Genetic background is different between sentinel and recurrent acute pancreatitis.
Genetic background is different between sentinel and recurrent acute pancreatitis.
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前哨急性胰腺炎和复发性急性胰腺炎的遗传背景不同。
DOI：
10.1111/j.1440-1746.2011.06691.x
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发表时间：
2011
期刊：
影响因子：
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通讯作者：
正宗 淳
中科院分区：
文献类型：
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作者：
Masamune A;Nakano E;Kume K;Kakuta Y;Ariga H;Shimosegawa T;正宗 淳
背景和目的：先前的研究表明胰蛋白酶相关基因的变体，如阳离子胰蛋白酶原（PRSS 1）和丝氨酸蛋白酶抑制剂Kazal 1型（SPINK 1）与胰腺炎相关。然而，这些基因变异是否与急性胰腺炎（AP）相关仍在很大程度上是未知的，特别是当首次发作与复发性attacks.Methods分离时：总共261例AP患者（174例为哨兵发作，87例为复发性发作）和健康对照者的PRSS 1基因中的p.R122H突变，SPINK 1基因中的p.N34S和IVS 3 + 2 T > C变异，阴离子胰蛋白酶原基因中的p.G191R变异，通过 聚合酶链反应-限制性内切酶消化和直接测序法检测中胰蛋白酶原（PRSS 3）基因中的p.E32del变异体和单核细胞趋化蛋白-1（MCP-1）基因中的− 2518 G> A变异体。与复发性胰腺炎患者相比，哨兵性胰腺炎患者中胆源性胰腺炎和重症病例的比例较低，而特发性胰腺炎的比例较高。检查的遗传变异的频率在对照组和哨兵胰腺炎患者之间没有差异。复发性AP患者中PRSS1p.R122H突变、SPINK1p.N34S变异和PRSS3p.E32del变异的频率高于对照组或哨兵AP患者。结论：PRSS1p.R122H突变、SPINK1p.N34S变异和PRSS3p.E32del变异与复发性AP相关，但与哨兵AP无关。哨兵AP和复发AP的遗传背景可能不同。
Background and Aim:Previous studies have shown an association of variants in trypsin‐associated genes, such as cationic trypsinogen (PRSS1) and serine protease inhibitor, Kazal type‐1 (SPINK1) with pancreatitis. However, whether these genetic variants are associated with acute pancreatitis (AP) remains largely unknown, especially when the first attack is separated from recurrent attacks.Methods:A total of 261 patients with AP (174 with a sentinel attack, and 87 with recurrent attacks) and healthy controls were genotyped for the p.R122H mutation in thePRSS1gene, p.N34S and IVS3 + 2T > C variants in theSPINK1gene, the p.G191R variant in the anionic trypsinogen gene, the p.E32del variant in the mesotrypsinogen (PRSS3) gene, and the −2518G > A variant in the monocyte chemoattractant protein‐1 gene by polymerase chain reaction–restriction enzyme digestion and direct sequencing.Results:Patients with recurrent attacks were younger. The proportions of biliary pancreatitis and severe cases were lower, and that of idiopathic pancreatitis was higher in patients with a sentinel attack than in those with recurrent attacks. The frequencies of the genetic variants examined did not differ between controls and patients with sentinel pancreatitis. The frequencies of thePRSS1p.R122H mutation,SPINK1p.N34S variant, andPRSS3p.E32del variant, but not other genetic variants, were higher in patients with recurrent attacks than in controls or those with a sentinel attack.Conclusions:ThePRSS1p.R122H mutation,SPINK1p.N34S, andPRSS3p.E32del variants were associated with recurrent, but not sentinel AP. The genetic background could possibly be different between sentinel and recurrent AP.