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Alcohol & Alcoholism Vol. 39, No. 1, pp. 20-24, 2004
© Medical Council on Alcohol 2004; all rights reserved

GENETIC POLYMORPHISMS IN ALCOHOL-METABOLIZING ENZYMES AND CHRONIC PANCREATITIS

Mariette Verlaan1,*, René H. M. Te Morsche1, Hennie M. J. Roelofs1, Robert J. F. Laheij1, Jan B. M. J. Jansen1, Wilbert H. M. Peters1 and Joost P. H. Drenth1,2

1 Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Centre St Radboud, Nijmegen, The Netherlands and 2 Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA

* Author to whom correspondence should be addressed at: Department of Medicine, Division of Gastroenterology and Hepatology, University Medical Centre St Radboud, PO Box 9101, 6500 HB Nijmegen, The Netherlands. Tel.: +31 24 3616520; Fax +31 24 3540103; E-mail: m.verlaan{at}mdl.umcn.nl

(Received 16 January 2003; first review notified 13 March 2003; in revised form 18 August 2003; accepted 25 August 2003)

Aims: Alcohol misuse is now regarded as an important risk factor for development of chronic pancreatitis (CP). However, not every alcohol misuser develops CP and it therefore might be suggested that susceptibility could be further influenced by inter-individual variations in the activities of alcohol-metabolizing enzymes. Several genetic polymorphisms that may affect the activities of alcohol-metabolizing enzymes have been described. Therefore we determined whether polymorphisms in the genes for alcohol dehydrogenase 3 (ADH3) or cytochrome P450 2E1 (CYP2E1) predispose to the development of CP. Methods: DNA samples were obtained from 142 adult CP patients with hereditary (n = 21), alcoholic (n = 82) or idiopathic (n = 39) CP. DNA from 128 healthy controls and from 93 alcoholic controls was analysed for comparison. Patients and controls were all of Caucasian origin. Genetic polymorphisms in ADH3 and CYP2E1 were determined by PCR, followed by restriction-fragment-length-polymorphism analyses in all subjects. Results: The frequencies of ADH3 and CYP2E1 c1c2 genotypes did not differ between CP patients and alcoholic and healthy controls. However, a trend for a higher frequency of the CYP2E1 intron 6 D allele was demonstrated in patients with alcohol-induced CP, compared to that of healthy controls (OR = 3.03, 95%CI = 1.0–9.1) or alcoholic controls (OR = 2.76, 95%CI = 0.9–8.7). Conclusions: These data suggest that the presence of the CYP2E1 intron 6 DD genotype might confer a higher risk of alcoholic CP.


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