• Francisco J Bosques-Padilla, Genaro Vázquez-Elizondo, Omar González-Santiago, Lourdes Del Follo-Martínez, Oscar P González, Jose A González-González, Héctor J Maldonado-Garza, and Elvira Garza-González.
• Gastroenterology Unit (FJBP, GVE, LDFM, OPG, JAGG, HJMG, EGG), University Hospital José Eleuterio González MD, Universidad Autónoma de Nuevo León, Monterrey, Mexico; Chemistry School (OGS), Universidad Autónoma de Nuevo León, San Nicolás de Los Garza, Mexico; and Clinical Pathology Department (EGG), University Hospital José Eleuterio González MD, Universidad Autónoma de Nuevo León, Monterrey, Mexico.
• Am. J. Med. Sci. 2015 Mar 1; 349 (3): 206-11.

BackgroundThe mechanisms responsible for the development of acute pancreatitis (AP) and its complications are not fully understood.AimTo assess the role of clinical and host molecular factors for the development and outcome of persistent systemic inflammatory response syndrome (SIRS) in patients with AP.MethodsWe included 191 patients with AP in the study. The considered variables were demographic characteristics, prognosis and outcome, etiology, laboratory findings and complications. Interleukin (IL) 10 (-1082 G/A, -592 C/A), TNFA-308 (G/A) and ILB-31 (C/T) polymorphisms were determined by pyrosequencing. An amplification refractory mutation system-polymerase chain reaction method was used to genotype the IL8-251 (A/T) polymorphism.ResultsDemographic characteristics were not statistically significant risk factors for the acquisition of persistent SIRS in patients with AP. Patients with hypertriglyceridemia were more likely to develop persistent SIRS (P < 0.05). No association with the TNFA, ILB, IL8-251 (A/T) and IL10 single-nucleotide polymorphisms was detected from the allele, genotype or haplotype frequencies.ConclusionsPatients with hypertriglyceridemia-induced AP were more likely to develop persistent SIRS.

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