SUN-317 Reactive Hypoglycemia in a Post-Partum Patient: A Diagnostic Conundrum

Abstract

Background: Both insulinoma and non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS) are known causes of insulin overproduction. The common presentation of insulinoma is symptomatic fasting hypoglycemia. The stereotyped presentation of NIPHS is reactive hypoglycemia. This is a case report of a patient with reactive hypoglycemia more typical of NIPHS who was later diagnosed with insulinoma by endoscopy. Clinical Case: A 34-year-old previously healthy female four weeks status post uncomplicated vaginal delivery presented with multiple episodes of hypoglycemia with blood glucose <60 mg/dL; reactive hypoglycemia was more frequent. CT scan showed no pancreatic masses, and lab work drawn during a period of fasting hypoglycemia demonstrated c-peptide level of 2.8 ng/ml and an insulin level of 4 uIU/ml. The working diagnosis was NIPHS; she was managed initially with acarbose 25mg every 8 hours and diet with goal 15-30g of net carbohydrates per day. She initially experienced reduced episodes of hypoglycemia with acarbose with blood glucose in the 70-90 mg/dL range but was unable to sustain glucose levels above 100 mg/dL. After four days on acarbose the patient was switched to diazoxide 1mg/kg every 8 hours, which resulted in frequent sugars in the 60-70 mg/dL range, so acarbose was resumed. Subsequent endoscopic ultrasound demonstrated insulinoma. Clinical Lessons: One would expect that acarbose and low carbohydrate diet would be ineffective in a patient with an insulinoma; however, this patient experienced reduction of hypoglycemic episodes with these therapies. Given her improved blood sugars on acarbose, we postulate that she had both an insulinoma and some degree of beta cell hyperplasia, possibly related to her recent pregnancy. This case demonstrates a challenging diagnostic dilemma and reveals subtle nuances in the workup and management of a post-partum patient with hypoglycemia. It also raises interesting questions regarding the effects of pregnancy hormones on the growth and presentation of insulinomas. Estrogen has been shown to inhibit rat insulinoma cell mitophagy in vitro.1 It is possible our patient experienced increased growth of the insulinoma during pregnancy due to a similar estrogen mediated mechanism but was simultaneously protected from severe hypoglycemia due to insulin resistance of pregnancy. In the less insulin resistant post-partum state, hypoglycemia ensued. Further investigation should be done to evaluate why some insulinomas present with post-prandial hypoglycemia, to determine an effective medical therapy for NIPHS and insulinoma prior to surgical intervention, and to fully elucidate effects of pregnancy on the presentation of insulinoma. 1. Zhang L., Zhao Y., Guo L. 17beta-estradiol protects INS-1 insulinoma cells from mitophagy via G protein-coupled estrogen receptors and the PI3K/Akt signaling pathway. Int J Mol Med. 2018;41:2839–2846.