ANGIOTENSIN-CONVERTING ENZYME GENOTYPE AND ACUTE PANCREATITIS IN TURKEY
Kasap E1*, Akyıldız M2, Tekin F2, 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: 39

INTRODUCTION

Acute pancreatitis (AP) is an acute inflamma­tory process of variable of etiology [1]. While etiol­ogy and pathogenesis of AP have been intensively investigated, it is still unclear why some patients progress to organ failure and others do not [2,3]. Blockage of the duodenal papilla or ampulla of Vater is the common characteristic of the disease. In developed countries, obstruction of the common bile duct by stones (38%) and alcohol abuse (36%) are the most frequent causes [4,5], but iatrogenic factors, sphincter of Oddi dysfunction and eating disorders are also important [6]. Acute pancreatitis is viewed as an event and chronic pancreatitis as a process that is sequentially linked to AP and reflects a complex interaction between genetic and environ­mental factors [7]. The major common genetic risk factors have yet to be defined [8].

The renin-angiotensin system (RAS) has been investigated in the pathogenesis of several diseases. Local RAS components exist in brain, heart, kid­ney, pancreas, adrenal glands and gonads [9-11], and contribute in the regulation of cell growth, dif­ferentiation, proliferation and apoptosis, reactive oxygen species generation, tissue inflammation and fibrosis, and hormonal secretion [12]. Renin-angio-tensin system has been implicated in pathogenesis


of AP and chronic pancreatitis [8]. Although the etiology of AP is believed to be multifactorial, the activation of proteolytic enzymes, lipase, kinins and other active peptides may be responsible for altera­tions of RAS expression [13,14]. In fact, the activ­ity of the plasma RAS is significantly increased in AP [15,16]. Renin-angiotensin system is important in regulation of electrolyte balance, fluid and blood pressure. Angiotensin-converting enzyme is the key enzyme which activates the RAS [8,9] by convert­ing angiotensin I to angiotensin II, which is a potent vasoconstrictor. The ACE inactivates bradykinin, a vasodilator of the kallikrein-kinin system, which has major influence in inflammatory processes. Since angiotensinogen and angiotensin receptors may play a role in induction of inflammation and mi-crocirculatory regulation in the pancreas, they may contribute to its injury in AP [16,17]. Association of severe AP and impairment of pancreatic micro-circulation has been demonstrated in experimental models of AP [18]. Indeed, vasoconstriction, capil­lary stasis, decreased oxygen tension, and progres­sive ischemia occur early in the course of AP [19].

The ACE gene is located on human chromo­some 17q23. Three genotypes are associated with an Alu repetitive sequence about 287 bp long on in-tron 16. These genotypes are insertion (I) and dele­tion (D) alleles, respectively [16,17].

The DD genotype has been linked to several in­flammatory diseases [8,9] and results in higher lev­els of circulating ACE than the II and DI genotypes. It is also significantly more frequent in patients with myocardial infarction or diabetic proteinuria than in controls [10]. However, several studies have re­ported that the ACE I/D polymorphism was not a risk factor in AP and chronic pancreatitis [8,9]. In this study, we investigated the I/D polymorphism in AP.




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