Acute Alcoholic Hepatitis

Beckett, A. Gordon; Livingstone, Angus; Hill, K. R.

doi:10.1136/bmj.2.5260.1113

Cited by 123 publications

(37 citation statements)

References 20 publications

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“…We identified adult subjects who were more than 18 years of age with biopsy-proven FLD. FLD was initially defined by the minimal criteria of hepatic steatosis (>5%) with or without lobular inflammation, Mallory–Denk bodies, cytological ballooning and fibrosis 1 9 21 22…”

Section: Methodsmentioning

confidence: 99%

Portal inflammation is associated with advanced histological changes in alcoholic and non-alcoholic fatty liver disease

et al. 2010

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Section: Methodsmentioning

confidence: 99%

Portal inflammation is associated with advanced histological changes in alcoholic and non-alcoholic fatty liver disease

et al. 2010

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“…1, a and b). Mallory bodies are not essential for the diagnosis of alcoholic hepatitis in man (11,(17)(18)(19)(20).…”

mentioning

confidence: 99%

Experimental alcohol-induced hepatic necrosis: suppression by propylthiouracil.

Israel¹,

Kalant²,

Orrego³

et al. 1975

Proc. Natl. Acad. Sci. U.S.A.

205

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We have previously reported that a hypermetabolic state, resembling that produced by thyroid hormones, exists in the livers of animals treated chronically with ethanol. We propose that this alteration produces a relative hypoxia in the centrilobular zone of the liver which, if severe enough, leads to cellular death and to the production of hepatitis.Rats consuming ethanol for 30 days, given with a nutritionally adequate diet, and exposed to reduced oxygen tensions for only 6 hr, developed histological and biochemical evidence of hepatocellular necrosis and inflammatory lesions confined to the centrilobular zone. The severity was proportional to the degree of hypoxia. Pair-fed (nonalcohol) controls showed no such lesions. Treatment of the animals with propylthiouracil for 3-10 days abolished the hypermetabolic state of the liver in ethanolconsuming animals, and drastically reduced the histological and biochemical effects of hypoxia in them. These findings may have implications for pathogenesis and treatment of alcoholic hepatitis in man.Livers of rats chronically treated with ethanol utilize oxygen at higher rates than control livers (1-5). The hypermetabolic state results from increased utilization of ATP by the cell membrane (Na+K)-ATPase (ATP phosphohydrolase, EC 3.6.1.3), associated with an increase in the active transport of monovalent cations across the membrane (2, 6). We have also reported that the hypermetabolic state can be completely abolished by ouabain, an inhibitor of the (Na+K)-ATPase (2, 3).Similar changes in (Na+K)-ATPase activity, cation transport, and oxygen consumption occur in livers of animals treated with thyroid hormones, and can also be completely abolished by ouabain (3, 4, 7-10). We have also pointed out other similarities between the livers of animals chronically treated with ethanol and those treated with thyroid hormones (3, 4, 7). These similarities suggested that a functional hyperthyroid state exists in the livers of alcohol-treated animals (3, 7).In human alcoholic hepatitis (11,12), hepatocellular necrosis is most commonly seen in the central region of the hepatic lobule (zone 3 of Rappaport). Since the livers of ethanoltreated animals consume oxygen at higher rates (1-5), the possibility exists that the gradient of decreasing oxygen tension from the portal to the central venous end of the sinusoid is accentuated. We propose that, when the availability of oxygen is reduced, it is this accentuation of centrilobular hypoxia which leads to necrosis.Abbreviations: PTU, 6-propyl-2-thiouracil; SGOT, serum glutamic-oxalacetic transaminase [aspartate transferase]; SOCT, serum ornithine carbamyltransferase.To test this hypothesis we have exposed rats briefly to atmospheres with reduced oxygen tensions (5-11%). In animals treated chronically with ethanol, but not in controls, this period of hypoxia resulted in various degrees of centrilobular damage ranging from focal necrosis to massive confluent necrosis with accompanying inflammatory reaction. We have also found that a short pr...

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“…Alcoholic hepatitis is a clinical/histopathologic diagnosis first described by Beckett et al [1]. The severity can be measured using Maddrey's discriminant function, and values above 32 indicate severe disease [2].…”

Section: Introductionmentioning

confidence: 99%

Clinical and histological recovery from “life-threatening” severe acute alcoholic hepatic failure with complete hepatofugal portal blood flow

Fujiwara

Toriyabe

Fukuda

et al. 2010

Clin J Gastroenterol

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A 25-year-old man who was a heavy alcohol drinker was admitted to our hospital after presenting with general malaise, dyspnea, abdominal distension, systemic edema and jaundice. His liver function tests showed hyperbilirubinemia and prolonged prothrombin time, and a computed tomography scan and ultrasound showed liver atrophy and massive ascites. Furthermore, Doppler ultrasound revealed complete hepatofugal portal blood flow in the portal trunk and intrahepatic portal branches. Causes other than alcohol were excluded, and he was diagnosed as having severe acute alcoholic hepatic failure (Maddrey's discriminant function score 43.3, MELD score 21), although not clinically typical. He was treated with anti-coagulation therapy according to the precise evaluation of portal blood flow by Doppler ultrasound, and marked clinical, biochemical and hemodynamic improvements were observed. Liver biopsy performed 2 months after onset showed submassive necrosis with pericellular fibrosis. Liver biopsy performed three years after onset showed mild portal fibrosis with a marked improvement. Doppler ultrasound is an indispensable tool for evaluating patients with severe acute hepatitis.

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Acute Alcoholic Hepatitis

Cited by 123 publications

References 20 publications

Portal inflammation is associated with advanced histological changes in alcoholic and non-alcoholic fatty liver disease

Portal inflammation is associated with advanced histological changes in alcoholic and non-alcoholic fatty liver disease

Experimental alcohol-induced hepatic necrosis: suppression by propylthiouracil.

Clinical and histological recovery from “life-threatening” severe acute alcoholic hepatic failure with complete hepatofugal portal blood flow

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