Abstract
Introduction: Alcohol use and biliary stones cause the majority of cases of acute pancreatitis (AP). Hypercalcemia is considered a relatively uncommon sole reason for AP. The incidence of hypercalcemia induced AP is about 1.5%. AP as the first presentation of primary hyperparathyroidism (PHPT), in the absence of any other precipitating factors, is extremely rare. We present a case of AP combined with obstructive uropathy as the first clinical manifestations of occult PHPT. The clinical and biochemical recovery of the patient followed parathyroidectomy suggested the correlation between AP and PHPT. Case Presentation: A 63-year-old patient with a history of type 2 diabetes mellitus, hypertension, and coronary artery disease presented to the emergency room with progressive abdominal pain that started two days prior. The pain radiated to his back and was associated with nausea and vomiting. Additionally, he reported black urine and dysuria. He did not report any alcohol or illicit drug use. His surgical history was significant for cholecystectomy. Physical examination showed elevated blood pressure and severe epigastric tenderness. Laboratory findings were significant for calcium level 14.3 mg/dL (8.5–10.5 mg/dL), serum lipase level 679 U/L (13–60 U/L), serum amylase 327 U/L (28–100 U/L), serum PTH 239 pg/mL (15–65 pg/mL), and leukocytosis 11.9K (4-11K) with neutrophilia of 86.4 %, Hemoglobin 13.3 g/dL, and normal platelet count. Vitamin D 25 (OH) level was 12.5 ng/mL (30–80 ng/mL). Urine analysis had moderate hematuria. Lipid panel showed normal triglycerides and cholesterol concentrations. HbA1c was 6.1 % (4–5.6%). Normal levels of metanephrines were found. CT of the abdomen showed acute pancreatitis with peripancreatic edema and right ureteric stone. Thyroid ultrasound revealed a hypervascular mass posterior to the left thyroid lobe. Sestamibi scan further demonstrated abnormal retention of activity in the neck near the left thyroid lobe consistent with parathyroid adenoma. After hydration and a short course of calcitonin, Cinacalcet was started as a bridge to parathyroidectomy. The patient clinically improved with normalization of Calcium levels. The ureteric stone was removed and elective left parathyroidectomy was performed two weeks later. The histopathological exam confirmed a parathyroid adenoma. Postoperatively, intact PTH level was 26 pg/mL with Calcium level of 10.4 mg/dL. The patient was completely asymptomatic. Conclusion: Although AP is a rare presentation of a silent PHTP, it should warrant the measurement of serum calcium and PTH levels in absence of more common causes of AP, especially if combined with urinary stones. Furthermore, MEN type 2 should be considered in the setting of the thyroid mass with PHPT. Medical therapy could improve the clinical condition of the patient; however, the surgical resection of a parathyroid adenoma remains the curative treatment.
Primary Hyperparathyroidism due to Parathyroid adenoma presenting as recurrent acute pancreatitis