Endocrine Abstracts

Primary hyperparathyroidism (PHPT) is rarely associated with the development of acute pancreatitis (AP). The incidence of AP induced by hypercalcemia in PHPT varies between 1.5 and 7%. PHPT is most commonly caused by parathyroid adenoma and infrequently by parathyroid hyperplasia, carcinoma or cyst and multiple endocrine neoplasia (MEN) types 1 and 2A. The present case is a 48-year-old man referred to our service for further investigation 1 month after an acute hemorrhagic necrotic pancreatitis in context of hypercalcemia, complicated with caudal pancreatic pseudocyst, partial thrombosis of portal vein, hepatosplenomegaly, moderate anemia and acute renal failure. His history included 3 AP attacks managed conservatively throughout the last 2 years, left renal microlithiasis, essential hypertension, chronic renal insufficiency, hyperuricemia, without additional risk factors for AP like alcohol ingestion, hyperlipidemia and gallstones. Laboratory findings revealed increased serum ionized calcium (6.29 mg/dl) and total serum calcium (11.98 mg/dl), hypophosphatemia (2.06 mg/dl) associated with elevated parathyroid hormone (PTH=320 pg/ml), high serum amylase (167 U/l), lipase (318.8 U/l), C-reactive protein (9.94 mg/dl), azotate retention (creatinine=1.75 mg/dl, serum urea=47 mg/dl), hyperglycemia (130 mg/dl) and moderate anemia (haemoglobin=9.3 g/dl). Cervical ultrasonography showed a 5.8/4.04/3.74 cm, mixed, echogenic and transonic, well-defined mass located postero-inferior of the right thyroid lobe. Single photon emission computed tomography (SPECT) with technetium-99 m sestamibi combined with X ray–based computed tomography (CT) revealed a right posterior cystic parathyroid adenoma, extended in the superior mediastinum, measuring 5/3.5/4 cm. After conservative management, hydratation, forced diuresis and calcitonine, the patient underwent right inferior parathyroidectomy. Histopathological examination confirmed the diagnosis of parathyroid adenoma. Postoperatively, the patient developed mild hypocalcemia and was treated by intravenous calcium infusions, followed by oral calcium and vitamin D. Serum calcium and PTH levels returned to normal and the patient was asymptomatic at the follow-up examinations. Although hypocalcemia is expected to appear during an AP attack, identifying hypercalcemia should always raise the suspicion of either hyperparathyroidism or malignancy. High PTH helps differentiate the two. As AP can have fatal consequences, it is important to reassess calcium levels after resolution of AP, especially in patients with idiopathic recurrent AP, because early recognition and treatment prevent reappearance.