8179 Complicated Pancreatitis Unveiled: A Case Of Untreated Primary Hyperparathyroidism

Abstract Disclosure: A. Rehan: None. H. Al Jumaili: None. J. Lim: None. Introduction: Acute pancreatitis (AP) triggered by hypercalcemia stemming from primary hyperparathyroidism (PHPT) is an infrequent occurrence, with a prevalence of about 1.5-7%. The proposed mechanism involves deposition of calcium in the pancreatic ducts and activation of pancreatic enzymes. While a causal connection between AP and PHPT has been described, it remains controversial. Calcium levels are thought to play a major role in determining the severity of the pancreatitis. Additionally, it is thought that genetic mutations may contribute to the development of AP in PHPT. Here, we report a case of necrotizing pancreatitis in a patient with untreated PHPT. Clinical Case: Patient is a 59-year-old male with a medical history of hypertension, nephrolithiasis and PHPT secondary to parathyroid hyperplasia (scheduled for parathyroidectomy) who presented with abdominal pain, nausea, vomiting and was found to have AP. He reported no history of alcohol use, trauma or insect bites. His workup was unrevealing for cholecystitis, choledocholithiasis or hypertriglyceridemia. He represented with calcium level of 16 mg/dL (NR 8.7-10.1) due to PHPT. PHPT was deemed the likely cause of AP. Course was further complicated by necrotizing pancreatitis and pseudocyst. A few months later, patient started having coffee ground emesis, worsening epigastric pain and weight loss of 60 lbs due to poor oral intake. CT abdomen/pelvis showed walled off pancreatic necrosis with peripancreatic stranding and concern for gastric outlet obstruction. EGD with PEG-J placement was done with plans for future endoscopic drainage. Few weeks after, he had another bout of worsening abdominal pain. Labs at the time showed corrected calcium between 11-13 mg/dL, PTH 147 pg/ml (NR 5-44), phosphorus 1.6 mg/dL (NR 2.5-4.5), vitamin D 25 hydroxy 19.5 ng/ml (NR 22-110). His condition became more complex with a hemorrhagic walled off pancreatic necrosis and splenic artery pseudoaneurysm requiring ICU care. The repeated escalation of symptoms resulted in multiple delays for the scheduled parathyroidectomy. Patient was started on treatment with Cinacalcet and vitamin D while in the hospital. Due to constraints in resources, he was unable to continue Cinacalcet outpatient. He subsequently was able to undergo parathyroidectomy with pathology showing benign adenoma. Conclusion: Hypercalcemic hyperparathyroidism causing AP, although rare, is often severe and poses a greater risk of complications making it important to be aware of this association, especially when more common causes have been excluded. Imaging techniques like cervical ultrasound, CT, and scintigraphy using 99mTc-Sestambi should be utilized to confirm suspicion. Surgical resection is the mainstay treatment, and having a multidisciplinary team with gastroenterologists, endocrinologists, and surgeons helps improve outcomes. Presentation: 6/2/2024