully treated for 7.7 +/- 7.6 months (range 1 to 22 months). Amiodarone toxicity occurred in 66 of 91 patients (72.5%) treated for more than 1 week. Fourteen patients had therapy-limiting toxicity. Of these 14, six had pulmonary toxicity, four had arrhythmia exacerbation, one had hepatitis, one had renal toxicity, one had rash, and one had erythema nodosum. The actuarial incidence of therapy-limiting side effects was 27 +/- 7% at 15 months. We conclude that amiodarone is useful in the treatment of refractory tachyarrhythmias but that the rate of efficacy in VT/VF is lower and the incidence of significant toxicity is higher than has been generally appreciated.
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PMID:Amiodarone: clinical efficacy and toxicity in 96 patients with recurrent, drug-refractory arrhythmias. 685 Oct 57

Lyme disease, caused by a tick-transmitted spirochete, typically begins with a unique skin lesion, erythema chronicum migrans. Of 314 patients with this skin lesion, almost half developed multiple annular secondary lesions; some patients had evanescent red blotches or circles, malar or urticarial rash, conjunctivitis, periorbital edema, or diffuse erythema. Skin manifestations were often accompanied by malaise and fatigue, headache, fever and chills, generalized achiness, and regional lymphadenopathy. In addition, patients sometimes had evidence of meningeal irritation, mild encephalopathy, migratory musculoskeletal pain, hepatitis, generalized lymphadenopathy and splenomegaly, sore throat, nonproductive cough, or testicular swelling. These signs and symptoms were typically intermittent and changing during a period of several weeks. The commonest nonspecific laboratory abnormalities were a high sedimentation rate, an elevated serum IgM level, or an increased aspartate transaminase level. Early Lyme disease can be diagnosed by its dermatologic manifestations, rapidly changing system involvement, and if necessary, by serologic testing.
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PMID:The early clinical manifestations of Lyme disease. 685 26

Thirty-six patients with advanced Hodgkin's disease who were treated primarily with MOPP were evaluated to determine the reasons for MOPP failure. Complete remission was achieved in 22 (61%) of the patients, and the predicted 5-year survival rate for all patients is 60%. Reasons for the failure of MOPP to cure patients in this series included: 1) Idiosyncratic drug reactions in 2 patients (6%). MOPP was discontinued after one cycle because of drug-related hepatitis or skin rash; 2) Resistant disease in 8 patients (22%). Primary treatment failure was significantly associated with the presence of B symptoms (p = .005) and age greater than 40 years (p = .02); 3) Death from complicating infection in 5 patients (14%). Four patients died without evidence of Hodgkin's disease while responding to MOPP from pneumocystis pneumonia, viral pneumonia, bacterial pneumonia, or bacterial septicemia. One patient died in complete remission from sudden, overwhelming sepsis; 4) Relapse from complete remission in 4 patients (11%). All patients who relapsed had deviations from the planned dose or timing of MOPP. Remission duration was shorter (p = .06) in patients with documented deviations in MOPP administration than in patients without such changes. It appears that new treatment approaches are needed for patients with B symptoms, and that failure to deliver MOPP on schedule in the planned dose increases the risk of relapse.
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PMID:Reasons for failure of MOPP to cure Hodgkin's disease: The importance of dose and schedule. 689 61

Respiratory tract infections with mycoplasma can cause severe infiltrating pneumonia (with pleuritis), associated with marked inflammatory reactions (maximal E.S.R., high leucocytosis with shift to the left and marked alpha 2-proteinaemia). Serial measurements of cold-agglutinin titres as well as complement-fixation reaction to Mycoplasma pneumoniae will confirm the diagnosis. Atypical forms of pneumonia can also be documented in that they respond only to erythromycin and extrapulmonary complications accompany the disease, giving them a protean character. In two such patients there was the clinical picture of pneumonia with high fever and marked inflammatory reaction, associated with anicteric hepatitis. In one there was also thoracic lymphadenitis, myositis and rash, in the other a meta- and post-infectious polyarthritis.
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PMID:[Severe forms of mycoplasma pneumonia (author's transl)]. 705 63

The clinical signs and gross and microscopic lesions of Lassa virus infection in the rhesus monkey are described. Of 17 monkeys infected with Lassa virus, nine died or were killed when moribund. The clinical signs were lethargy, aphagia, constipation, fever, conjunctivitis, and skin rash. Pulmonary congestion, pleural effusion, pericardial edema, hydropericardium, and a few visceral hemorrhages were present grossly. Major microscopic lesions were necrotizing hepatitis and interstitial pneumonia. Other microscopic changes were present in the heart, small intestine, spleen, lymph nodes, kidney, urinary bladder, adrenal glands, and central nervous system; however, most of these lesions were mild. In fact, death could not always be attributed to the morphologic changes; therefore, function alterations must be examined.
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PMID:Pathology of Lassa virus infection in the rhesus monkey. 712 56

A 75 year-old man developed fever after one month of quinidine administration 800 mg/day. Significant enlargement of the liver and spleen became evident, associated with marked rise in serum GOT, GPT and alkaline phosphatase. Arthritis also developed, but there was no skin rash nor any changes in the haemoglobin, leucocytes or platelets. The signs and biochemical findings regressed within a few days of stopping quinidine and the temperature became normal. Rechallenge with four doses of the drug produced a rise in the GOT, GPT and alkaline phosphatase. It is thought that this hypersensitivity response is consistent with the description of granulomatous hepatitis, and represents a much less common manifestation of quinidine hypersensitivity than the well known skin, gastro-intestinal and haematological side-effects.
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PMID:Hepatosplenomegaly as a manifestation of quinidine hypersensitivity. 721 71

We encountered 11 patients who had rashes associated with hepatitis. Five of six acute hepatitis cases, but only one of five chronic hepatitis cases, were related to hepatitis B. Nine of the 11 patients had rash in the absence of clinically overt liver disease. Skin biopsy specimens showed histologic evidence of cutaneous vascular injury; specimens of urticarial and maculopapular rashes, which were seen in this series only with acute hepatitis, showed a primarily lymphocytic venulitis with focal necrosis, while palpable purpura, which was seen in this series only in chronic hepatitis, showed a primarily neutrophilic necrotizing vasculitis involving small vessels. One patient had lichen planus-like lesions. Demonstration of vascular deposits of immunoglobulins, complement, and fibrin in skin, as well as hypocomplementemia, circulating immune complexes, and mixed cryoglobulinemia, in these patients suggests that cutaneous lesions associated with liver disease resulted from immune complex-mediated vascular injury.
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PMID:Cutaneous vasculitis associated with acute and chronic hepatitis. 722 43

A case of salicylate hepatitis in a seven-week-old boy with Kawasaki's disease, mucocutaneous lymph node syndrome, is reported. The infant was admitted to the hospital with fever and a diffuse maculopapular petechial rash. He was treated with antibiotics for 72 hours for presumed septicemia. His condition deteriorated and he developed mucous membrane lesions and edema in his hands and feet. When the cultures of spinal fluid, blood, and urine were found to be negative, the antimicrobial therapy was discontinued; however, the cyanosis of his extremities progressed and gangrenous regions developed in his toe and finger pads. Oral aspirin therapy was started at a dosage of 100 mg/kg/day, every six hours. After five days, the rash, membrane lesions, and swelling in his hands and feet resolved. The cyanosis regressed. Liver enzyme tests revealed mild elevations of SGOT and LDH, and on the 12th hospital day these values peaked to a level consistent with salicylate hepatitis. The aspirin therapy was discontinued and within four days the liver function test results were normal. Aspirin therapy was reinstituted at a single daily dose of 30 mg/kg with no recurrence of hepatitis. The careful monitoring of liver function tests is recommended for children with Kawasaki's disease receiving aspirin therapy to avoid salicylate-induced hepatitis.
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PMID:Salicylate hepatitis: a complication of the treatment of Kawasaki's disease. 727 May 63

Although the toxicity of diphenylhydantoin in a number of target organs is discussed in numberous reports, hepatotoxic reactions are quite rare. The hepatic lesion has mostly been described as necrosis or hepatitis. Tissue sections from 20 patients who had validated diphenylhydantoin hepatotoxicity were reviewed to define this entity. The morphologic lesions included ground-glass transformation of liver cells, hepatocellular degeneration and/or necrosis (with changes resembling those occurring in viral hepatitis or infectious mononucleosis), granulomatous reactions with or without associated hepatocellular injury or vasculitis, and infiltration by malignant cells of reticuloendothelial origin. The interval between the beginning of therapy and the adverse drug reaction varied from one to eight weeks. Clinically, 75% of the patients had fever, 62.5% had rash, and 89% had eosinophilla. Most patients recovered after the drug was discontinued. The clinical and morphologic differential diagnosis includes a number of diseases, such as granulomatous hepatitis, infectious mononucleosis, and viral hepatitis.
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PMID:Hepatic injury associated with diphenylhydantoin therapy. A clinicopathologic study of 20 cases. 742 26

A patient with Sulindac-induced hepatitis is presented. Sulindac was confirmed as the cause of the patient's liver disease when hepatic dysfunction abruptly recurred after an inadvertent reexposure to Sulindac and quickly resolved when the drug was withdrawn. The prompt reappearance of fever, chills, pruritus, rash, tender hepatomegaly, and abnormal liver tests after only two doses of Sulindac suggested a hypersensitivity reaction.
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PMID:Sulindac (Clinoril) hepatitis. 745 Apr 49


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