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Title
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Noncirrhotic human nonalcoholic fatty liver disease induces portal hypertension in relation to the histological degree of steatosis
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Author
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Abstract
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| Introduction: We earlier showed in an animal model that steatosis, in the absence of fibrosis or inflammation, induces a significant rise in portal pressure. The relevance of these findings for human pathology is unknown till date. Aims: To study portal pressure in nonalcoholic fatty liver disease patients and to identify factors possibly related to steatosis-induced changes in liver haemodynamics. Materials and methods: Patients presenting with a problem of overweight and with noninvasive signs of liver involvement were proposed for transjugular liver biopsy. The biopsy was scored according to the Nonalcoholic Steatohepatitis Clinical Research Network scoring system. Results: Fifty consecutive patients were studied. Mean age was 47.9+/-13.6 years; 31 (62%) of them were female. Hepatic venous pressure gradient (HVPG) was normal in 27 patients (54%), borderline (5 mmHg) in nine (18%) and elevated in 14 patients (28%). For further analysis those with a HVPG of 5 mmHg were considered normal (group 1). HVPG was 8.8+/-2.6 mmHg in those with an elevated HVPG (group 2) versus 3.4+/-1.2 mmHg in group 1 (P<0.0001). In both the groups, only one patient had cirrhosis; 26 of 36 (group 1) and nine of 14 patients (group 2) had fibrosis score 0. Fibrosis score was not significantly different (P=0.530). Perisinusoidal fibrosis score was not significantly different (P=0.186). Steatosis was the only histological feature that significantly differed between the groups (P=0.016). The degree of steatosis (P=0.010) was the only independent predictor of the presence of portal hypertension. Conclusion: Human nonalcoholic fatty liver disease can, even in the absence of significant fibrosis, induce portal hypertension, correlated with the severity of the steatosis. |
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Language
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English
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Source (journal)
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European journal of gastroenterology & hepatology. - Melville, N.Y.
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Publication
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Melville, N.Y.
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2010
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ISSN
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0954-691X
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DOI
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10.1097/MEG.0B013E32833F14A1
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Volume/pages
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22
:12
(2010)
, p. 1449-1457
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ISI
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000283802700010
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Full text (Publisher's DOI)
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Full text (publisher's version - intranet only)
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