Brief Article
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jun 28, 2012; 18(24): 3105-3111
Published online Jun 28, 2012. doi: 10.3748/wjg.v18.i24.3105
Alcohol consumption in patients with primary sclerosing cholangitis
Hannes Hagström, Per Stål, Knut Stokkeland, Annika Bergquist
Hannes Hagström, Per Stål, Annika Bergquist, Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, 14186 Stockholm, Sweden
Knut Stokkeland, Department of Medicine, Visby Hospital, Karolinska Institutet, 14186 Stockholm, Sweden
Author contributions: Hagström H, Stål P, Stokkeland K and Bergquist A designed the study; Stokkeland K contributed to the lifetime drinking history survey; Hagström H, Stål P and Bergquist A analysed the data; and Hagström H and Bergquist A wrote the paper.
Supported by Wallenberg Foundation Bengt Ihres Fund
Correspondence to: Hannes Hagström, MD, Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, Huddinge K63, 14186 Stockholm, Sweden. hannes.hagstrom@ki.se
Telephone: +46-8-58582328 Fax: +46-8-58582335
Received: November 16, 2011
Revised: February 20, 2012
Accepted: February 26, 2012
Published online: June 28, 2012
Abstract

AIM: To assess the alcohol drinking patterns in a cohort of primary sclerosing cholangitis (PSC) patients and the possible influence on the development of fibrosis.

METHODS: Ninety-six patients with PSC were evaluated with a validated questionnaire about a patient’s lifetime drinking habits: the lifetime drinking history (LDH) questionnaire. In addition, clinical status, transient elastography and biochemistry values were analysed and registered. Patients were defined as having either significant or non-significant fibrosis. Significant fibrosis was defined as either an elastography value of ≥ 17.3 kPa or the presence of clinical signs of cirrhosis. Patients were divided into two groups depending on their alcohol consumption patterns; no/low alcohol consumption (one drink or unit/d) and moderate/high alcohol consumption (≥ 1 drink or unit/d). LDH data were calculated to estimate lifetime alcohol intake (LAI), current alcohol intake, drinks per year before and after diagnosis of PSC. We also calculated the number of episodes of binge-drinking (defined as consuming ≥ 5 drinks per occasion) in total, before and after the diagnosis of PSC.

RESULTS: The mean LAI was 3882 units of alcohol, giving a mean intake after onset of alcohol consumption of 2.6 units per week. Only 9% of patients consumed alcohol equal to or more than one unit per day. Current alcohol intake in patients with significant fibrosis (n = 26) was less than in patients without significant fibrosis (n = 70), as shown by lower values of phosphatidylethanol (B-PEth) (0.1 μmol/L vs 0.33 μmol/L, respectively, P = 0.002) and carbohydrate-deficient transferrin (CDT) (0.88% vs 1.06%, respectively, P = 0.02). Self-reported LAI was similar between the two groups. Patients with significant fibrosis reduced their alcohol intake after diagnosis from 103 to 88 units per year whereas patients without fibrosis increased their alcohol intake after PSC diagnosis from 111 to 151 units/year. There were no correlations between elastography values and intake of alcohol (units/year) (r = -0.036).

CONCLUSION: PSC patients have low alcohol consumption. The lack of correlation between fibrosis and alcohol intake indicates that a low alcohol intake is safe in these patients.

Keywords: Alcohol, Fibrosis, Cirrhosis, Lifetime drinking history, Primary sclerosing cholangitis