Pancreatitis and primary hyperparathyroidism: Forty cases

Background: Pancreatitis is associated with primary hyperparathyroidism (PHPT) in 1.5-7% of cases. The relationship of cause and effect between the two diseases has been debated. Methods: To evaluate this relationship, the clinical, biochemical and pathological data on 1435 patients operated on for hyper parathyroidism (HPT) over the past 30 years were retrospectively reviewed. A total of 1224 of these patients had biologically proven and cured PHPT and 211 patients had renal HPT (RHPT). The diagnosis of pancreatitis (PTS) was based on a high serum amylase level and/or abnormalities on ultrasound or computed tomography (CT) scan explorations. Only patients without biliary stones were included in the PTS group associated with HPT. Results: A total of 3.2% (n = 40) of patients with PHPT had PTS, which was acute in 18 cases, subacute in 8 cases and chronic in 14 cases. This rate of PTS is higher than in a random hospital population. Surgical cure of HPT was followed by the spontaneous healing of 17/18 acute PTS, whereas six of the 22 patients with subacute or chronic PTS developed complications due to the evolution of their disease (diabetes, pancreatic duct stenosis treated by surgery). A single diseased gland was found in 27 patients with PTS, which is in favour of primary parathyroid disease, being responsible for, and not a consequence of, PTS. Only the serum calcium (13.0 vs 12.1 g/dL) level was significantly increased in PHPT patients with PTS, when compared to those without PTS, The calcium level is probably of major importance in the development of PTS, which was never encountered in 211 patients with RHPT, who had low calcium and high PTH levels. Conclusions: The data suggest that (i) the PTS-PHPT association is not incidental; (ii) PTS is the consequence and not the cause of PHPT; (iii) hypercalcaemia seems to be a major factor in the development of PTS in PHPT patients; and (iv) cure of PHPT leads to the healing of acute PTS, whereas it does not affect the evolution of subacute and chronic PTS.