Endocrine Abstracts

Introduction: Primary hyperparathyroidism(PHPT) is a prevalent endocrine disorder characterized by hypercalcemia due to the overproduction of parathyroid hormone(PTH) from one or more parathyroid glands. While PHPT is typically diagnosed incidentally through routine laboratory testing due to asymptomatic hypercalcemia, acute pancreatitis as the initial symptom is a rare occurrence. This article presents three cases where acute pancreatitis served as the first manifestation ofPHPT.

Case reports: A 69-year-old patient was with an acute digestive presentation of transfixing epigastric pain and bilious vomiting, revealing pancreatitis classified as Balthazar stage D. The etiological assessment revealed primary hyperparathyroidism. Scintigraphy with SestamibiTc99m identified 2 focal retention areas in the MIBI-Tc99m. The patient received rehydration followed by bisphosphonate infusion and underwent successful surgical intervention. A 35-year-old patient was admitted for an acute digestive presentation, revealing pancreatitis classified as stage B. The etiological assessment showed hypercalcemia at 132 mg/l with hypophosphatemia at 19 mg/l. PTH was elevated at 985 pg/ml. Cervical ultrasound revealed a hyper-vascularized right retro-thyroid formation. SestamibiTc99m scintigraphy revealed a focus below the lower right thyroid pole. The patient underwent an adrenalectomy, with pathological examination confirming a parathyroid adenoma. A 28-year-old patient was admitted for epigastric pain, nausea. Lipase levels were elevated, and a CT scan revealed pancreatitis stage C. Primary hyperparathyroidism was diagnosed in the etiological assessment, with a PTH level of 3111 pg/ml, hypercalcemia of 136 mg/l, and hypophosphatemia of 22 mg/l. Sestamibi scintigraphy revealed three focal retention areas in the MIBI-Tc99m. The patient underwent a 7/8 parathyroidectomy with total thyroidectomy. Histological examination indicated parathyroid carcinoma, and unfortunately, the patient’s condition became fatal after the development of multiple metastases.

Discussion: Hypercalcemia is a rare cause of acute pancreatitis, even more so if secondary to primaryhyperparathyroidism, with a prevalence varying from 1.5% to 5%. The association between hyperparathyroidism and acute pancreatitis has been debated, with three proposed mechanisms supporting this connection. These mechanisms involve hypercalcemia triggering trypsinogen conversion, calcium accumulation obstructing pancreatic ducts, and elevated calcium levels combined with genetic mutations increasing pancreatitis risk in PHPT patients. Patients with PHPT exhibit a higher pancreatitis rate than those without, and given the high morbidity and mortality associated with acute pancreatitis, immediate treatment is crucial. The primary focus should be on managing pancreatitis initially. Once pancreatitis subsides, parathyroidectomy becomes imperative as it is the sole treatment for symptomatic PHPT. This comprehensive approach aims to address both acute pancreatitis and the underlying primary hyperparathyroidism to optimize patient outcomes.