6666 Asymptomatic Fasting Hypoglycemia After Sleeve Gastrectomy
Authors: Mitrollari Kristjana , Deveaux Hillary Kieran , Gundeti Anjali , Calimag Angela Pauline , Yasmeen Tahira 
Published: October 2024

Disclosure: K. Mitrollari: None. H.K. Deveaux: None. A. Gundeti: None. A.P. Calimag: None. T. Yasmeen: None.

Introduction: Post-bariatric surgery hypoglycemia (PBSH), though previously considered rare, is increasingly recognized, occurring not only after Roux-en-Y gastric bypass (RYGB,) but also following various bariatric procedures. PBSH can manifest as postprandial or fasting hypoglycemia, requiring thorough investigation and prevention due to potential asymptomatic presentations that may lead to severe consequences, including coma and death. Case Report A 45-year-old female with a history of type 2 DM, ESRD on HD, gastric sleeve surgery, bilateral trans-metatarsal amputations, coronary artery disease, and congestive heart failure presented with bilateral lower extremity wounds. On admission her venous blood glucose was 71 mg/dL. Glycohemoglobin was 3.9% and fructosamine was 225 (205-285 umol/L). Her glycohemoglobin levels consistently remained below 6.4% status post sleeve gastrectomy off diabetes medications. Throughout admission, she experienced almost daily episodes of fasting asymptomatic hypoglycemia correlated with venous sample with lowest blood glucose reading 38 mg/dL. Initially, these episodes were attributed to NPO status for procedures or decreased PO intake. Her diet consisted of fast food brought by her family, which she reported was similar to her diet at home. Workup during a hypoglycemic episode (glucose 51 mg/dL,) revealed insulin 4 mUnits/L, proinsulin 7.1 pmol/L (&lt;=7.2 pmol/L), C-peptide 25.7 ng/mL (0.8-3.9 ng/mL), and beta-hydroxybutyrate 0.5 mmol/L (0.0-0.3 mmol/L). Negative insulin antibodies and sulfonylurea panel, normal cortisol, and ACTH levels were noted. The patient was placed on a 10% dextrose infusion to avoid further episodes of hypoglycemia. However, she continued to experience hypoglycemia and was started on oral diazoxide. A CT pancreas with and without contrast was unremarkable, and endoscopic ultrasonography only revealed a 10 mm accessory spleen. The patient was discharged with counseling on glucose monitoring, dietary changes, and follow-up with endocrinology. Conclusion: PBSH should be considered as a differential diagnosis in patients with unexplained hypoglycemia and a history of bariatric surgery. PBSH mimics insulinoma or non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS) with elevated insulin, proinsulin, C-peptide, and low beta-hydroxybutyrate during hypoglycemia, however NIPHS is exclusive to non-bariatric patients. Imaging is crucial to rule out insulinoma, and invasive tests such as endoscopic ultrasound aid diagnosis. PBSH is a diagnosis of exclusion; therefore, workup involves ruling out other causes of hypoglycemia. First-line treatment involves diet modification, with medications like diazoxide or acarbose considered if dietary changes prove insufficient. This case underscores the complexity of hypoglycemia, implicating bariatric surgery as a contributing factor.

Presentation: 6/3/2024