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The Association of Primary Hyperparathyroidism With Pancreatitis

Bai, Harrison X. MD, BS*; Giefer, Matthew MD; Patel, Mohini MD*; Orabi, Abrahim I. BS; Husain, Sohail Z. MD

Journal of Clinical Gastroenterology:
doi: 10.1097/MCG.0b013e31825c446c
Clinical Reviews
Abstract

The association between primary hyperparathyroidism (PHPT) and acute or chronic pancreatitis is controversial. For this reason, we conducted a review of the literature over the past 30 years to explore the relationship between these 2 disorders. Ten retrospective studies each with >50 patients diagnosed with PHPT were identified. With the notable exception of 2 studies, the rate of pancreatitis among patients with PHPT was higher than that reported in general among hospitalized patients without PHPT. A higher serum calcium level may contribute to pancreatitis in these cases, along with additional genetic or environmental insults. Hypercalcemia may predispose the pancreatic acinar cell to abnormal, sustained calcium levels, lead to premature pancreatic protease activation, and pancreatitis. Although there was only short-term follow-up, most reports cited that definitive treatment of PHPT by parathyroidectomy led to the resolution of pancreatitis attacks. The published cohorts of patients with PHPT and pancreatitis are subject to bias, because serum calcium screening was not universally performed among all control nonpancreatitis patients to evaluate for PHPT. However, the pooled clinical and experimental data suggest an association between PHPT and pancreatitis and implicate hypercalcemia. For clinicians, it is important to recognize pancreatitis in patients with PHPT and, conversely, to consider PHPT by checking serum calcium levels in patients, who present with an unexplained pancreatitis.

Author Information

*Departments of Pediatrics, Yale University School of Medicine, New Haven, CT

Seattle Children’s Hospital, Seattle, WA

University of Pittsburgh Medical Center, Pittsburgh, PA

H.X.B. and M.G. have contributed equally.

Supported by National Institutes of Health Grants DK093491, DK083327, HD001401 (Yale Child Health Research Center), DK34989 (Yale Liver Center), and a Children’s Digestive Health and Nutrition Young Investigator Award (to S.Z.H.).

The authors declare that they have nothing to disclose.

Reprints: Sohail Z. Husain, MD, Department of Pediatrics, 4401 Penn Avenue, Pittsburgh, PA 15224 (e-mail: sohail.husain@chp.edu).

© 2012 Lippincott Williams & Wilkins, Inc.