MON-614 - Bactrim'S Bitter Aftertaste: Trimethoprim/Sulfamethoxazole Induced Hypoglycemia

Introduction:
Trimethoprim-sulfamethoxazole (TMP-SMX) is a widely prescribed antibiotic, yet its potential to induce hypoglycemia remains underrecognized.

Case presentation:
An 82-year-old non-diabetic female presented with decreased responsiveness and confusion in the setting of hypoglycemia. Her mental status improved after glucose administration, and on exam, she was hemodynamically stable with a healing skin ulcer on the left lower extremity without signs of infection. Preliminary laboratory evaluation revealed normal electrolytes, liver and renal function. Upon further questioning, she reported having started TMP-SMX five days prior for treatment of left lower extremity cellulitis. The patient remained persistently hypoglycemic despite continuous dextrose infusion, prompting further biochemical evaluation which revealed serum glucose 52 mg/dL, insulin 29 (2.6–24.9 μU/mL), c-peptide 6.0 (1.1–4.4 ng/mL), proinsulin 17 (0–10 pmol/L), and beta-hydroxybutyrate 0.1 ( < 0.4 mmol/L), consistent with endogenous hyperinsulinemia. A negative sulfonylurea panel excluded exogenous secretagogue use. Insulinoma was deemed unlikely given the acute onset of hypoglycemia and absence of a pancreatic lesion on abdominal CT. Due to concern for TMP-SMX induced hypoglycemia, the medication was held. Within 16 hours of the last dose, her glucose levels normalized, confirming TMP-SMX as the causal agent.

Discussion:
The glucose-lowering effect of TMP-SMX is caused by its sulfamethoxazole component that shares structural similarity to sulfonylureas and thus, can stimulate pancreatic insulin release. Although rare, TMP-SMX induced hypoglycemia is likely underreported due to limited familiarity with this adverse effect and misattribution of hypoglycemia to the underlying infection being treated. Most reported cases occur in patients who are malnourished or have hepatic or renal dysfunction which can reduce drug clearance, extending the 10-hour half-life of TMP-SMX. In fact, renal dysfunction has been identified in more than 75% of documented cases. In contrast, our patient had normal renal function, which likely contributed to her relatively mild presentation, and fast resolution of hypoglycemia following drug discontinuation.

Conclusion:
TMP-SMX can precipitate hypoglycemia even in patients without risk factors, though the likelihood and severity are amplified in those with predisposing conditions. Clinicians should therefore maintain suspicion for TMP-SMX as a potential cause of unexplained or refractory hypoglycemia.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*