Cases reported "Liver Diseases, Alcoholic"

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1/14. Fulminant hepatitis A in patients with chronic liver disease.

    Fulminant hepatitis is a rare complication of acute hepatitis a virus (HAV) infection. We report three cases of fulminant hepatic failure with death due to HAV infection in patients with pre-existing chronic liver disease. Data from the literature also indicate a high case fatality rate during HAV superinfection in patients with chronic hepatitis b, particularly those with cirrhosis, and in patients with alcoholic cirrhosis. In patients with chronic hepatitis c, results are conflicting with some reports indicating a high fatality rate of HAV superinfection and others not, irrespective of the presence or absence of cirrhosis. Based on our observations and this review of the literature, we suggest that patients with chronic liver disease should be vaccinated against hepatitis A.
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2/14. Pseudo-budd-chiari syndrome: decompensated alcoholic liver disease mimicking hepatic venous outflow obstruction.

    Three patients with rapid onset decompensated liver disease who were referred to our hospital with presumed budd-chiari syndrome are described. This diagnosis was based on marked hepatomegaly, caudate lobe hypertrophy and failure to visualize hepatic veins by Doppler-ultrasound examination. Detailed history, biochemistry, and histology were, however, highly suggestive of alcoholic liver cirrhosis with steatohepatitis-induced hepatomegaly. On angiographic examination narrowed but patent hepatic veins were demonstrated in 2 patients. A third patient died before further work-up could be performed; autopsy showed patent hepatic veins. These cases show that the radiological diagnosis of budd-chiari syndrome due to hepatic vein obstruction can be false positive and that suspected hepatic vein occlusion on Doppler-ultrasound should be confirmed by angiographic studies and on liver histology.
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3/14. Severe steatosis as the initial histologic manifestation of recurrent hepatitis c genotype 3.

    Steatosis is a common finding that is seen in patients with both chronic hepatitis c and alcoholic liver disease; however, the extent of involvement in the former is generally minimal to mild. We present 2 patients who underwent live donor liver transplantation for end-stage liver disease that was caused by chronic hepatitis c (genotype 3) and alcohol abuse. Both patients presented with liver allograft dysfunction, with liver biopsy findings of moderate to marked steatosis. Exclusion of a relapse of alcohol use required intense questioning of both the patients and their families. A definitive diagnosis of recurrent hepatitis c was established by viral markers with institution of the proper therapy and resolution of graft dysfunction. We conclude that recurrent hepatitis c, particularly genotype 3, may present with severe steatosis. Recognition of this phenomenon is important, and confirmation with viral markers is necessary to provide optimal patient care.
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4/14. Strategy for hepatic hyperplastic nodules in heavy drinkers.

    BACKGROUND: Increased detection of nodular lesions that have not yet been definitively diagnosed as hepatocellular carcinoma (HCC) has occurred with the use of advanced imaging techniques. In heavy drinkers, the differential diagnosis between a hyperplastic nodule and early HCC on the basis of results of fine-needle biopsy is often difficult. Negation of diagnosis of HCC after surgical resection has been reported, and nodular lesions have been found to decrease during follow-up observation. On the basis of findings, a suitable strategy for the management of such lesions is suggested. methods: We identified six patients who had hepatic nodular lesions on ultrasonography and were heavy drinkers. This group included five men and one woman with a mean age of 45.3 /- 3.8 years. Two patients had solitary lesions; four had multiple lesions, and of these, two were hepatitis c virus antibody positive (C ). In the five men, the nodular lesions were detected during hospitalization for ruptured or prophylactic treatment of gastroesophageal varices. RESULTS: Five of the six patients had hypervascular lesions characterized by increased hepatic artery blood flow. However, dynamic computed tomography and magnetic resonance imaging studies during late-phase imaging could not confirm any decrease in portal blood flow. HCC was diagnosed by detailed imaging studies and liver biopsy in one C patient with a solitary nodule. In two of the other four patients, imaging findings were compatible with hypervascular HCC. Findings on liver biopsy do not always permit an easy differential diagnosis between a regenerative lesion (hyperplastic nodule) and a dysplastic or neoplastic lesion. One patient with a hypovascular lesion was C , and liver biopsy showed a dysplastic nodule. CONCLUSION: Heavy drinkers with alcoholic liver disease often develop hypervascular, hyperplastic nodules. The accurate diagnosis of these nodules requires careful consideration of clinical factors, including a combination of images and histologic examination. However, some cases were still difficult to distinguish between HCC by applying advanced imaging techniques and biopsy results.
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5/14. liver transplantation in a patient with undiagnosed bipolar disorder.

    We present the case of a 55-year-old woman with no previous diagnosis of bipolar disorder, who underwent orthotopic liver transplantation for hepatitis c and alcohol-related liver disease. Two weeks posttransplant, she exhibited manic symptoms including hyperactivity, racing thoughts, and pressured speech. Although drug and alcohol abuse had been in remission for a 10-year period, a long history consistent with bipolar disorder was only identified after surgery. This article discusses the role of psychiatric evaluation prior to undergoing liver transplantation, and provides the transplant team with suggestions for comprehensively assessing psychiatric disorders in addition to alcohol and drug use.
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6/14. Acute liver failure: a message found under the skin.

    Acute liver failure is a rare syndrome with rapid progression and high mortality. It is characterised by the onset of coma and coagulopathy usually within six weeks but can occur up to six months after the onset of illness. Viral hepatitis, idiosyncratic drug induced liver injury, and acetaminophen ingestion are common causes. This report describes the case of a 35 year old man who presented with acute liver failure shortly after binge drinking. Repeated history taking disclosed a gluteal disulfiram implant that the patient had received to treat his alcohol dependence. The patient recovered with maximum supportive care after surgical removal but without liver transplantation. This case illustrates that only meticulous history taking will disclose the sometimes bewildering causes of acute liver failure.
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7/14. A case of alcoholic liver injury with an unusual polyacrylamide-gel disc-electrophoretic pattern of serum lipoproteins.

    An unusual lipoprotein pattern on polyacrylamide-gel disc-electrophoresis was observed in 37 year-old male diagnosed as alcoholic liver injury. The electrophoretic lipoprotein pattern consisted of a major band of pre-beta mobility and minor intermediate, fast-beta and slow-alpha bands. The normal beta band was virtually absent and the alpha band was diminished. The abnormal lipoprotein pattern was observed one week after discontinuing alcohol consumption when marked hypertriglyceridemia demonstrated earlier had already normalized leaving a moderate hypercholesterolemia with reduced esterified cholesterol and abnormal liver function tests. The lipoprotein abnormalities were completely normal one month later. The appearance of a major pre-beta band with normal triglyceride and high cholesterol levels is discussed in relation to the formation of larger triglyceride-rich LDL particles in recovery from alcoholic hepatitis.
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8/14. acetaminophen hepatotoxicity in alcoholics. A therapeutic misadventure.

    We have treated 6 chronic alcoholics and identified an additional 19 reported in the literature who developed severe hepatotoxicity from acetaminophen taken in apparently moderate doses. The clinical disease in these 25 patients had a characteristic pattern: mild to moderate jaundice; mild to severe coagulopathy; and strikingly abnormal aminotransferase levels, values inconsistent with either acute alcoholic hepatitis or viral hepatitis. The possible causes for the injury from ostensibly nontoxic drug levels appear to be either the induction by chronic alcohol intake of the cytochrome P-450 system responsible for converting acetaminophen to a toxic metabolite, or the effect of alcoholism and the associated malnutrition in reducing the glutathione concentration, responsible normally for preventing hepatotoxicity by conjugation with the toxic metabolite. The research data pertaining to the apparent enhanced toxicity from chronic alcoholism are reviewed. Despite the low frequency of ethanol-potentiated acetaminophen hepatotoxicity, alcoholics should be cautioned about the use of acetaminophen while they persist in heavy consumption of alcohol.
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keywords = hepatitis
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9/14. Post-transfusion hepatitis: fatal outcome in two cases with underlying alcoholic liver disease.

    Two patients with underlying alcoholic liver disease who were doing well before receiving multiple blood transfusions for gastrointestinal bleeding died after developing post-transfusion hepatitis (PTH). This hepatitis was associated with an uncharacteristic disparity between transaminase levels.
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10/14. Acute cholestasis, hepatic failure, and fatty liver in the alcoholic.

    Three alcoholic patients are described who presented with acute cholestasis and liver cell failure. In each patient the liver biopsy showed severe fatty change with cholestasis, but without typical alcoholic hepatitis. There was no evidence of extra-hepatic biliary obstruction, although one patient had chronic pancreatitis. Two of the three patients died of hepatic failure, but the third recovered and has remained well while abstaining from alcohol.
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