Treatment of Pancreatic Insufficiency

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Chapter 342 Treatment of Pancreatic Insufficiency

Steven L. Werlin

Treatment of exocrine pancreatic insufficiency by oral enzyme replacement usually corrects creatorrhea, but steatorrhea is difficult to correct completely. This may be due to inadequate dosage, incorrect timing of doses in relation to food consumption or gastric emptying, lipase inactivation by gastric acid, and the observation that chymotrypsin in the enzyme preparation digests and thus inactivates lipase. In 2010 the FDA removed all pre-existing enzyme preparations from the U.S. market. The previous practice of overfilling capsules was banned. To date, 3 new preparations have been approved. All have been tested and shown to reduce malabsorption in cystic fibrosis patients. Modern enzyme products are enteric-coated to resist gastric acid inactivation.

The dosage of pancreatic replacement for children depends on the amount of food eaten and is established by trial and error. Because these products contain excess protease compared with lipase, the dosage is estimated from the lipase requirement of 500-2,500 IU/kg/meal, with a maximum of 10,000 IU/kg/day. An adequate dose is one that is followed by the return of the stools to normal fat content, which can be verified by a 72-hour fecal fat collection, and normalization of stool consistency color, and odor. Enzyme replacement should be given at the beginning of and with the meal. In children unable to swallow enzyme capsules, the granules can be mixed with a small quantity of food, typically applesauce. Enzymes should not be chewed, crushed or dissolved in food, which would allow gastric acid to penetrate the enteric coating and destroy the enzymes. Enzymes must also be given with snacks. Increasing enzyme supplements beyond the recommended dose does not improve absorption, might retard growth, and can cause fibrosing colonopathy.

When adequate fat absorption is not achieved, gastric acid neutralization with an H₂-receptor antagonist or, more commonly, a proton pump inhibitor decreases enzyme inactivation by gastric acid and improves delivery of lipase into the intestine. Enteric coating also protects lipase from acid inactivation.

Untoward effects secondary to pancreatic enzyme replacement therapy include allergic reactions, increased uric acid levels, and kidney stones. Fibrosing colonopathy, consisting of colonic fibrosis and strictures, can occur 7-12 mo after high-dose pancreatic supplement therapy (6,500-58,000 IU lipase/kg/meal).

Baker SS, Borowitz D, Duffy D. Pancreatic enzyme therapy and clinical outcomes in cystic fibrosis. J Pediatr. 2005;146:189-193.

Borowitz D, Baker RD, Stallings V. Consensus report in nutrition for pediatric patients with cystic fibrosis. J Pediatr Gastroenterol Nutr. 2002;35:246-259.

Schall JI, Bentley T, Stallings V. Meal patterns, dietary fat intake and pancreatic enzyme use in preadolescent children with cystic fibrosis. J Pedatr Gastroenterol Nutr. 2006;43:651-659.

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