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Hypertriglyceridemia-induced pancreatitis and risk of persistent systemic inflammatory response syndrome
Francisco J Bosques-Padilla1, Genaro Vázquez-Elizondo, Omar González-Santiago
1Gastroenterology 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.
Background:
The mechanisms responsible for the development of acute pancreatitis (AP) and its complications are not fully understood.
Aim:
To 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.
Methods:
We 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.
Results:
Demographic 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.
Conclusions:
Patients with hypertriglyceridemia-induced AP were more likely to develop persistent SIRS.
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