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A 49-year-old female with past medical history of Huntington’s disease presents to the ED after being found unresponsive at her assisted-living facility. She was noted to be hypoglycemic with a glucose of 21 and responded to dextrose. For the past several months, patient had symptoms of dizziness, tremors. She has no history of diabetes, and only home medication is Zyprexa. Patient required D10 drip to maintain glucose levels. Given patient’s psychiatric history, there was concern for surreptitious use of diabetic medications. Labwork showed an insulin level of 163 and an elevated C-peptide of 7.0 consistent with endogenous insulin secretion. Patient underwent a 72-hour fasting protocol which revealed a glucose of 23, C-peptide of 4.1 and insulin of 101, undetectable beta-hydroxybutyrate levels and pro-insulin level of 782 which is consistent with a diagnosis of insulinoma. She was started on diazoxide, which diminishes insulin secretion, to treat the hypoglycemia. Patient underwent a pancreas CT protocol which showed multiple hypervascular hepatic masses up to 9 cm and one 4 cm mass in pancreatic tail concerning for metastasis. Pathology revealed metastatic well-differentiated neuroendocrine tumor grade 3. She was not a candidate for surgical resection of tumors and she was started on Octreotide 200 mcg TID. Patient underwent two Y90 radioembolization treatments, 2 months apart with improvement of hypoglycemia and discontinuation of diazoxide. Patient remains on Octreotide LAR injection every 4 weeks. Insulinoma, although rare, occurs in 1-4% of the population and is the most common type of functional neuroendocrine tumor of the pancreas. It secretes insulin which results in hyperinsulinemic hypoglycemia. Diagnosis involves persistent hypoglycemia with glucose

Immune Checkpoint Inhibitors (ICI) have been approved since 2011 to treat patients with advanced solid and hematological malignancies and have had remarkable results. However, case reports of endocrine adverse events are becoming increasingly reported and can be fatal if not recognized early. Here we present two unique cases of rare endocrinopathies after the use of ICIs. A 47 year old male with metastatic melanoma presented with nausea, vomiting, polyuria, polydipsia of 5 days. Three weeks prior, he was started on nivolumab and ipilimumab. On presentation, he was tachycardic and tachypneic. Lab work was remarkable for a glucose of 676, Na 129, K 6.2, CO2 6, Cr 2.43 (baseline of 1.1) and beta-hydroxybutyrate of 11.7 with elevated HgA1c of 7.1%. DKA was diagnosed and fluids and insulin drip were started. Further work up revealed a normal cortisol level, TFTs and C-peptide

Background: Excess thyroid hormone alters the hemodynamics of the heart and vascular system resulting in a hyper-dynamic circulatory state which can lead to thyrotoxic heart disease. Clinical case: A 48-year-old male presented to the hospital with several days of rapid heart rate and weakness. He denied prior medical history, medication or supplement intake. Pertinent exam revealed a very thin, hoarse gentleman with shallow breathing and obvious hand tremors; heart exam with irregular rate and tachycardia, absent peripheral edema and bibasilar crackles bilaterally. EKG was consistent with atrial fibrillation with rapid ventricular response. Lab work revealed a pro-BNP of 4000 and positive D-dimer. CTA-Thorax was consistent with CHF with cardiomegaly, large pleural effusions, pulmonary edema and an incidental finding of thyromegaly. Echocardiogram revealed global LV hypokinesis with Ejection Fraction of 10-15%. TSH was 8.00, and Triiodothyronine was 27.04. Thyroid ultrasound showed heterogeneous enlarged gland with hypervascularity and no focal nodules. Graves’ Disease was confirmed with thyroid stimulating Immunoglobulin of 507. Methimazole and hydrocortisone were initiated along with Metoprolol and digoxin for rate control. Thyroid hormone has significant impact on cardiac function, structure and the vascular system. In the vasculature, T3 works to decrease systemic vascular resistance via direct vasodilatation. The decrease in SVR activates RAAS resulting in retention of sodium and fluid. Thyroid hormone also stimulates erythropoiesis which results in an increase in blood volume and stroke volume. In the heart, T3 enters the myocyte via specific transport proteins and via transcription-and non-transcription-mediated effects, increases contractility and relaxation of the cells. Given the increased metabolism, low SVR and increase in total blood volume, this creates a high cardiac output state. Untreated high-output state leads to ventricular dilatation, persistent tachycardia and eventual heart failure. Thus, prompt diagnosis and treatment of cardiac dysfunction is key. Of most importance is correction of thyroid dysfunction with either anti-thyroid medication, radioactive iodine ablation or thyroidectomy. This can possibly reverse and “cure” patient’s systolic heart failure. Conclusion: We present a case of thyrotoxicosis -induced cardiomyopathy with left ventricular ejection fraction of 10% secondary to undiagnosed Graves disease and emphasize the importance of thyroid disease as a possible cause of systolic heart failure. References: Riaz K, Forker AD, Isley WL, Hamburg MS, McCullough PA. (2007). Hyperthyroidism: A “Curable” Cause of Congestive Heart Failure - Three Case Reports and a Review of the Literature. Congestive Heart Failure.2007; 9: 40-46