2019-06-12
AUTHORSAtsushi Masamune , Tooru Shimosegawa
ABSTRACTThe association between alcohol misuse and chronic pancreatitis (CP) has been recognized for a long time. CP is a multifactorial and a complex disease, and the combination of genetic, environmental, and metabolic factors contributes to its development. Extensive research has been done to clarify the genetic factors. Candidate-gene approaches have focused on variants in the alcohol metabolizing enzymes (alcohol dehydrogenase 1B (ADH1B) and aldehyde dehydrogenase 2 (ALDH2)) and known pancreatitis susceptibility genes such as cationic trypsinogen (PRSS1), serine protease inhibitor Kazal type 1 (SPINK1), and chymotrypsin C (CTRC). It has been increasingly acknowledged that these previously known pancreatitis susceptibility genes identified in non-alcoholic (hereditary and idiopathic) CP also play a role in alcoholic CP. In addition, recent genome-wide association studies have identified new risk loci: the polymorphisms in the PRSS1-PRSS2 and the CLDN2-RIPPLY1-MORC4 loci and the inversion in the CTRB1-CTRB2 locus. The genetic alterations might at least in part explain a long-standing unsolved question: why only a small portion of heavy drinkers develop pancreatitis. More... »
PAGES139-149
Alcoholic/Non-Alcoholic Digestive Diseases
ISBN
978-981-13-1464-3
978-981-13-1465-0
http://scigraph.springernature.com/pub.10.1007/978-981-13-1465-0_12
DOIhttp://dx.doi.org/10.1007/978-981-13-1465-0_12
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