title: The clinical course of alcoholic cirrhosis: effects of hepatic metabolic capacity, alcohol consumption, and hyponatremia--a historical cohort study.
abstract: BACKGROUND
  The cirrhosis complications hepatic encephalopathy, ascites, and variceal bleeding increase mortality but develop in random sequence. Therefore prognoses based on the presence or absence of these clinical complications are inherently inaccurate, and other determinants of the clinical course should be identified. Here we present our study of patho-etiological factors that may be causally involved in the development of specific complications to alcoholic cirrhosis; it was based on a model of cirrhosis pathophysiology encompassing hepatic metabolic capacity, continued alcohol consumption, and circulatory dysfunction.
  
  
  METHODS
  We followed a Danish community-based cohort of 466 patients with alcoholic cirrhosis. Stratified Cox regression was used to examine the effects of GEC (a measure of hepatic metabolic capacity), alcohol consumption, and plasma sodium concentration (a measure of circulatory dysfunction) on the hazard rates of first-time hepatic encephalopathy, first-time ascites, first-time variceal bleeding, and mortality. We adjusted for confounding by comorbidity, gender, and age. Data on risk factors and confounders were updated during follow-up.
  
  
  RESULTS
  A low GEC increased the risk of first-time hepatic encephalopathy (hazard ratio [HR] 1.21 per 0.1 mmol/min GEC loss, 95% CI 1.11-1.31), but was unassociated with other adverse events. Alcohol consumption increased the risk of first-time ascites (HR 3.18, 95% CI 1.19-8.47), first-time variceal bleeding (HR 2.78, 95% CI 1.59-4.87), and mortality (HR 2.45, 95% CI 1.63-3.66), but not the risk of first-time hepatic encephalopathy. Hyponatremia increased the risk of all adverse events.
  
  
  CONCLUSIONS
  Reduced hepatic metabolic capacity, alcohol consumption, and hyponatremia were causally involved in the development of specific complications to alcoholic cirrhosis.
authors.affiliation: Department of Medicine V (Hepatology and Gastroenterology), Aarhus University Hospital, Aarhus, Denmark. pj@dce.au.dk
authors.forename: Peter
authors.initials: P
authors.lastname: Jepsen
authors.forename: Peter
authors.initials: P
authors.lastname: Ott
authors.forename: Per Kragh
authors.initials: PK
authors.lastname: Andersen
authors.forename: Hendrik
authors.initials: H
authors.lastname: Vilstrup
mesh_terms: D000428:Alcohol Drinking / Q000009:adverse effects*; D001201:Ascites / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D015331:Cohort Studies; D018450:Disease Progression; D004932:Esophageal and Gastric Varices / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005690:Galactose / Q000378:metabolism; D006470:Hemorrhage / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D006501:Hepatic Encephalopathy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007010:Hyponatremia / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008104:Liver Cirrhosis, Alcoholic / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors; D012964:Sodium / Q000097:blood
chemical_list: D012964:Sodium; D005690:Galactose