CHOLANGITIS OF PANCREATITIS? DOES THE ANGIOTENSIN-CONVERTING ENZYME GENOTYPE FAVOR EITHER?
Kasap E1*, Akyıldız M2, Akarca U2
*Corresponding Author: Elmas Kasap, Department of Gastroenterology, Faculty of Medicine, Celal Bayar University, Manisa, Turkey; Tel.: +90-236-2330115-+90-542-2457238; Fax: +90- 236-2370213 ; e-mail: elmaskasap@ yahoo.com
page: 53

INTRODUCTION

Gallstones are frequent in the Western world, with up to 10% of the general population affected. Gallstone prevalence is higher in the elderly and in women [1]. Most series indicate that the prevalence rate of gallstones in women between the ages of 20 and 55 years varies from 5 to 20%, and in those older than 50 years, from 25 to 30%. The prevalence rate in men is approximately one-half that in women for a given age group and the prevalence in children is 0.13% [2]. Acute cholangitis and pancreatitis are the most serious complications of gallstones, with con­siderable morbidity and mortality [1,3].

Acute cholangitis is an infectious disease of the biliary tract ranging in severity from a mild form with fever and jaundice to a severe form with sep­tic shock. Patients are febrile, often have abdominal pain, and are jaundiced [4]. There is usually leukocy-tosis, and serum alkaline phosphatase and bilirubin levels are generally elevated [4,5]. Approximately 85% of cases are caused by an impacted stone in the common bile duct, with resulting bile stasis [6].

Acute pancreatitis is an acute inflammatory pro­cess with varied etiologies [7], but its pathogenesis is not fully understood [8]. Blockages of the duodenal papilla or ampulla of Vater are the common charac­teristics of the disease being most commonly due to gallstones, causing approximately 40% of cases [9]. Gallstone pancreatitis may be associated with cho-langitis but is also common as a separate entity [10]. A popular mechanism of gallstone pancreatitis is that an impacted gallstone in the distal common bile duct obstructs the pancreatic duct, increasing pancreatic pressure and damaging ductal and acinar cells [11].

Several studies have shown the existence of lo­cal renin-angiotensin system (RAS) components in brain, heart, kidney, pancreas, adrenal glands and gonads [12,13]. Local RAS functions include the regulation of cell growth, differentiation, prolifera­tion and apoptosis, reactive oxygen species (ROS) generation, tissue inflammation and fibrosis, and hor­monal secretion [14].

The systemic hormonal RAS regulates electro­lyte balance, fluid and blood pressure. The angio-tensin-converting enzyme (ACE) is responsible for the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor [15,16] and also inactivates bradykinin, a vasodilator produced by the kallikrein-kinin system, which has major impli­cation in acute pancreatitis and other inflammations [17,18]. The ACE gene insertion/deletion (I/D) poly­morphism is localized in intron 16 of the human ACE gene and corresponds to a repetitive sequence about 287 bp long [18,19].

In our clinical experience, some individuals with common bile duct stones are hospitalized more than once for treatment of biliary pancreatitis or for cho-langitis. Why do some of the people with common biliary duct stone suffer cholangitis, while others develop pancreatitis? The answer to this question is not yet quite clear. Angiotensin is a proinflammatory molecule and may have a role in cholangitis (an in­fectious disease) and pancreatitis (a sterile inflamma­tion). To determine if the ACE genotype determines the occurrence of cholangitis or biliary pancreatitis, we studied patients with these diseases and healthy controls.




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