Abstract

Introduction: Octreotide is used for a wide arrange of disorders particularly with endocrinologic and gastrointestinal diseases. We present a case of an uncommon side effect of octreotide in a patient with Familial hypocalciuric hypercalcemia (FHH). Clinical case: 59 year old male presented in late 2011 for persistent hypercalcemia (age 52 at the time). He carried a diagnosis of suspected FHH. Medical records were available for review and demonstrated repeated, persistent hypercalcemia (~12.5-13.4 mg/dL) with no history of normo-calcemia, repeated low urine calciums (31 - 56 mg/24hr), PTH 74-130 pg/ml. Other testing included normal PTH-rp, 25 OH Vitamin D, 1,25 OH Vitamin D, and albumin. Hypercalcemia was confirmed with elevated ionized calcium. PMH also included recurrent pancreatitis since 2007 (admitted ~ 20 times for pancreatitis). No alcohol abuse. A cholecystectomy was completed but pancreatitis persisted. In 2010, triglycerides 1350 mg/dL during a hospitalization and he was treated with gemfibrozil. Despite follow up levels <200 mg/dL he continued to have episodes of pancreatitis. Due to persistent hypercalcemia without another etiology for pancreatitis, in early 2011 he underwent 3.5 gland parathyroidectomy with half a gland implanted in sternocleidomastoid muscle. PTH dropped immediately from ~150 to 30-40 pg/ml postoperatively with normal calcium levels. However, within 2 months calcium increased to 11-12.5 mg/dL with PTH 40-48 pg/ml. The patient continued to have episodes of pancreatitis. FH was limited due to both parents deceased but no report of calcium disorder. The patient had negative genetic testing for FHH. In April 2011, he was started on cinacalcet and titrated until calcium normalized. A few months later GI placed a biliary stent due to biliary/pancreatic duct strictures, initiated octreotide LR and titrated to 30mg monthly. In general, his episodes of pancreatitis decreased but did not resolve. In mid-2014 while he was still taking cinacalcet, he developed hypocalcemia and cinacalcet was stopped and calcium remained mostly WNL. Then in 6/2017 when admitted for liver phlegmon he had hypocalcemia and suspected symptomatic based on carpal symptoms. He also had new hyperglycemia. Discussion with GI led to a dose decrease in octreotide to 10mg. However patient developed pancreatitis and octreotide dose increased back to 20mg daily. Calcium remained in the low normal range on this dose. Conclusion: We believe this is the first published case of octreotide induced hypocalcemia in a patient with FHH. The occurrence of hypocalcemia in patient with a suspected inactivating mutation of the calcium sensing receptor (CASR) gene may assist in understanding the mechanism of octreotide induced hypocalcemia. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. s presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.

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