Cases reported "Hepatitis, Alcoholic"

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1/7. Triggering of acute alcoholic hepatitis by alpha-interferon therapy.

    BACKGROUND/AIMS: Alcohol may induce autoimmunity by recognition of acetaldehyde-modified proteins which may be implicated in the pathogenicity of acute alcoholic hepatitis. We report here the potential role of alpha-interferon, a potent inducer of the autoimmunity process, in inducing alcoholic hepatitis. methods: We analyzed clinical, biological, virological and histological features in two cases where alpha-interferon treatment for HCV-related hepatitis led to a marked increase in aminotransferase activities. RESULTS: alpha-interferon as treatment of HCV-related hepatitis seemed to exacerbate acute alcoholic hepatitis despite moderate alcohol consumption. In Case 1, moderate daily alcohol intake of 40 g during therapy led to biopsy-proven acute alcoholic hepatitis, while the same consumption before therapy did not. In Case 2, before treatment, the liver biopsy showed mild acute alcoholic hepatitis; aminotransferases increased during alpha-interferon therapy, although no increase in alcohol intake was observed. CONCLUSION: alpha-interferon therapy by its immunomodulatory properties could be implicated in alteration of the course of acute alcoholic hepatitis. These observations emphasize that the decision to treat with alpha-interferon when there is even moderate alcohol consumption should be carefully weighted in HCV-infected patients.
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2/7. A clinicopathological study of acute hepatitis in heavy drinkers, unrelated to hepatitis a, B, or C viruses.

    BACKGROUND: There are six histological classifications of alcoholic liver disease (ALD) in japan. However, it is unclear whether all cases of the disease conform to these criteria. This study investigated the clinicopathological features of eight histologically unusual cases of ALD. methods: The characteristic features of alcohol drinking behavior, subjective and objective symptoms, laboratory data on admission, and progress after admission were analyzed for eight patients with acute-onset hepatitis. RESULT: The eight patients showed histologically acute hepatitis, with much spotty necrosis that contained granular ceroid pigment by kupffer cells, which indicated acute parenchymal damage of the liver, but with no mallory bodies and unremarkable intrasinusoidal neutrophilic infiltration. The only etiological factor for all the cases was habitual alcohol consumption, with increased consumption just before the onset of symptoms. In five cases that were tested, the patients were negative for hepatic viral markers, which included hepatitis G virus rna and TT virus dna. CONCLUSION: Some cases of ALD may not conform to the current histological classifications in either japan or Western countries. It seems natural to consider that these cases are developed by other, unknown causes that overlap with ALD rather than as a result of damage from alcoholic overload.
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3/7. Severe alcoholic hepatitis accompanied by Fournier's gangrene.

    Fulminant necrotizing soft-tissue infection of the external genitalia and perineum (Fournier's gangrene) occurred in a patient with severe alcoholic hepatitis. By means of radical debridement and disinfection of the necrotizing tissue, use of broad-spectrum antibiotics and prednisolone, and other supportive measures, Fournier's gangrene and severe alcoholic hepatitis eventually subsided with broad skin defects in the waist and external genitalia. Later, the skin defects were successfully reconstructed with skin grafts. Although the route of bacterial intrusion could not be defined, Fournier's gangrene presumably developed in a background of impaired immunological defences, principally associated with habitual massive alcohol consumption and profound liver dysfunction. This present case highlights not only the underlying immunocompromised condition but also the need for concern regarding the urogenital and anorectal areas as potential foci of life-threatening infection in patients with liver dysfunction, especially when related to alcohol intake.
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4/7. Discrepancy between pancreatographic and histopathological findings in the ventral pancreas of pancreas divisum.

    CONTEXT: pancreas divisum is a congenital anomaly in which the ventral and dorsal pancreatic ducts do not communicate. CASE REPORT: autopsy case of pancreas divisum with a history of heavy consumption of alcohol was presented. Pancreatography via the major duodenal papilla showed a short ventral pancreatic duct of 1 cm in length, and hypoplasia of the ventral pancreas was suspected. As large cysts were confined to the dorsal pancreas, isolated dorsal pancreatitis was also suspected. At autopsy, extensive fibrosis was detected in both the ventral and dorsal pancreas. Immunohistochemical examination revealed that PP-rich islets were scattered in the fibrotic area between the ventral pancreatic parenchyma and the neck of the pancreas, suggesting that this fibrotic area originated from the ventral pancreas. These facts suggest that the short ventral pancreatic duct was not induced by hypoplasia of the ventral pancreas but was shortened secondarily by the alcohol-induced fibrosis. CONCLUSIONS: In pancreas divisum, a short ventral pancreatic duct resulting from secondary factors may be confused with that originating from hypoplasia of the ventral pancreas.
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5/7. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management.

    Two cases of right hepatic hydrothorax occurring in the absence of clinical ascites are reported. diagnosis was confirmed by the intraperitoneal and intrapleural injection of radioisotope 99mTc-sulfur colloid that demonstrated the one-way transdiaphragmatic flow of fluid from the peritoneal to pleural cavities. In contrast, radioisotope injected into the peritoneal cavity of 5 patients with pleural effusions secondary to pulmonary or cardiac disease failed to traverse the diaphragm and localize in the pleural space. Medical therapy with salt and water restriction and diuretics resulted in both of the patients with hepatic hydrothorax developing signs of intravascular volume depletion without significant mobilization of the pleural fluid. thoracotomy allowed identification of the diaphragmatic defects that were repaired by chemical and traumatic pleurodesis followed by postoperative peritoneal and pleural drainage. This therapy resulted in complete resolution of the pleural effusions, which have not recurred despite the subsequent development of clinical ascites in both patients.
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keywords = water
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6/7. Diabetic hepatitis preceding the onset of glucose intolerance.

    A patient who abstained from alcohol consumption but who had asymptomatic chronic progressive hepatomegaly, mild disturbance of liver function tests and hepatitis resembling alcoholic hepatitis (nonalcoholic steatohepatitis) developed glucose intolerance several years after the hepatitis was diagnosed. The patient had a family history of both diabetes and chronic liver disease. A lesion resembling alcoholic hepatitis in a patient who denies alcohol consumption, may be diabetic or pre-diabetic in aetiology and such a patient should be followed up with glucose tolerance tests.
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7/7. Improvement of renal failure with repeated head-out water immersions in patients with hepatorenal syndrome associated with alcoholic hepatitis.

    Two patients with severe hepatorenal syndrome associated with alcoholic hepatitis are reported, in whom repeated daily courses of head-out water immersion were dramatically effective in producing an improvement of the renal function. Using repeated 2-hour courses of head-out water immersion for 7 days in the 1st patient, an immediate increase in urine output was observed. A slight increase in renal sodium excretion was also noted. The patient lost 7 kg over 1 week. serum creatinine decreased from 520 to 370 mumol/l, and the renal function continued to improve thereafter. In the 2nd patient, repeated head-out water immersion was associated with a progressive improvement of the renal function, an effect that was absent during an initial therapy of volume load. The acute effects of immersion in in this 2nd patient were characterized by a dramatic increase in urine output and renal sodium excretion as well as in p-aminohippurate and creatinine clearances. These effects were associated with a decrease in the activity of the renin-angiotensin system and a modest increase in plasma atrial natriuretic peptide levels. Thus, these 2 cases emphasize the potential benefits of repeated head-out water immersions in improving the renal function of patients with hepatorenal syndrome.
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