Abstract #1401957: Hypoglycemia in a Patient with Malnutrition After Bariatric Surgery and Cirrhosis from Alpha-1 Antitrypsin Deficiency

Abstract

Hypoglycemia is rare in patients who do not have diabetes treated by insulin or insulin secretagogues. However, severe malnutrition can predispose to hypoglycemia through substrate limitation of gluconeogenesis and glycogen depletion, and severe hepatic insufficiency may lead to hypoglycemia due to reduced capacity for gluconeogenesis and synthesis and storage of glycogen. We report a case of hypoglycemia occurring in a patient with malnutrition after Roux-en-Y gastric bypass (RYGB) surgery and cirrhosis due to alpha1-antitrypsin (AAT) deficiency. Endocrinology was consulted to evaluate a 67-year-old female for possible hypoglycemia. Her history was notable for RYGB surgery and AAT deficiency complicated by cirrhosis. The patient reported a 3-y history of dizziness and palpitations that resolved after eating. BMI was 18 kg/m2, and bitemporal wasting and sarcopenia were observed. Markers of liver function were abnormal, including prothrombin time (16.3 sec, 11.7-14.7) and albumin level (2.2 g/dL, 3.5-5.7). GFR calculated to 81 mL/min/1.73 m2. During a diagnostic fast, plasma glucose fell to 47 mg/dL, and simultaneously measured insulin and C-peptide levels were 0.8 mIU/mL (expected < 3) and 1.4 ng/dL (expected < 0.6), respectively. Beta-hydroxybutyrate level was 0.1 mM (expected > 2.7). An insulin secretagogues panel, ACTH-stimulation test, and IGF-2 level were unremarkable. Malnutrition is a well-known risk factor for hypoglycemia, and approximately 5% of hospitalized patients with malnutrition experience hypoglycemia. Significant protein-energy malnutrition, though uncommon after RYGB, has been documented in nearly 5% of patients in some series. Severe hepatic insufficiency is also an independent risk factor for hypoglycemia, and 10-15% of patients with AAT deficiency develop hepatic injury due to accumulation of Z-type AAT polymers in the liver. Though the patient had advanced liver failure as indicated by elevated prothrombin time and inability to mount a ketogenic response to hypoglycemia, AAT deficiency induced cirrhosis alone has not been documented to cause hypoglycemia in adults. C-peptide is metabolized mostly by the kidneys, and the discrepancy between insulin and C-peptide levels was most likely due to impaired renal function, with GFR artifactually high due to low serum creatinine level from sarcopenia. This case of hypoglycemia is unusual because it was due to the co-occurrence of two unusual disorders – severe protein malnutrition following RYGB and cirrhosis due to AAT deficiency – and measurements of C-peptide and beta-hydroxybutyrate were confounded by the patient’s renal and hepatic function, respectively.