Updated: 08/21/07 08:12 AM
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Authors: D.R. Saunders, C.E. Rubin, and J.D. Ostrow
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N. Protein Malabsorption


Intestinal resection, pancreatic insufficiency are most common
The most frequent causes of protein malabsorption are loss of normal jejunal mucosal function and loss of exocrine pancreatic secretion of peptidases and of sodium bicarbonate to maintain the peptidase's neutral pH optimum. In children this is most commonly associated with the hereditary diseases in which gluten injures the duodenal jejunal mucosa (celiac sprue) or in which the pancreas is destroyed (cystic fibrosis). In adults it is most common with chronic pancreatitis, celiac sprue and shortened bowel secondary to surgical resection of an infarcted area.

When protein loss into the intestinal lumen is excessive, it is referred to as protein-losing enteropathy. This condition is caused by a variety of mucosal diseases which lead to exudation of plasma because of surface inflammation or a leaky mucosa that develops for other reasons.

Enterokinase activates trypsin Congenital enterokinase deficiency in children can prevent activation of trypsinogen to trypsin. The lack of trypsin in turn prevents activation of the other pancreatic peptidases. Thus, these patients cannot split their protein and therefore absorb it inefficiently.

Genetic defects Genetic defects in single amino acid transport systems are usually shared by kidney and intestine, i.e., in Hartnup's disease both organs lack the neutral amino acid pump and in cystinuria both organs lack the basic amino acid transport system for cysteine. Nevertheless, their di- and tripeptide transport systems are intact, providing an alternate mechanism for absorption of these amino acids as constituents of the di- and tri-peptides.

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