Objective The aim of the study was to study the prevalence and characteristics of sinistral portal hypertension (SPH) in acute pancreatitis (AP) and its correlation with the severity of AP. Methods Retrospectively studied 633 patients with AP admitted to our institution and underwent magnetic resonance imaging (MRI). Diagnosis of SPH was based on clinical manifestations, laboratory tests, and MRI. The venous system and pancreatitis were evaluated on T1 weighted imaging, T2 weighted imaging, and dynamic-enhancement MRI. Data on patients' demographics, etiology, organ failure, MR severity index, and clinical outcomes were all collected. Results The SPH was detected in 21 patients (3.3%, 21/633). There was no statistical difference in organ failure between patients with SPH and without SPH (P > 0.05). The prevalence of SPH in males and females was 5.1% (17/336) versus 1.3% (4/297) (χ2 = 6.775, P = 0.009), in edematous and necrotizing AP was 0.4% (2/510) versus 15.5% (19/123) (χ2 = 65.413, P = 0.000), and in mild, moderate, and severe AP, based on MR severity index, were 0.6% (2/334) versus 2.9% (8/276) versus 47.8% (11/23) (χ2 = 55.977, P = 0.000), respectively. Conclusions The SPH rarely occurs in AP, and its risk is higher in males. Its presence is strongly associated with the local conditions of pancreatitis.

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

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