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)

One hundred patients on chronic haemodialysis were studied prospectively over one year for evidence of hepatitis and of infection with hepatitis A or B virus. Five patients developed transient elevations of SGPT, accompanied by a consistent pattern of clinical manifestations, including low-grade fever, anorexia, nausea, hepatomegaly, and hypotension during dialysis. None of these patients had a positive test for A or B virus infection. Non-A non-B hepatitis appears to cause a specific syndrome in uraemic patients, and its transmission in a dialysis unit seems unrelated to blood transfusions.
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PMID:Non-A, non-B hepatitis: a new syndrome in uraemic patients. 12 59

The chief causes of liver disease in Ethiopia are reviewed, considering hospital data on admissions for hepatitis, cirrhosis, ascites and hepatoma. Liver diseases account for 11.4% of all medical admissions in 3 medical wards in Addis Ababa. The causes are viral hepatitis, post- hepatic and post necrotic and mixed cirrhosis and hepatocellular carcinoma. Alcoholic cirrhosis is rare. Viral hepatitis with shivering, rigor and fever and elevated direct bilirubin levels are common in Ethiopians, especially in child-bearing women. The hepatitis B surface antigen (HBsAg) is often associated with hepatitis. The disease may be transmitted by several species of mosquitoes, placental transmission, or feces, urine, saliva or semen. Blood products are not screened for hepatitis B. Cirrhosis is common, and causes significant mortality, usually from esophageal varices and hepatic coma. Chronic active hepatitis patients may live for a time, especially if they are near a hospital and are treated with steroids. In Ethiopia presenting symptoms for hepatoma are anorexia, weight loss, persistent, burning, right upper quadrant pain, and a hard, nodular, tender RUQ mass. Over 5% of malignancies seen are primary hepatocellular carcinomas. 50% have HBsAG, compared to 3.8% of controls. 65% have alpha-fetoglobulins. It is suggested that some viral hepatitis cases progress to cirrhosis, of which some go on to hepatocellular carcinoma. Herbal medicines, aflatoxins and other toxins may also contribute to liver disease.
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PMID:Current views on liver diseases in Ethiopia. 20 62

Vincristine-high-dose methotrexate-citrovorum factor (VCR-MTX-CF) was administered preoperatively at weekly intervals to eight patients, four with primary tumors and four with pulmonary metastases. These patients had not received prior VCR-MTX-CF treatment. A similar treatment program was administered to five patients with pulmonary metastases who had received prior VCR-MTX-CF. Among the eight patients who had not received prior VCR-MTX-CF, complete responses were obtained in three with primary tumors (this was followed by surgical excision) and two with pulmonary metastases. Partial responses occurred in two additional patients. Partial responses were also obtained in two patients who had received VCR-MTX-CF. Chemotherapy and surgery in one patient with an extremity lesion resulted in preservation of the limb and useful function. The major toxicity was anorexia and weight loss. Other side effects included stomatitis, myelosuppression, hepatitis and transient renal impairment. The weekly program was highly effective when compared to responses obtained with the tri-weekly schedule utilized in previous studies.
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PMID:Weekly high-dose methotrexate-citrovorum factor in osteogenic sarcoma: pre-surgical treatment of primary tumor and of overt pulmonary metastases. 29 28

Twelve patients with liver disease related to methyldopa were seen between 1967 and 1977. Illness occurred within 1--9 weeks of commencement of therapy in 9 patients, the remaining 3 patients having received the drug for 13 months, 15 months and 7 years before experiencing symptoms. Jaundice with tender hepatomegaly, usually preceded by symptoms of malaise, anorexia, nausea and vomiting, and associated with upper abdominal pain, was an invariable finding in all patients. Biochemical liver function tests indicated hepatocellular necrosis and correlated with histopathological evidence of hepatic injury, the spectrum of which ranged from fatty change and focal hepatocellular necrosis to massive hepatic necrosis. Most patients showed moderate to severe acute hepatitis or chronic active hepatitis with associated cholestasis. The drug was withdrawn on presentation to hospital in 11 patients, with rapid clinical improvement in 9. One patient died, having presented in hepatic failure, and another, who had been taking methyldopa for 7 years, showed slower clinical and biochemical resolution over a period of several months. The remaining patient in the series developed fulminant hepatitis when the drug was accidentally recommenced 1 year after a prior episode of methyldopa-induced hepatitis. In this latter patient, and in 2 others, the causal relationship between methyldopa and hepatic dysfunction was proved with the recurrence of hepatitis within 2 weeks of re-exposure to the drug.
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PMID:Patterns of hepatic injury induced by methyldopa. 42 37

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.
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PMID:Disseminated intravascular coagulation complicating aflatoxicosis in dogs. 55 87

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23

Disordered gustatory acuity was demonstrated in 22 patients with acute viral hepatitis and in 16 patients with chronic liver disease utilizing subjective responses and objective measurements of detection and recognition thresholds and scaling for NaCl, sucrose, HCl, and urea. In patients with early hepatitis and those with chronic liver disease, the magnitude and the uniformity of the threshold elevations were comparable, implying that disordered gustatory acuity reflects disordered hepatic function per se. Patients with acute hepatitis showed a significant fall in taste thresholds (improvement in acuity) as the hepatitis waned, indicating that the gustatory defect is reversible. This disorder of gustatory acuity may contribute to the anorexia commonly found in patients with liver disease.
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PMID:Disordered gustatory acuity in liver disease. 125 40

A retrospective study concerning ten patients with autoimmune hepatitis (AiH), diagnosed during a 2 1/2-year period is presented. The age of the patients ranged from 25 to 82 years and nine of the patients were women. Their symptoms included jaundice, pruritus, fever, anorexia and fatigue during a few weeks to years. Seven patients had increased serum aspartate aminotransferase (ASAT) levels. The three patients with normal ASAT levels had hypoalbuminaemia, decreased level of prothrombin or high levels of serum immunoglobulin G. Moderate or high levels of smooth muscle antibody titer were detected in nine patients, while none had increased levels of anti-nuclear antibody titer. Histological features of moderate or severe chronic active hepatitis were demonstrated in nine patients. One patient presented with clinical and histological features of acute hepatitis. Prednisolone therapy was followed by biochemical improvement in all the patients. In one patient, maintenance therapy with prednisolone was combined with azathioprine.
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PMID:[Autoimmune hepatitis. Forms of manifestation, diagnosis and treatment]. 141 30

We report a case of clinical hepatitis associated with occupational exposure to halothane in a research laboratory. A biochemist who for 3 y repeatedly used halothane for sedation and euthanization of rats suffered recurrent episodes of epigastric discomfort, culminating in an episode of malaise, anorexia, jaundice and elevated liver associated enzymes that promptly resolved after removal from exposure to halothane. Serologic testing for viral sources and risk factors for non-infectious hepatitis were negative. Halothane-induced hepatitis has been documented as an idiosyncratic reaction among anesthetized patients and has been reported once in operating room personnel. The mechanism for halothane-induced hepatitis is proposed to be a hypersensitivity reaction to liver neo-antigens produced by the halothane metabolite 2-chloro-1, 1, 1-trifluoroethane.
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PMID:Chemical hepatitis associated with occupational exposure to halothane in a research laboratory. 145 11

The Southwest Oncology Group studied the response rate and toxicity of didemnin B (3.47 mg/m2 i.v. q 28 days) in patients with advanced renal cell carcinoma. There were no responses in 22 response evaluable patients. Toxicity was significant with 10 patients having grade 3 or 4 toxicity. Toxicity seen included nausea and vomiting, exacerbation of coronary artery disease, hyperglycemia, anorexia, diarrhea and hepatitis. Didemnin B was toxic but inactive in patients with renal cell treated at this dose.
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PMID:Phase II evaluation of didemnin B in advanced adenocarcinoma of the kidney. A Southwest Oncology Group study. 160 54


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