The frequency of PD was higher in patients with CFTR gene-associated pancreatitis as compared with those with idiopathic and alcoholic pancreatitis (P<0.0001) and with those with SPINK1 and PRSS1 gene-associated pancreatitis (P<0.02).
Scope remains for further studies examining proteins related to cellular anti-oxidant defenses, minor cystic fibrosis (CF) mutations and trans-heterozygosity involving a combination of mutations of different genes (such as CFTR alterations combined with SPINK1 or PRSS1 variants), as potential triggers of alcoholic pancreatitis.
Genetic studies have suggested that in hereditary pancreatitis mutation of the cationic trypsinogen gene and serine peptidase inhibitor, Kazal type 1 (SPINK1) genes mutations of the may have pathogenetic importance; however, studies on alcoholic pancreatitis have produced disappointing results so far.