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Query: UMLS:C0028754 (obesity)
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Thirty patients with alcoholic cirrhosis, ascitic during 13.6 +/- 13 months (mean +/- S.D.) were cured of ascites and followed up during 2 to 9 years (4.3 +/- 2.7 years). Twenty six were compared with a same number of cirrhotics, matched for age and sex, who died during the year after the first admission. Many biological data show statistical difference. Nevertheless no valuable prognosis can be predicted in an individual case. The clinical improvement is associated with major, sometimes total biological recovery. Other complications of cirrhosis (gastro-intestinal bleeding, hepatoma) may occur (7 cases with 5 deaths) or alcoholic hepatitis if alcohol withdrawal is stopped (3 cases, 2 deaths). Some associated diseases look unexpectedly frequent: diabetes (4 cases), obesity (9), nodular lipomatosis (14 cases) whose frequency looks higher than that can be calculated for a similar group of healthy subjects.
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PMID:[Recovery after treatment for cirrhotic ascites : a study of 90 cases. Frequency of arterial hypertension (author's transl)]. 49 44

Obesity is associated either with hepatic steatosis, a well known and innocuous entity or with non alcoholic steatohepatitis. This latter lesion has been recently individualized. It affects mainly middle-aged, obese women, with diabetes and/or hyperlipidaemia. It is morphologically very similar to alcoholic hepatitis. We review the literature considering 1) histologic hepatic lesions of the obese, 2) epidemiologic, clinical and biological characteristics of the non alcoholic steatohepatitis, 3) evolution and treatment of the non alcoholic steatohepatitis and 4) present physiopathological considerations. We conclude by considering the clinician's attitude in front of an obese potentially afflicted by a non alcoholic steatohepatitis.
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PMID:[Obesity: danger for the hepatocytes?]. 133 21

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.
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PMID:Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. 205 45

About 90 per cent of morbidly obese patients show histological abnormalities of the liver. One third of patients have fatty change involving more than 50 per cent of hepatocytes. Fatty liver disease can be divided into four histological groups: Fatty liver, fatty hepatitis, fatty liver with portal fibrosis, and cirrhosis. Most patients show only fatty change. Alcohol, drugs, diabetes, poor nutrition, and weight-reducing surgery contribute to progressive liver damage, but morbid obesity alone may lead to severe disease showing all the features of alcoholic hepatitis and may end in cirrhosis and liver failure. The accumulation of fat alone is unlikely to be the stimulus to inflammation and fibrosis. Only one fifth of patients have complaints that arise from the liver. The development of severe fatty liver disease may also be asymptomatic and rarely shows the florid picture associated with alcoholic hepatitis. There is poor correlation of liver function test results with morphology in obesity. ALT levels exceeding twice the normal limit have some predictive value for histological grades of severity, but they are present in few patients. Pericentral and pericellular fibrosis in prebypass liver biopsies may be an important prognostic lesion for the development of fatty hepatitis and cirrhosis. In contrast with the frequent progression to massive fatty change, inflammation and fibrosis after bypass surgery, weight loss by low-calorie dieting, or starvation is accompanied by improvement in fatty change and return of liver function tests to normal.
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PMID:Fatty liver disease in morbid obesity. 331 4

Two groups, 16 nonalcoholic steatohepatitis patients (group I) and 22 alcoholic hepatitis patients (group II) classified according to the presence or absence of drinking and their histological characteristics, were compared on the basis of clinical, biochemical, and liver biopsy findings. The frequencies of female patients (p less than 0.01), obesity (p less than 0.001), and maturity-onset diabetes (p less than 0.005) were significantly greater in group I than in group II. The serum glutamic pyruvic transminase (p less than 0.05) and gamma-glutamyltranspeptidase (p less than 0.05) contents were significantly greater in group II than in group I. The cholinesterase content (p less than 0.05) was significantly less in group II. Significant differences were found in the grades of nuclear vacuolation (p less than 0.001, Fisher's exact probability test), periportal pericellular fibrosis, proliferation of bile ductules, and changes in the shape of the portal tracts (p less than 0.001, Wilcoxon's rank-sum test). Zonal necrosis in group I was seen in only severe steatohepatitis. These clinical and biochemical findings were found to be useful in differentiating nonalcoholic steatohepatitis from alcoholic hepatitis. Liver biopsy was of limited value at best in separating the two conditions.
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PMID:Comparison between nonalcoholic steatohepatitis and alcoholic hepatitis. 360 26

Nonalcoholic steatohepatitis is a rare complication of obesity with laboratory and histological features indistinguishable from alcoholic hepatitis. Three patients with 50-60% overweight and steatohepatitis are reported. All responded with normalization of the biochemical and/or histological changes after modest weight reduction.
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PMID:Nonalcoholic steatohepatitis in obesity: a reversible condition. 376 11

Clinical features and liver biopsy findings were studied in six patients with nonalcoholic steatohepatitis associated with hyalin. A comparative study was made on the ultrastructure of the hyalin in one patient with nonalcoholic steatohepatitis and in one patient with alcoholic hepatitis. The patients, all over 50 years old, comprised two females and one male with steatohepatitis and three females with micronodular cirrhosis. They showed obesity, hepatomegaly, and mild abnormalities on laboratory tests. Three of them showed maturity-onset diabetes. The hyalin was found in the cytoplasm of swollen hepatocytes of the centrilobular or in the peripheral region of nodules and was accompanied by necrosis. Ultrastructurally, the hyalin comprised filamentous structures and vesicular or angular structures resembling disorganized circular or branched rough endoplasmic reticulum. It resembled that found in the liver of patients with alcoholic hepatitis.
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PMID:Nonalcoholic steatohepatitis and cirrhosis with Mallory's hyalin with ultrastructural study of one case. 617 90

Hepatic damage resembling alcoholic hepatitis has been described after jejunoileal bypass surgery for morbid obesity, but has not been previously reported as a complication of gastric partitioning operations (gastric bypass and gastroplasty). A patient who developed an alcoholic hepatitislike clinical picture 8 mo after gastroplasty is described, suggesting that malnutrition superimposed on obesity may be responsible for the injury in both settings. Reversal of the gastroplasty was associated with clinical and biochemical improvement.
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PMID:Liver injury with alcoholiclike hyalin after gastroplasty for morbid obesity. 619 39

Problem areas in the necropsy diagnosis of alcoholic liver disease are reviewed, potential sources of confusion delineated, and diagnostic guidelines proposed. The entire spectrum of alcoholic liver disease, including alcoholic hepatitis, may be perfectly mimicked by severe obesity, diabetes, and perhexiline maleate toxicity. Focal fatty change in the liver introduces sampling errors in the assessment of steatosis. Nodular regenerative hyperplasia of the liver mimics a micronodular cirrhosis both clinically and macroscopically. Measurement of the liver iron concentration reliably differentiates between alcoholic liver disease with siderosis and idiopathic hemochromatosis. The evaluation of preexisting fibrosis or cirrhosis in cases of massive hepatic necrosis is aided by stains for elastic fibers. Alcohol abusers taking acetaminophen (paracetamol) in excessive, but not suicidal doses are at risk of developing fatal "late" acetaminophen hepatotoxicity. Fatal viral hepatitis may be overlooked in an alcoholic with preexisting liver disease.
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PMID:Problems in the necropsy diagnosis of alcoholic liver disease. 673 1

Nonalcoholic steatohepatitis is a poorly understood and hitherto unnamed liver disease that histologically mimics alcoholic hepatitis and that also may progress to cirrhosis. Described here are findings in 20 patients with nonalcoholic steatohepatitis of unknown cause. The biopsy specimens were characterized by the presence of striking fatty changes with evidence of lobular hepatitis, focal necroses with mixed inflammatory infiltrates, and, in most instances, Mallory bodies; Evidence of fibrosis was found in most specimens, and cirrhosis was diagnosed in biopsy tissue from three patients. The disease was more common in women. Most patients were moderately obese, and many had obesity-associated diseases, such as diabetes mellitus and cholelithiasis. Presence of hepatomegaly and mild abnormalities of liver function were common clinical findings. Currently, we know of no effective therapy.
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PMID:Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease. 2901 67


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