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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with the acquired immune deficiency syndrome (AIDS) frequently develop hepatic dysfunction. Although hepatic injury may indirectly result from malnutrition, hypotension, administered medications, sepsis, or other conditions, the hepatic injury is frequently due to opportunistic hepatic infection, directly related to AIDS. Infection with Mycobacterium avium intracellulare typically occurs in patients with advanced immunocompromise and with systemic symptoms due to widely disseminated infection. In contrast, hepatic tuberculosis often occurs with less advanced immunocompromise. Cytomegaloviral infection may produce a hepatitis. Cytomegaloviral and cryptosporidial infections have been implicated as causes of acalculous cholecystitis and of a secondary sclerosing cholangitis. About 10-20% of patients with AIDS have chronic hepatitis B infection. These patients tend to develop minimal hepatic inflammation and necrosis. The clinical findings in patients with hepatic cryptococcal infection are usually due to concomitant extrahepatic infection. Hepatic histoplasmosis usually develops as part of a widely disseminated infection with systemic symptoms. Hepatic involvement by Kaposi's sarcoma is rarely documented ante mortem because an unguided liver biopsy is an insensitive diagnostic procedure. Patients with non-Hodgkin's lymphoma of the liver typically have lymphadenopathy, hepatomegaly, and systemic symptoms. As a pragmatic approach, patients with liver dysfunction and HIV-related disease should have a sonographic or computerized tomographic examination of the liver. Patients with dilated bile ducts should undergo endoscopic retrograde cholangiopancreatography because opportunistic infection may produce biliary obstruction. Patients with a focal hepatic lesion should be considered for a guided liver biopsy. Patients with a significantly elevated serum alkaline phosphatase level should be considered for a percutaneous liver biopsy. When performed for these indications, liver biopsy will demonstrate a significant disease involving the liver in about 50% of patients with AIDS and in about 25% of patients who are HIV seropositive but who are not known to have AIDS. The clinical impact of a diagnostic biopsy is blunted by a lack of efficacious therapy for many opportunistic infections.
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PMID:Hepatobiliary manifestations of the acquired immune deficiency syndrome. 198 33

We describe the clinical features, liver histology, and ultrastructure in reversible diclofenac-induced hepatitis and review previous reports of this entity. Although rarely reported, diclofenac hepatitis may be severe, and even fatal. Symptoms, which develop from 1 week to 11 months after starting the drug, include jaundice, pruritus, fever, abdominal pain, nausea, vomiting, and rash. Bilirubin and alkaline phosphatase are mildly elevated, transaminases often markedly so. The nature of the idiosyncratic injury appears variable, some cases having features of a hypersensitivity reaction, most being more suggestive of a toxic metabolic effect. Light microscopy shows a nonspecific hepatitis with portal and lobular activity, and focal hepatocellular injury that may progress to zonal or massive necrosis. The ultrastructural features in our case are typical of drug or toxin injury. This may be of value in distinguishing this entity from other forms of hepatitis, which is important in view of the frequent reversibility of this potentially lethal form of injury.
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PMID:Reversible hepatitis associated with diclofenac. 203 30

This report described seventeen patients suffering from fulminant hepatitis and had a rapid fatal course. They were all residents of Southern Thailand. Fourteen cases were recognized between April and August which is the beginning of the rainy season in this part of the country. All age groups were found with males slightly predominant. Clinical manifestation presented with fever and later developed jaundice, convulsion and other central nervous system symptoms, liver failure and acute renal failure. Four cases had pneumonia and another three cases had pleural effusion. Laboratory investigations revealed hyperbilirubinemia, marked increase in serum transaminases, a variable alkaline phosphatase level and electrolytes derangement. HBsAg was positive in only two of fourteen cases. Blood cultures and serological examination for infections were unfruitful. Histopathological changes of the liver were classified into three types; type 1 massive hepatocellular coagulation necrosis; type 2 massive scattered hepatocellular necrosis and type 3 massive bridging hepatocellular necrosis. Electron microscopy of five cases revealed spherical viral-like particles ranging in size 70 to 90 nm in diameter, in the cytoplasm of liver cells. This is believed to be a unique type of fulminant hepatitis, possibly viral in origin, and were clinically and pathologically different from the previously described fulminant viral hepatitis.
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PMID:Fulminant hepatitis, possible virus origin: a report of seventeen cases in southern Thailand. 208 15

Properties differentiating 13 biochemical indexes of cholestasis within a group of patients suffering from acute virus hepatitis were examined. It has proved the existence of a set of parameters of optimal properties differentiating separate states of cholestasis. This set includes concentrations of bilirubin and cholesterol esters, together with the activity of alkaline phosphatase. The variables formed a function enabling to differentiate mathematically+ the states with and without cholestasis.
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PMID:[Biochemical criteria of intrahepatic cholestasis in hepatitis B]. 210 Aug 9

Sixty cases of acute viral hepatitis were studied from clinical, biochemical and in particular serological point of view. Majority of the patients had significant pre-icteric and icteric phase with moderate elevations of bilirubin, SGOT and SGPT and marginal elevations of serum alkaline phosphatase. Cholestatic features were observed only in 6.7% of cases. All subjects improved and there was no death in this series. Serological marker studies revealed hepatitis A in 8 (13.3%) cases and hepatitis B in 3 (5.0%) cases. Rest 49 cases were possibly due to non-A, non-B hepatitis. As there was no evidence of parenteral transmission, it was concluded that this epidemic was water borne from contaminated municipal water supply.
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PMID:Studies on outbreak of viral hepatitis at Calcutta with special reference to serological investigations. 212 96

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

A previously healthy woman developed acute anicteric hepatitis which slowly resolved, though bilateral anterior uveitis then appeared. No other cause than an occupational exposure to trichloroethylene was found, and rechallenge by resuming work has led to a transient increase in serum alkaline phosphatase. Both manifestations may constitute a rare systemic reaction to trichloroethylene.
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PMID:Anicteric hepatitis and uveitis in a worker exposed to trichloroethylene. 223 4

Lipoproteid-X was revealed at the onset of the disease in 59.6% of patients with acute viral hepatitis with prevalence of the cholestasis syndrome and cytolysis. Lipoproteid-X may be revealed in moderate activity of alkaline phosphatase. Lipoproteid-X was revealed in 66.7% of patients with chronic cholestatic hepatitis and biliary cirrhosis independent of the duration of the pathological process.
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PMID:[The diagnostic significance of lipoprotein-X]. 233 Jun 94

We report four cases of severe delayed cholestatic hepatitis induced by flucloxacillin. All patients presented with deep jaundice and pruritus which developed soon after ceasing flucloxacillin. Liver function tests were abnormal in all patients with markedly elevated serum bilirubin concentration, alkaline phosphatase and aspartate transaminase levels. Extrahepatic biliary obstruction and infective hepatitis were excluded in all cases. Liver biopsies showed centrilobular cholestasis with portal and lobular inflammation and eosinophil infiltration. Although symptoms resolved within six weeks in all patients, cholestatic liver function tests have persisted in two patients for more than six months. With the increasing usage of this drug and the delayed presentation of cholestasis, flucloxacillin needs to be considered in the differential diagnosis of all patients presenting with cholestatic jaundice.
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PMID:Flucloxacillin induced delayed cholestatic hepatitis. 237 76

This analysis of the morphology of suspected amiodarone (AD) liver disease is based on a study of liver specimens from 17 individuals. Changes similar to alcoholic liver injury were commonly seen. Steatosis, both macrovesicular and microvesicular, was the most frequent histopathologic feature. Ballooning of hepatocytes, Mallory bodies, and fibrosis were also common. Other changes included nuclear unrest, acidophilic bodies, foam cells, glycogenated nuclei, and portal inflammation. Characteristic lamellar lysosomal inclusion bodies representing phospholipidosis were found in two of 14 specimens studied ultrastructurally. These changes of pseudoalcoholic hepatitis and/or phospholipidosis were present in liver specimens from asymptomatic, anicteric patients with mild elevations in serum aminotransferase or alkaline phosphatase values with or without hepatomegaly, as well as in patients with clinically overt symptoms of hepatotoxicity. Phospholipidosis appears to be a generalized systemic effect of cationic amphophilic compounds, such as AD. The cytotoxic pseudoalcoholic changes appear to be an independent phenomenon in susceptible patients, whom we speculate may have been unable or less able to metabolize AD through normal pathways. The true incidence of hepatic injury from AD remains to be determined from prospective evaluations of pretreatment and follow-up liver biopsies.
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PMID:Histopathologic analysis of suspected amiodarone hepatotoxicity. 240 75


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