C49-02 A Bitter Brew: Bitter Gourd Tea and Metformin-associated Lactic Acidosis

Abstract Introduction Metformin-associated lactic acidosis (MALA) is a rare but life-threatening complication of one of the most prescribed antidiabetic agents. It carries a high mortality rate and is often precipitated by kidney injury, infection, or concomitant toxin exposure. Momordica charantia, also known as bitter melon, is a popular herbal supplement believed to have glucose-lowering properties in many cultures. However, it contains cucurbitacins (triterpenoid compounds), which may be toxic, causing nausea, vomiting, abdominal pain, and hypotension. Case Presentation A 62-year-old man with a history of type 2 diabetes, hyperlipidemia, and hypothyroidism was transferred from an outside hospital in the setting of shock, renal failure, and lactic acidosis for continuous renal replacement therapy. He initially presented after several days of persistent nausea and vomiting. On presentation, he was normothermic, normotensive, tachycardic, and tachypneic. Over the next few hours, he became confused and lethargic. His physical examination was unremarkable; however, his laboratory studies were significantly abnormal. He was profoundly acidotic, with a pH of 6.74 and a pCO2 of 30 mmHg. His lactic acid level was above assay (17 mmol/L) and had acute kidney injury with a BUN of 53 mg/dL, serum creatinine of 8.5 mg/dL, an anion gap of 34, and a serum bicarbonate of 6 mmol/L. Infectious workup was negative, and imaging did not reveal any acute pathology. Despite fluid resuscitation and empiric antibiotics, he continued to deteriorate, requiring intubation and transfer for emergent dialysis. Given his hemodynamic instability and need for vasopressors, he was started on continuous renal replacement therapy. Further discussion with his wife revealed that he had been on metformin for over two decades but had recently begun taking over-the-counter supplements and consuming large quantities of bitter gourd tea for glycemic control. The temporal relationship between his supplement use and clinical deterioration raised concern for a possible interaction contributing to his metabolic decompensation. He responded well to renal replacement therapy. After a prolonged ICU stay, he was successfully extubated, transferred to the medical floor with evidence of renal recovery, and ultimately discharged to a rehabilitation facility. Conclusion “Toxic squash syndrome,” a recognized complication of certain gourds, led to acute kidney injury through dehydration from GI loses that likely precipitated the development of MALA. This case underscores the importance of identifying the risks associated with commonly used dietary supplements and their potential interactions with prescription medications. Physicians should routinely inquire about supplement use and counsel patients on possible adverse effects. This abstract is funded by: None