Endocrine Abstracts

Introduction: The revelation of primary hyperparathyroidism by acute pancreatitis is an exceptional situation

Case report: We report the case of a 73 years old patient, hypertensive, having the antecedent of an ischemic cardiopathy complicated by cardiac insufficiency and atrial fibrillation, admitted to the emergency for an abdominal pain evolving since 10 days, associated with vomiting, the initial biological assessment showed lipasemia at 2543IU/l, kidney failure and malignant hypercalcemia at 142mg/l. The etiological work-up showed primary hyperparathyroidism with double localizations, the patient benefited from a Para thyroidectomy with a good clinic biological evolution.

Discussion: Hypercalcemia is a rare cause of acute pancreatitis, even more so if it is secondary to primary hyperparathyroidism, its prevalence varies, according to studies, from 1.5 to 5% [1]. Authors suggest that this association is not coincidental, and several pathophysiological explanations have been proposed, but none has been experimentally proven to date. the highest prevalence of acute pancreatitis in patients with hyperparathyroidism has been observed in those with hypercalcemia [2], and the hypercalcemia-acute pancreatitis link is currently well established. For Prinz and his team [3], acute pancreatitis is the consequence of a deposit of lithiasis secondary to an accumulation of calcium in the gastric juice. The second explanation is that of intra-pancreatic trypsinogen activation, which is widely accepted as the lever leading from acinar cell injury to acute pancreatitis [4]. Recently, the role of a genetic substrate has been suggested; mutations in the SPINK1 and CFTR genes have been detected in hyper parathyroid patients who developed acute pancreatitis[5].

Conclusion: The association hyperparathyroidism - acute pancreatitis was most often explained by the link of hypercalcemia, most of the above theories have not presented scientific evidence, and the current challenge is to seek a direct link between these two pathologies, the genetic theory remains an option, but its role is not clear.

Bibliography: [1] Kusnierz-Cabana B, and al. Currents concepts on diagnosis and treatment of acute pancreatitis. Adv Clin Chem 2003;37:47–81. [2] Carnaille B, and al. Pancreatitis and primary hyperparathyroidism: forty cases. ANZ J Surg 1998; 68:117–9. [3] Prinz RA, Aranha GV. The association of primary hyperparathyroidism and pancreatitis. Am Surg 1985;51:325–9. [4] Pandol SJ, and al. Acute pancreatitis: bench to the bedside. Gastroenterology 2007;132: 1127–51. [5] Felderbauer MD, and al. Pancreatitis risk in primary hyperparathyroidism: relation to mutations in the SPINK1 trypsin inhibitor (N34S) and the cystic fibrosis gene. Am J Gastroenterol. 2008; 103:368–74.