The clinical course of alcoholic cirrhosis: effects of hepatic metabolic capacity, alcohol consumption, and hyponatremia – a historical cohort study

Abstract

BackgroundThe 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.MethodsWe 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.ResultsA 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.ConclusionsReduced hepatic metabolic capacity, alcohol consumption, and hyponatremia were causally involved in the development of specific complications to alcoholic cirrhosis.

Propranolol treatment of portal hypertension in cirrhosis patients is better the higher the untreated pressure: a single-centre prospective experience

“…Our finding that alcohol consumption was not associated with the response to propranolol is in contrast to a recent epidemiological study showing that continued alcohol consumption is predictive for variceal bleeding [19]. The discrepancy may be related to the finding that patients with excessive alcohol consumption cease to have effect of propranolol at a third HVPG measurement [6,20].…”

Epidemiology, disease burden and outcomes of cirrhosis in a large secondary care hospital in South Auckland, New Zealand

“…Log-rank test was used to compare time-dependent variables. The crude age-and ethnic-adjusted incidence rates for age stratified groups (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44), 45-59, 60-79, >80 years) and ethnic groups were calculated by dividing age-specific and ethnicity-specific liver events by age-and ethnic-specific (weighted) CMDHB population sizes data from the NZ Health Statistics (Ministry of Health). Projected cirrhosis Accepted Article incidence per year was calculated by dividing the year-specific number of total cirrhosis patients under active follow-up by the year-specific CMDHB population data from NZ Health Information Services and using results form year 2000-2011 to extrapolate the cumulative cirrhosis patients under active follow-up until 2023.…”

“…10 Currently, chronic hepatitis C (CHC) infection is estimated to affect about 1% of New Zealanders and CMDHB rates are believed to be similar to the population as a whole with much remaining undiagnosed. 11 While cirrhosis and its complications may be preventable, [12][13][14][15] the incidence and the impact of cirrhosis are not known in NZ or the South Pacific region. Therefore, our aim was to describe the epidemiology and disease burden of the four most common known causes of cirrhosis in the CMDHB area (alcoholic liver disease (ALD), NAFLD, CHC and CHB infection) over a 12-year period.…”

A Model for Predicting Development of Overt Hepatic Encephalopathy in Patients With Cirrhosis

“…32 We recognize that our model had some limitations. Comorbidities or a quantitative evaluation of liver metabolic activity 33 were not considered. The role of precipitants of HE also was not considered by the model, although it is possible to hypothesize different effects of a precipitant in patients with different predispositions to HE.…”