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)

We report a case study of an 86-year-old female patient with severe cholestatic hepatitis who was undergoing treatment with oral ticlopidine 250 mg daily for coronary artery disease. The patient had nausea and vomiting and was jaundiced after taking ticlopidine for 6 weeks. She was admitted to the hospital for further evaluation. Ultrasound and endoscopic retrograde cholangiopancreatography eliminated the presence of biliary obstruction. Results from a liver biopsy showed a histopathologic picture consistent with cholestatic hepatitis. Ticlopidine-induced cholestatic hepatitis has been reported 32 times in the foreign literature. This is the first reported severe cholestatic hepatitis (total bilirubin up to 43 mg/dl) case in Taiwan. Ticlopidine-related blood dyscrasia is a renowned adverse drug effect; liver function should be monitored in patients receiving ticlopidine therapy.
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PMID:Ticlopidine-induced severe cholestatic hepatitis. 1096 55

Cholestasis resulting from drugs is an increasingly recognized cause of liver disease. It produces a broad clinical-pathologic spectrum of injury that includes simple jaundice, cholestatic hepatitis, and bile duct injury that can mimic extrahepatic biliary obstruction, primary biliary cirrhosis, and sclerosing cholangitis. Although the risk of drug-induced cholestasis leading to a fatal outcome is quite rare, knowledge and recognition of the various forms of cholestatic injury assumes an importance whenever clinicians are confronted with jaundice or other manifestations of liver disease in patients receiving medicinal or chemical agents.
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PMID:Drug- and chemical-induced cholestasis. 1129 Dec 33

Histologic cholestasis and clinical jaundice may be seen in all stages of alcoholic liver disease. In rare cases, isolated cholestasis without significant steatosis, hepatitis, or cirrhosis is identified in an alcoholic patient. The mechanisms of ethanol-induced cholestasis are not well studied but may involve compression of intrahepatic biliary radicals or interference with basolateral uptake and intracellular transport of bile acids. In the evaluation of the jaundiced alcoholic patient, clinical, biochemical, and radiologic data are usually sufficient to distinguish alcohol-induced liver disease from extrahepatic biliary obstruction. In cases where the diagnosis is not readily apparent, more invasive studies such as liver biopsy or ERCP may be necessary. The risk of these invasive studies is directly related to the degree of underlying hepatic dysfunction.
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PMID:Cholestasis and alcoholic liver disease. 1129 Dec 40

1. Recurrent primary biliary cirrhosis (PBC) after transplantation is controversial, but most studies support disease recurrence within the graft. 2. Granulomatous destructive cholangitis should be present, and exclusion of acute and chronic rejection, graft-versus-host disease, biliary obstruction, viral hepatitis, and drug effects is mandatory before making a diagnosis of recurrent PBC. 3. Recurrent primary sclerosing cholangitis (PSC) after transplantation is difficult to diagnose because of the lack of a diagnostic gold standard. 4. Well-defined cholangiographic and histological criteria should be present, and exclusion of preservation injury, blood group type incompatibility between donor and recipient, chronic rejection, hepatic arterial occlusion, and viral infection is mandatory before making a diagnosis of recurrent PSC. 5. Most studies support recurrent autoimmune hepatitis (AIH) after transplantation based on clinical, biochemical, serological, and histological criteria. Exclusion of rejection, viral infection, drug effects, and biliary obstruction is mandatory before making a diagnosis of recurrent AIH. 6. Intermediate-term patient and graft survival are excellent for patients with recurrent autoimmune liver diseases within the transplanted liver, but additional studies are required to address the impact of disease recurrence on long-term patient and graft survival.
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PMID:Recurrent primary biliary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis after transplantation. 1168 82

We studied nondiagnostic liver biopsy specimens from 20 patients with definite primary biliary cirrhosis (PBC) and 18 with definite autoimmune hepatitis (AIH) to identify distinguishing features. All patients had early-stage disease; biopsy specimens were devoid of granulomas or diagnostic features of PBC or AIH. Diagnoses were based on serologic and clinical variables. Sixteen specimens from each group were immunostained with cytokeratin 7. The density of portal tract eosinophils and number with cytokeratin 7-reactive periportal hepatocytes were quantified. Sixteen of 18 patients with AIH and 13 of 20 with PBC had no or minimal bile duct injury. Histologic activity index scores were 5.8 in AIH and 5.7 in PBC. The mean portal eosinophil score was greater in PBC than in AIH. Cytokeratin 7 identified many central bile ducts that were obscured by portal inflammation. The mean periportal cytokeratin 7-reactive hepatocyte score was greater in PBC than in AIH. Portal eosinophils and cytokeratin 7 reactivity in periportal hepatocytes are supportive of PBC rather than AIH. No morphologic features were supportive of AIH. Cytokeratin 7 reactivity in periportal hepatocytes may be an early response to PBC-induced biliary obstruction in other regions of the liver.
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PMID:Portal tract eosinophils and hepatocyte cytokeratin 7 immunoreactivity helps distinguish early-stage, mildly active primary biliary cirrhosis and autoimmune hepatitis. 1176 73

Liver biopsy is used to determine the pathogenesis of liver dysfunction after liver transplantation. One or more causative factors may be identified on biopsy. The pathologist must be familiar with the histopathology of acute rejection to differentiate it from other potential complications, including biliary obstruction, intercurrent cytomegalovirus hepatitis, or recurrent disease. Consensus documents from the Banff international panel provide useful guidelines for the appropriate grading of acute and chronic rejection.
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PMID:Diagnostic issues in liver transplantation pathology. 1212 70

Liver fibrosis represents a major medical problem with significant morbidity and mortality. Worldwide hepatitis viral infections represent the major cause liver fibrosis; however, within the United States chronic ethanol consumption is the leading cause of hepatic fibrosis. Other known stimuli for liver fibrosis include helminthic infection, iron or copper overload and biliary obstruction. Fibrosis can be classified as a wound healing response to a variety of chronic stimuli that is characterized by an excessive deposition of extracellular matrix proteins of which type I collagen predominates. This excess deposition of extracellular matrix proteins disrupts the normal architecture of the liver resulting in pathophysiological damage to the organ. If left untreated fibrosis can progress to liver cirrhosis ultimately leading to organ failure and death if left untreated. This review will discuss the molecular events leading to liver fibrosis. The discussion will include collagen gene regulation and proliferative signals that contribute to the amplification of the hepatic stellate cell, the primary fibrogenic cell type that resides in the liver.
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PMID:Liver fibrosis: signals leading to the amplification of the fibrogenic hepatic stellate cell. 1245 23

Two patients developed acute cholestatic hepatitis during treatment with propafenone. Viral infections, alcohol abuse, hepatotoxicity by other drugs, and biliary obstruction were excluded as causes. In one patient, liver biopsy showed changes consistent with a drug-associated injury. Another patient had autoimmune antibodies (ANA) in the serum. Following propafenone withdrawal, the clinical and biochemical profiles of both patients improved. Hepatic toxicity from the antiarrhythmic drug propafenone is highly uncommon. Moreover, the drug produces hepatocellular injury by an unknown mechanism. Most of the seven cases reported here had acute cholestatic hepatitis after a latency period of two to four weeks.
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PMID:Propafenone hepatotoxicity: report of two new cases. 1264 15

Liver involvement is nearly universal in healthy persons with Epstein-Barr Virus (EBV) infection-induced infectious mononucleosis. It is usually mild, undetected clinically and resolves spontaneously. Jaundice is distinctly uncommon and may reflect either more severe hepatitis or an associated hemolytic anemia. Cholestatic hepatitis due to EBV infection is infrequently reported and may pose a diagnostic quandary. We describe a patient who presented with jaundice and a markedly elevated serum alkaline phosphatase level due to serologically confirmed acute infection with EBV. Imaging studies excluded biliary obstruction. Symptoms and laboratory abnormalities resolved spontaneously. EBV infection should be included in the differential diagnosis of cholestatic hepatitis in adults.
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PMID:Cholestatic hepatitis induced by Epstein-Barr virus infection in an adult. 1275 67

We report a patient with fibrosing cholestatic hepatitis (FCH)-like syndrome in renal transplant recipient, who was negative for hepatitis-B and C-virus infection. The patient presented initially with extrahepatic biliary obstruction due to stricture at the lower end of the common bile duct. Cholestasis persisted inspite of effective biliary drainage. He was operated for empyema of the gallbladder and histological examination showed the presence of cytomegalovirus inclusions in the wall of the gallbladder. The patient died inspite of aggressive management; autopsy examination of the liver revealed evidence of FCH-like changes.
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PMID:Fibrosing cholestatic hepatitis-like syndrome in a hepatitis B virus and hepatitis C virus-negative renal transplant recipient: a case report with autopsy findings. 1297 14


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