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Genetic basis of chronic pancreatitis in Asia Pacific region
Author(s) -
Reddy D Nageshwar,
Prasad S Siva
Publication year - 2011
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2010.06598.x
Subject(s) - trypsinogen , pancreatitis , medicine , gastroenterology , genetic predisposition , pancreas , pancreatic disease , etiology , endocrinology , disease , trypsin , biology , biochemistry , enzyme
Chronic pancreatitis (CP) is a disease characterized by irreversible destruction and fibrosis of the parenchyma, leading to pancreatic exocrine insufficiency. In developed countries, the etiology for 60% to 70% of CP amongst male patients is alcohol and 25% are classified as idiopathic chronic pancreatitis (ICP). The genetic predisposition to CP could be an inappropriate activation of trypsinogen in the pancreas. Two common haplotypes, c.101A > G (p.N34S) and c.−215G > A, and four intronic alterations of the serine protease inhibitor Kazal type 1 ( SPINK1 ) gene have been found to increase the risk for CP in the Asia Pacific region. Hence, SPINK1 is thought to be a candidate gene for pancreatitis. A loss‐of‐function alteration in chymotrypsinogen C ( CTRC ) gene has been shown to be associated with tropical calcific pancreatitis (TCP). Cathepsin B ( CTSB ) is also found to be associated with TCP. However mutations in cationic and anionic trypsinogen gene do not play an important role in causing CP in Asia Pacific region.