MON-613 - Persistent Hypoglycemia Secondary to Infliximab Therapy: A Rare but Clinically Relevant Case Report

Hypoglycemia in non-diabetic adults is uncommon and may result from hyper insulinemic states, adrenal insufficiency, critical illness, or medication side effects. We present a 35-year-old male with inflammatory bowel disease who developed recurrent hypoglycemia following infliximab therapy.

A 35-year-old man with past medical history of inflammatory bowel disease (IBD), opioid dependance on methadone, chronic anemia, hypertension, and hyperlipidemia presented with recurrent bloody diarrhea requiring transfusions. Colonoscopy confirmed IBD, and infliximab was initiated. After two infusions, he developed recurrent hypoglycemia, prompting discontinuation of therapy and initiation of prednisone 40 mg daily. Soon after discharge, patient returned with chest pain and was diagnosed with non–ST elevation myocardial infarction and triple-vessel coronary artery disease, requiring transfer for coronary artery bypass graft (CABG) evaluation. During early hospitalization, he continued to have hypoglycemia with fingerstick glucose as low as 45mg/dL (74-200mg/dL), prompting Endocrinology consultation. He reported hypoglycemia with glucose values as low as 40 mg/dL (70–99 mg/dL) during prior hospitalization. Symptoms included diaphoresis, tremulousness, and dizziness, which resolved with improvement of glucose levels. He denied history of diabetes or insulin/sulfonylurea exposure.

Initial work up revealed C-peptide of 4.8 ng/mL (1.0 – 5.0 ng/mL) and insulin of 12.6 µIU/mL (2–25 µIU/mL), both collected after correction of hypoglycemia and venous glucose 171mg/dL (59-140mg/dL). Further investigation showed A1C 4.5% ( < 5.7%), creatinine 0.5mg/dL (0.5-1.3mg/dL), and normal thyroid and liver function test. Cortisol could not be evaluated due to high-dose prednisone therapy. CT scan showed fatty liver without focal mass, unremarkable adrenal glands and pancreas without masses.

Oral intake optimized, resolving hypoglycemia. The patient was advised to eat every 4–6 hours and avoid large carbohydrate loads. CABG surgery was deferred until steroid taper; he was discharged with cardiology and gastroenterology follow-up.

Our case highlights a rare but important metabolic effect of infliximab, recurrent symptomatic hypoglycemia in a nondiabetic patient. Resolution after drug discontinuation, along with exclusion of other causes, including renal/hepatic dysfunction, adrenal insufficiency or pancreatic neoplasm, supports a causal link. TNF-α inhibition reverses inflammation-driven insulin resistance, enhancing insulin signaling and GLUT4-mediated glucose uptake, which can trigger hypoglycemia, especially during catabolic states like IBD flares. Patients with diabetes starting infliximab require close glucose monitoring and timely insulin dose adjustments, as failure to anticipate this may cause iatrogenic hypoglycemia from relative over-replacement.

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