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Hypocalcemia and steatorrhea—Clues to etiology

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Abstract

Two boys with idiopathic hypoparathyroidism had extensive studies of gastrointestinal function during hypocalcemia accompanied by steatorrhea. No evidence of generalized gastrointestinal moniliasis or abnormal mucosal structure or function was observed. Studies of pancreatic function and bile salt metabolism during hypocalcemia demonstrated deficient meal-stimulated intraluminal pancreatic enzyme concentrations in both subjects and reduced bile salt concentrations in one subject. However, following stimulation with exogenous octapeptide of cholecystokinin, intraluminal pancreatic enzyme and bile salt concentrations were normal in both. Cholic acid pool sizes were markedly increased in both subjects during hypocalcemia (9 and 12 times larger than during normocalcemia) and cholic acid turnover was reduced during hypocalcemia in one subject. Our findings suggest that during hypocalcemia, insufficient endogenous cholecystokinin is released by the duodenal mucosa during a meal stimulus to stimulate normal gallbladder contraction and pancreatic enzyme secretion.

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Authors and Affiliations

  1. Division of Gastroenterology and the General Clinical Research Center, Children's Hospital Research Foundation, Children's Hospital Medical Center, 45229, Cincinnati, Ohio

    James E. Heubi MD, John C. Partin MD & William K. Schubert MD

  2. the Department of Pediatrics, University of Cincinnati, 45229, Cincinnati, Ohio

    James E. Heubi MD, John C. Partin MD & William K. Schubert MD

Authors
  1. James E. Heubi MD
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  2. John C. Partin MD
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  3. William K. Schubert MD
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Additional information

Supported in part by USPHS grant RR-00123 and Clinical Associate Physician's Award 3-MDI-RR00123-16SI from the General Clinical Research Centers Branch, National Institutes of Health, and a Trustee Grant, Children's Hospital Research Foundation.

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Heubi, J.E., Partin, J.C. & Schubert, W.K. Hypocalcemia and steatorrhea—Clues to etiology. Digest Dis Sci 28, 124–128 (1983). https://doi.org/10.1007/BF01315141

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  • DOI: https://doi.org/10.1007/BF01315141

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