We present a rare case of a 49-year-old female with very severe hypertriglyceridemia (HTG) having a total triglyceride (TG) count of > 10,000 mg/dL in the absence of pancreatitis. Based on literature review, this is one of the highest recorded TG counts in an adult without evidence of pancreatitis. HTG is a common occurrence in clinical practice, but rarely do numbers exceed 2000 mg/dl. It is crucial to evaluate and rapidly lower TG levels to prevent potentially life-threatening complications such as severe pancreatitis. Removal of potential predisposing medications, control of underlying diseases known to cause HTG, and maintenance therapies are essential to prevent reoccurrence.

We present here the case of a 55-year-old male who presented to the emergency department with severe abdominal pain and respiratory distress secondary to mesenteric ischemia. His critical illness on preexisting chronic kidney disease, previously undiagnosed alcoholic cirrhosis, and congestive heart failure led to a rare yet fatal consequence of refractory hypoglycemia. Critical illness associated hypoglycemia generally occurs as a result of high metabolic consumption with relative insulin excess and insufficient nutritional intake that is seen frequently in critically ill patients. This, along with reduced hepatic and renal gluconeogenesis seen in preexisting liver and renal disease, can cumulate to life-threatening hypoglycemia and is seen as a poor prognostic factor in the ICU setting.

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Introduction: Hypoglycemia in non-diabetic patients can be diagnostically challenging. It can have various etiologies including medications, tumors, post gastric bypass surgery, alcohol use, critical illness, liver/renal disease and adrenal insufficiency. We present a case of a 55-year old male with persistent, refractory hypoglycemia in the absence of Diabetes Mellitus (DM). Case Description: Patient is a 55-year old male with past medical history of Congestive Heart Failure with ejection fraction of 30%, Chronic Kidney Disease, Atrial Fibrillation, and alcohol abuse. He presented with sudden onset severe abdominal pain. Admission vitals were stable except oxygen saturation of 70% on room air. Labs were significant for lactic acid of 5.3 mmol/L and Acute Kidney Injury (AKI). CT scan of the abdomen was unremarkable. The patient was admitted to the ICU for severe acute hypoxic respiratory failure and mesenteric ischemia. On hospital day-3, he became unresponsive. At that time, his labs revealed blood sugar of less than 10 mg/dl and worsening renal failure. The patient was given multiple ampules of Dextrose 50% and infusion of dextrose 5% was started. He was initiated on Continuous Renal Replacement Therapy (CRRT) as well. Despite this, his blood sugar remained in the 40’s. His IV fluids were switched to Dextrose 10% and eventually to Dextrose 20% because of persistent hypoglycemia, also requiring intermittent IV Glucagon. He had no family or personal history of DM. HbA1c was 5.6%. Cortisol, Pro-insulin, Insulin, C-peptide levels were normal. Sulfonylurea screen was negative. Liver Function Tests were normal. Endoscopic Ultrasound did not reveal any pancreatic mass. Paracentesis of ascitic fluid was suggestive of underlying liver cirrhosis. It was then determined that the patient’s hypoglycemia was likely secondary to critical illness along with underlying severe hepatic and renal failure. The patient’s overall prognosis was poor and his condition declined rapidly. He refused any further intervention and opted for hospice care. Conclusion: Patients with critical illness especially those with underlying advanced liver/renal disease, malnutrition and advanced age may develop profound hypoglycemia even in the absence of diabetes. These patients should have frequent monitoring of blood sugar levels. Prompt support for decompensated disease is vital for overall survival. References: 1. Desimone ME, Weinstock RS. Non-Diabetic Hypoglycemia. [Updated 2017 Sep 23]. In: De Groot LJ, Chrousos G, Dungan K, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK355894/ Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. Abstracts presented at a news conference are embargoed until the date and time of the ...

Introduction Hypertriglyceridemia (HTG) is a common form of dyslipidemia. It has been shown to increase the risk for acute pancreatitis and cardiovascular disease. The risk of pancreatitis increases when TG levels exceed 1000-2000 mg/dL. Based on literature review, this patient has perhaps the highest recorded TG count without evidence of pancreatitis 1 . Case Description A 49-year-old Hispanic female with history of hypertension and asthma presented with chest tightness. Medications included Albuterol inhalers, Losartan, Montelukast, Verapamil, and intermittent Prednisone tapers for asthma exacerbations. She denied alcohol/drug use and quit smoking 13 years ago. Vitals were stable on admission. BMI was 27.7. Chest wall was tender to palpation which was ruled to be musculoskeletal. The remainder of the examination including skin was normal. Initial centrifuged blood on gross examination was heavily lipemic. Lipid panel revealed serum triglyceride of >10,000 mg/dL, serum cholesterol of 1,029 mg/dL, LDL of 33 mg/dL, and HDL of 22 mg/dl. Serum lipase, blood glucose, TSH, and HbA1c were all within normal limits. Urine protein-creatinine ratio was normal. Cardiovascular work-up was negative. IV insulin drip was initiated with IV fluids containing dextrose along with Heparin subcutaneously. These are potent activators of lipoprotein lipase 2,3 . A lipid panel from 2016 revealed serum triglycerides of 212 mg/dL and serum cholesterol of 182 mg/dL. On day 9, serum TG levels came down to 825 mg/dL and serum cholesterol was noted to be 360 mg/dL. She was discharged on Rosuvastatin, Fenofibrate and prescription omega-3 fatty acids. Labs one month after discharge revealed serum TG levels of 142 mg/dL and serum cholesterol of 117 mg/dL. The cause of HTG was believed to be repeated Prednisone courses precipitating an underlying genetic HTG disorder. The patient did not follow up for further genetic testing. Conclusion Hypertriglyceridemia is frequently encountered in clinical practice. In cases of severely elevated TG levels (above 1000-2000 mg/dL), rapid lowering to levels < 500-1000 mg/dL must be achieved with aggressive therapy (IV insulin drip and heparin) to prevent the development of acute pancreatitis. References 1. Vangara, S. S., Klingbeil, K. D., Fertig, R. M., & Radick, J. L. (2018). Severe hypertriglyceridemia presenting as eruptive xanthomatosis. Journal of Family Medicine and Primary Care , 7 (1), 267-270. http://doi.org/10.4103/jfmpc.jfmpc_270_17 2. Berger Z, Quera R, Poniachik J, Oksenberg D, Guerrero J. heparin and/or insulin treatment of acute pancreatitis caused by hypertriglyceridemia. Rev Med Chil , 2001;129:1373-8. 3. Jabbar M, Zuhri-yafi M, Larrea J. Insulin therapy for a non-diabetic patient with severe hypertriglyceridemia. J Am Coll Nutr , 1998;17: 458-61.