Metformin is a US FDA-approved oral anti-hyperglycemic medication used to treat non-insulin-dependent diabetes mellitus (NIDDM). Metformin, a biguanide drug, works by reducing glucose production in the liver, decreasing intestinal absorption, and improving insulin sensitivity, leading to lower blood glucose levels. Metformin is generally considered to be a medication with a good safety profile and high tolerability. However, metformin therapy is associated with an uncommon but potentially serious complication known as metformin-associated lactic acidosis (MALA), which is marked by severe lactic acid accumulation in the bloodstream. This case introduces an elderly female with multiple comorbidities who presented with confusion, malaise, and lethargy. Her laboratory findings revealed acute renal failure, severe metabolic acidosis, and significantly elevated lactic acid levels consistent with sepsis and possibly MALA. Aggressive resuscitation with fluids and sodium bicarbonate was initiated. Antimicrobial drugs were started for urinary tract infections. She subsequently required endotracheal intubation with invasive ventilation, pressor support, and continuous renal replacement therapy. Her condition gradually improved over several days. The patient ultimately recovered, and at the time of discharge, metformin was discontinued, and a sodium-glucose cotransporter-2 (SGLT-2) inhibitor was initiated. This case underscores the relevance of MALA as a potential complication of metformin therapy, particularly in patients with underlying kidney disease or other risk factors. Timely detection and prompt management of MALA can prevent progression to a critical stage and thus avoid potentially fatal outcomes.
Immune checkpoint inhibitors are becoming of more use as clinicians are prescribing them for patients with different malignancies. As their use continues to increase, clinicians must be aware of the side effects, which are autoimmune in nature. Autoimmune diabetes has been described in the past while patients were being treated with programmed cell death protein 1 (PD-1) inhibitors, but it usually occurs after the patient's fourth or fifth cycle. In this case presentation, we describe a patient with no history of type 1 or 2 diabetes presenting to the emergency department with severe diabetic ketoacidosis. At the time of presentation, he was on his 22nd cycle of nivolumab for metastatic renal cell carcinoma. The patient was eventually treated successfully, but upon discharge, he was prescribed a large dose of insulin regimen to control his blood sugar levels at home. We attributed his new diagnosis of insulin-dependent diabetes to the PD-1 inhibitor nivolumab.
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