Bosques-Padilla Francisco J, Vázquez-Elizondo Genaro, González-Santiago Omar, Del Follo-Martínez Lourdes, González Oscar P, González-González Jose A, Maldonado-Garza Héctor J, Garza-González Elvira
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;349(3):206-11. doi: 10.1097/MAJ.0000000000000392.
The mechanisms responsible for the development of acute pancreatitis (AP) and its complications are not fully understood.
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.
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.
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.
Patients with hypertriglyceridemia-induced AP were more likely to develop persistent SIRS.
急性胰腺炎(AP)及其并发症发生的机制尚未完全明确。
评估临床和宿主分子因素在AP患者持续性全身炎症反应综合征(SIRS)发生及预后中的作用。
本研究纳入191例AP患者。研究变量包括人口统计学特征、预后与转归、病因、实验室检查结果及并发症。采用焦磷酸测序法测定白细胞介素(IL)10(-1082 G/A、-592 C/A)、肿瘤坏死因子α(TNFA)-308(G/A)和白细胞介素β(ILB)-31(C/T)基因多态性。采用扩增阻滞突变系统-聚合酶链反应法对IL8-251(A/T)基因多态性进行基因分型。
人口统计学特征并非AP患者发生持续性SIRS的统计学显著危险因素。高甘油三酯血症患者更易发生持续性SIRS(P < 0.05)。未从等位基因、基因型或单倍型频率中检测到与TNFA、ILB、IL8-251(A/T)和IL10单核苷酸多态性的关联。
高甘油三酯血症诱导的AP患者更易发生持续性SIRS。