Results 161 to 170 of about 137,068 (205)
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Alcoholic steatohepatitis

Best Practice & Research Clinical Gastroenterology, 2010
Severe alcoholic steatohepatitis has a poor prognosis and is characterized by jaundice and signs of liver failure. Its incidence is unknown, but prevalence is around 20% in cohorts of alcoholics undergoing liver biopsy. Diagnosis is established with elevated liver transaminases, neutrophil counts, serum bilirubin, and impaired coagulation and a history
Felix, Stickel, Helmut K, Seitz
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Nonalcoholic Steatohepatitis

Seminars in Liver Disease, 1999
Nonalcoholic steatohepatitis (NASH) is an hepatic disorder with histologic features of alcohol-induced liver disease that occurs in individuals who do not consume significant alcohol. NASH is believed to be one of the most common explanations for abnormal liver chemistries in American adults.
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Non-alcoholic steatohepatitis

Current Opinion in Endocrinology & Diabetes, 1998
NASH is an important form of chronic liver disease that is increasingly recognized. The diagnosis is secured by biopsy findings with similarities to alcoholic hepatitis in a patient with a confirmed history of abstinence. Obesity is a major risk factor, but the disease also occurs in the nonobese.
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Non-alcoholic steatohepatitis

Medicina Clínica (English Edition), 2022
Non-alcoholic steatohepatitis belongs to the spectrum of metabolic-associated fatty liver diseases characterized by steatosis linked to obesity, diabetes, metabolic syndrome, dyslipidemia and immune-mediated disorders. The main features of MAFLD include high prevalence, heterogeneity, complexity and dynamic disease.
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Nonalcoholic steatohepatitis

Gastroenterology, 2001
Nonalcoholic steatohepatitis (NASH) is a condition characterized by hepatomegaly, elevated serum aminotransferase levels, and a histologic picture similar to alcoholic hepatitis in the absence of alcohol abuse. Most patients with NASH are obese women, and many have diabetes mellitus, hypercholesterolemia, or hypertriglyceridemia.
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Mitochondria in Steatohepatitis

Seminars in Liver Disease, 2001
For the first time in history, populations in affluent countries may concomitantly indulge in rich food and physical idleness. Various combinations of obesity, diabetes, and hypertriglyceridemia, with insulin resistance as the common feature, cause hepatic steatosis, which can trigger necroinflammation and fibrosis.
D, Pessayre   +3 more
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Drug-induced steatohepatitis

Clinics in Liver Disease, 2003
Drugs rarely cause steatohepatitis, but amiodarone, perhexiline, and DH, have unequivocally been found to independently induce the histologic picture of alcoholic liver disease or NASH. All three agents have similar pathogenetic mechanisms of hepatotoxicity, targeting mitochondrial ATP production and fatty acid catabolism. Other drugs that occasionally
R Todd, Stravitz, Arun J, Sanyal
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REVIEW: Nonalcoholic steatohepatitis

Journal of Gastroenterology and Hepatology, 1997
Nonalcoholic steatohepatitis (NASH) is a reasonably well‐defined clinicopathological entity; it has been reported more commonly in women than in men or children of both sexes and it appears to be most closely associated with obesity, diabetes mellitus and related abnormalities, such as hyperlipidaemia and hyperglycaemia.
J, Ludwig, D B, McGill, K D, Lindor
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Liver Cirrhosis with Steatohepatitis: Nonalcoholic Steatohepatitis and Alcoholic Steatohepatitis

2019
Nonalcoholic steatohepatitis is a phenotype of metabolic diseases in the liver, associated with eating disorders and lack of exercise. In contrast, alcoholic steatohepatitis develops due to alcohol abuse. Although the causes are different, each type of steatohepatitis exhibits the same histological features, such as steatosis, lobular and portal ...
Teruki Miyake, Yoichi Hiasa
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Pathogenesis of steatohepatitis

Best Practice & Research Clinical Gastroenterology, 2002
Understanding the pathogenesis of non-alcoholic steatohepatitis has recently assumed great importance with the recognition that it has the potential to progress to fibrosis and cirrhosis. The 'two-hit' model of pathogenesis was proposed in 1998, with the first 'hit' - steatosis - increasing the sensitivity of the liver to the second 'hits' mediating ...
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