Delivery of Pancreatin in Microsphere Preparations: Transit, Timing, Physiological Needs

Abstract

While maldigestion and malabsorption of dietary protein are usually eliminated with treatment (Harris et al. 1955; Regan et al. 1977; Durie et al. 1980), steatorrhea is commonly refractory to any form of pancreatin therapy in patients who have pancreatic insufficiency (PI) (Fig. 1). Fat absorption can be normalized in about 10% of patients (Durie et al. 1980; Schneider et al. 1985), but the majority excrete 10%–30% of dietary fat on current treatments (Table 1). In about 8% of patients, outputs of fecal fat remain much above 30% of intake and are almost completely unaffected by any form of pancreatin (Henker 1989; Durie et al. 1980). A consequence of failure to normalize fat absorption is the need for heavy supplementation with fat-soluble vitamins (Hahn et al. 1974; Farrell et al. 1977; Mischler et al. 1979; Dutta et al. 1982; Hanly et al. 1985; Gibbens et al. 1988; Raynor et al. 1989), especially with vitamin E. Serum levels of vitamin E in patients with cystic fibrosis vary inversely with the amount of fat lost in the feces (Congdon et al. 1981). Undernutrition, reduced appetite relative to caloric needs, and inadequate consumption of calories are common in treated patients with PI. Fecal loss of ingested calories contributes significantly to caloric imbalance (Buchdal et al. 1989).