MON-026 Orthostatic Hypotension (OH), Postural Orthostatic Tachycardia Syndrome (POTS), and Reactive Hypoglycemia: Are they connected?

Abstract Disclosure: M. Fathima: None. A. Khan: None. J. Gilden: Novartis Pharmaceuticals. Introduction: Hypoglycemia without diabetes mellitus (DM) is rare and is often associated with other comorbidities. When autonomic dysfunction (AN) occurs, there can be defective hormonal counter regulation which can lead to prolonged or recurrent hypoglycemia in patients without DM [1]. After a hypoglycemic episode (HYPO), patients may experience orthostatic intolerance as a symptom, relating to neurogenic orthostatic hypotension (nOH) and postural orthostatic tachycardia syndrome (POTS). Case presentation:Case 1: A 64-year-old female with known neurogenic orthostatic hypotension (nOH) and AN began experiencing dizziness/lightheadedness and had a fainting spell while taking a shower. She was also noted to have postprandial symptoms of tremors, lightheadedness, and anxiety. A continuous glucose monitor (CGM) was placed for 2 weeks. Episodes of postprandial HYPO with blood glucose values <80 were recorded, corresponding to symptoms. Lab values demonstrated: Glucose of 99, Hemoglobin A1C of 5.5%, proinsulin 5.6 pmol/L (normal <18.8 pmol/L), C-peptide 2.7 ng/ml (normal 0.81 - 3.85 ng/mL), ACTH 10 pg/ml (normal 0 - 47 pg/ml), and AM cortisol 15.47 ug/dl (normal 5.3 - 22.5 ug/dl). The patient was diagnosed with reactive HYPO without DM due to AN. Although the HYPO episodes decreased with starting acarbose 25 mg with meals, she was unable to tolerate this due to gastrointestinal symptoms and HYPO episodes increased with lightheadedness on changes in position. Case 2: A 61-year-old male with complaints of syncopal episodes and low systolic blood pressure readings was referred to Endocrinology for evaluation and management of nOH. A 13 day CGM was placed to rule out HYPO as a cause for syncope in a nondiabetic patient. Frequent readings of fasting and postprandial low blood glucose trends of hypoglycemia were recorded. Lab values demonstrated: Glucose of 88, Hemoglobin A1C of 6.1%, proinsulin 6.4 pmol/L (normal <18.8 pmol/L), C-peptide 0.98 ng/ml (normal 0.81 - 3.85 ng/mL), fasting insulin 5.02 mIu/L (normal <25), ACTH 9 pg/ml (normal 0 - 47 pg/ml), and AM cortisol 15.9 ug/dl (normal 5.3 - 22.5 ug/dl). Patient was diagnosed with reactive HYPO due to AN and was started on acarbose 25 mg with meals. HYPO and hypotensive episodes were both attenuated. Conclusion: While therapy of non-neurogenic OH is mostly straight-forward, nOH is often difficult to treat. A structured approach is important in the management of patients with nOH. Our cases highlight that there is an interaction between the autonomic nervous system and glucose homeostasis. Furthermore, therapeutic interventions may be similar. References: 1. Freeman, R. (2007). Hypoglycemia and the Autonomic Nervous System. In: Veves, A., Malik, R.A. (eds) Diabetic Neuropathy. Clinical Diabetes. Humana Press. https://doi.org/10.1007/978-1-59745-311-0_23 Presentation: Monday, July 14, 2025