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).
Key findings include the relationship between pancreas divisum and CFTR mutations, the role of trypsin in acute and recurrent acute pancreatitis, and the discovery of a pancreatitis modifier gene on the X chromosome that provides new clues to why the vast majority of patients with alcoholic pancreatitis are men.
This association, however, does not definitely confer a pathophysiological role for PD in pancreatitis but may denote that PD co-mingles with CFTR mutations without influencing pancreatitis or CFTR mutations influence pancreatic duct embryogenesis.
Further studies on CFTR mutations and abnormal nasal airway ion transport in patients with PD, either with or without recurrent AP, should be conducted.