MON-146 Prolonged Hypoglycemia in the Setting of Synthetic Cathinone Abuse

Abstract

INTRODUCTION Amphetamine and amphetamine-analogues, such as synthetic cathinones, popularly known as “bath salts”, should induce hyperglycemia, due to their increased dopaminergic activity. However, a handful of case reports have described paradoxical hypoglycemia with the use of synthetic cathinones. CLINICAL CASE A 39-year-old man with no known prior medical history was admitted to the Medical ICU after being found agitated and combative; he was intubated at the scene. In the ED fingerstick glucose monitoring was 57mg/dL and later confirmed by venous blood chemistry. The rest of his chemistry was remarkable for a creatinine of 2.14mg/dL (0.7-1.20mg/dL), a mild elevation of AST-SGOT at 85 units/L (0-40 units/L), and a creatinine kinase of 1937 units/L (20-200 units/L). His CBC revealed a WBC count of 22.39 x 109/L (3.50-10.50 x 109/L), with normal differential. A comprehensive urine drug screen was positive for amphetamine and methamphetamine and a screen for hypoglycemic agents was negative. He remained hypoglycemic for the initial 48h of his hospital admission, despite continuous supplementation with D10W and frequent administration of D50% boluses. Patient was weaned off the ventilator and admitted to the ingestion of “bath salts” prior to his hospitalization. His physical examination was essentially unremarkable, except for noted tachycardia and intermittent episodes of confusion and disorganized speech; with these findings improving within 48 hours of admission. His hospital course was complicated and prolonged due to concomitant sepsis secondary to MRSA and Klebsiella pneumoniae bacteremia, with acute liver and kidney failure. Euglycemia was achieved once oral intake was initiated; remaining this way for the rest of his hospital stay and continuous dextrose infusion was weaned off in 4 days. Our patient’s hypoglycemia was suspected to be derived from the use of synthetic cathinones, and to a lesser degree from the combination of early starvation and impaired gluconeogenesis in the setting of acute liver and kidney failure. CONCLUSIONS Although amphetamine derivatives, including synthetic cathinones, have been shown to produce hypoglycemia in a few animal studies (1), this remains to be confirmed in humans. The suspicion or confirmation of the use of illicit stimulants, including “bath salts” in the setting of prolonged hypoglycemia, should prompt the clinician to include this as a major contributing factor to disruptions in glucose metabolism. REFERENCES Soto-Montenegro, Marisa & Vaquero, Juan Jose & Arango, C & Ricaurte, G & García-Barreno, P & Desco, Manuel. (2007). Effects of MDMA on blood glucose levels and brain glucose metabolism. European journal of nuclear medicine and molecular imaging. 34. 916-25. 10.1007/s00259-006-0262-8.