Acute pancreatitis (AP) is a complex disease that results in significant morbidity and mortality. For many decades, it has compelled\nresearchers to explore the exact pathogenesis and the understanding of the pathogenesis of AP has progressed dramatically.\nCurrently, premature trypsinogen activation and NF-�ºB activation for inflammation are two remarkable hypotheses for the\nmechanism of AP. Meanwhile, understanding of the influence of genetic polymorphisms has resulted in tremendous\ndevelopment in the understanding of the advancement of complex diseases. Now, genetic polymorphisms of AP have been\nnoted gradually and many researchers devote themselves to this emerging area. In this review, we comprehensively describe\ngenetic polymorphisms combined with the latest hypothesis of pathogenesis associated with AP.
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