Gallstone disease is a common disorder of the gastrointestinal tract. The prevalence of gallstones in the United States is approximately 10 to 15%. Symptoms occur in approximately 20% of those with gallstones, and this group is at the highest risk for serious complications from simple recurrent biliary colic to severe, life-threatening ascending cholangitis and/or pancreatitis [20]. This is the first study to evaluate the role of the ACE gene polymor­phism in cholangitis and pancreatitis. The ACE gene insertion/deletion polymorphism has been studied in several inflammatory diseases, such as urinary tract infections, acute pyelonephritis, in children with sepsis and septic shock, sepsis-induced acute respi­ratory distress syndrome (ARDS) and osteoarthritis [22-27]. In Turkey, patients who were carriers of the

I allele ( I/D and II genotypes) had increased risk of developing sepsis compared to the control group [23]. A study from Korea found that the frequency of the I allele was significantly higher in early os­teoarthritis [26]. The other study with inflammation and infections did not find any correlation between inflammation, infections and ACE gene polymor­phisms [22,24,25, 27].

We found no statistical significant difference in frequency of this polymorphism between cholangitis and biliary pancreatitis patient groups. However, the ACE II genotype frequency was significantly higher in cholangitis and biliary acute pancreatitis than in healthy controls. In the European population, the ra­tio for the DD/ID/II was found to be 1:2:1, respec­tively, but in Turkey the ratio for DD/DI/II genotype is 2/3/1 [27,28]. Ethnic variation and gender have been reported to play a significant role in the fre­quency of the ACE I/D genotype [26].

Homozygous deletions (DD) show highest ACE activity, whereas, conversely, homozygous insertion (II) exhibits lowest ACE activity in the inflamma­tory process [17]. In carriers of the I allele (I/D and

II genotype), the bradykinin inactivity is decreased because of lower ACE activity [17]. Therefore, de­pressed angiotensin II cannot sufficiently inactivate bradykinin, which has a major implication in the in­flammatory process and this may be the reason for inflammation.

The ACE II genotype frequency may have a re­lationship with inflammation, however, it is remark­able that the ACE DD genotype frequency is higher in patients having a recurrence of cholangitis and/or pancreatitis.