Cystic fibrosis is the most common, lethal, genetic defect of white populations (1). Once limited largely to infants and children, the immediate prognosis has changed drastically over the last three decades so that now the majority of patients survive into adolescence, and nearly 80% live beyond their twentieth birthdays (2-4). The diagnosis is established in 2% of cases after 18 yr of age. Internal medicine and pediatrics, therefore, now share the complications and consequences of cystic fibrosis. Cystic fibrosis is a genetic syndrome of apparent exocrine dysfunction, characterized by obstructive lesions throughout multi pie-organ systems and disturbances of mucus and electrolyte secretion (5, 6). Although reported in various racial groups, cystic fibrosis is more commonly found among whites. It is inherited in an autosomal recessive fashion, and it is estimated to occur in 1: 2000 live births (5). The specific genetic defect remains obscure. Elevated concentrations of sweat sodium and chloride are integral and diagnostic features (7). A diversity of symptoms is produced. Cystic fibrosis is a major cause of malabsorption in infants and children in the United States, and it is responsible for a large pro-