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Gastrointestinal Manifestations of Cystic Fibrosis

Cy ystic fibrosis (CF) is due to a defect in chloride transport that is a result of a defective cystic fibrosis transmembrane regulator (CFTR). The CFTR functions as a cyclic adenosine monophosphate (cyclic AMP) regulated chloride channel. The CFTR gene has been localized to chromosome 7 and over 750 mutations have been identified.' The most common mutation associated with symptoms of CF is A508 which accounts for approximately 70% of all cases of CF worldwide. Other mutations account for no more than 2-4% of the CF population. The dysfunction of CFTR results in a diminished secretion ofwater and electrolytes in ductular epithelium. The concentration of macromolecules in the lumen of the effected organ increases and proteins tend to precipitate into plugs which slow ductule flow leading to duct obstruction. Since the discovery of the CFTR gene in 1989, there has been a dramatic addition to our understanding of the pathogenesis of disease and the clinical spectrum of abnormalities associated with CFTR mutations.2 The degree of organ dysfunction depends on both the specific mutation in the gene and the localization of the