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World J Gastroenterol. Sep 7, 2014; 20(33): 11788-11792
Published online Sep 7, 2014. doi: 10.3748/wjg.v20.i33.11788
Published online Sep 7, 2014. doi: 10.3748/wjg.v20.i33.11788
PRSS1 and SPINK1 mutations in idiopathic chronic and recurrent acute pancreatitis
Mario Pelaez-Luna, Guillermo Robles-Diaz, Research Division, School of Medicine, UNAM, Pancreas Clinic-Gastroenterology Department, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, CP 14000, Mexico
Samuel Canizales-Quinteros, Maria T Tusié-Luna, Unit of Molecular Biology and Genomic Medicine, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, CP 14000, Mexico
Author contributions: All authors participated equally in the study design and analysis, and manuscript writing, review and approval; Pelaez-Luna M collected data and performed all experiments.
Correspondence to: Mario Pelaez-Luna, MD, Associate Professor of Medicine, Research Division, School of Medicine, UNAM, Pancreas Clinic-Gastroenterology Department, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga 15, Colonia Sección XVI, Tlalpan, Mexico City, CP 14000, Mexico. mariopl@prodigy.net.mx
Telephone: +52-5-55733418 Fax: +52-5-56550942
Received: November 5, 2013
Revised: April 10, 2014
Accepted: June 12, 2014
Published online: September 7, 2014
Processing time: 306 Days and 12.8 Hours
Revised: April 10, 2014
Accepted: June 12, 2014
Published online: September 7, 2014
Processing time: 306 Days and 12.8 Hours
Core Tip
Core tip: Chronic and recurrent idiopathic pancreatitis has been associated with mutations in genes responsible for the synthesis of pancreatic proteases (PRSS1) and protease inhibitors (SPINK1). The distribution of these mutations varies among countries, but has not been examined in detail in Latin American countries. This study examined PRSS1 and SPINK1 in 19 Mexican subjects with chronic pancreatitis and/or idiopathic recurrent acute pancreatitis and identified two novel PRSS1 mutations and one novel SPINK1 mutation.