SAT-594 A Metabolic Muddle : Thyrotoxicosis Causing Diabetic Ketoacidosis

Abstract

INTRODUCTION: Diabetic Ketoacidosis (DKA) is a metabolic state developing in diabetic patients whenever a stressor shifts the metabolism towards ketogenesis with resultant metabolic acidosis. Common stressors for DKA are infections and medication non-compliance. We present a peculiar case of DKA which was precipitated by thyrotoxicosis. CASE DESCRIPTION: 32-year-old female with past medical history of Type 1 Diabetes Mellitus presented for evaluation of nausea, vomiting and chest pain. She reported as being compliant with her insulin regimen. Physical examination showed rapid breathing and acetone breath. Initial blood tests revealed elevated blood sugars at 745 MG/DL with a high anion gap metabolic acidosis. Beta hydroxybutyrate levels were elevated suggesting diabetic ketoacidosis. Rest of the workup to identify the precipitating cause, including urinalysis, EKG, Chest X ray had been negative. Another striking feature noted on patient's examination was bilateral exophthalmos. No thyroid enlargement was appreciated. A thyroid function panel was ordered which demonstrated elevated free T4 at 3.42 NG/DL (normal range 0.7-1.9 NG/DL), T3 at 26.01 PG/ML (normal range 1.7-3.71 PG/ML) and a depressed TSH level <0.01 mcIU/mL (normal range 0.35-.5 mcIU/ml) suggesting primary hyperthyroidism. Our patient improved upon administration of IV fluids and insulin with resultant closure of anion gap and resolution of DKA. Tachycardia persisted despite the resolution of DKA. Treatment was begun with propylthiouracil and propranolol to control thyrotoxicosis with remarkable improvement at the time of discharge. DISCUSSION: Treatment of Diabetic Ketoacidosis requires a thorough investigation of the precipitating event. In clinical practice, the most common triggers are noted to be infections like pneumonia and urinary tract infections, missed or inadequate insulin dose and myocardial infarction. Hyperthyroidism is rarely considered as a culprit for the same. In literature, there is only mention of few cases of hyperthyroidism causing DKA. Hyperthyroidism affects glucose and insulin metabolism in multiple ways. In untreated hyperthyroidism, proinsulin processing becomes abnormal resulting in a reduced C peptide to pro insulin ratio. Hyperthyroidism also leads to increased glucose absorption in the intestinal tract. Lastly, excessive thyroid hormone activity reduces the half-life of insulin via increased degradation into biologically inactive molecules. Our case emphasizes the need to consider thyrotoxicosis as an independent risk factor for development of DKA in appropriate clinical settings, especially when tachycardia persists despite resolution of DKA and infection has been ruled out. Women with Type 1 Diabetes have been found to have a higher prevalence of Graves’ disease. Correction of underlying hyperthyroidism decreases the insulin requirements in these patients.