Abstract Introduction Hypertriglyceridemia-induced diabetic ketoacidosis (DKA) is a rare and severe metabolic emergency, particularly in solid-organ transplant recipients. Calcineurin inhibitors, mTOR inhibitors, and corticosteroids can collectively impair beta-cell function, induce insulin resistance, and promote dyslipidemia, resulting in an increased risk of new-onset diabetes after transplantation (NODAT). We present a case of hypertriglyceridemic DKA in a cardiac-transplant recipient receiving triple immunosuppression where immunosuppressive therapy could not be modified due to prior rejection history. Case Presentation A male with congenital d-transposition of the great arteries status-post Mustard palliation and orthotopic heart transplant in 2020 presented with 48 hours of nausea, vomiting, and poor oral intake. His chronic immunosuppressive regimen included tacrolimus, sirolimus, and prednisone. Laboratory evaluation revealed high-anion-gap DKA (anion gap 31, bicarbonate 9 mmol/L), HbA1c 10.8% consistent with new-onset diabetes, and severe hypertriglyceridemia (3578 mg/dL) without evidence of pancreatitis. Chest imaging showed mild pulmonary edema, necessitating cautious fluid resuscitation. An insulin infusion was initiated, resulting in rapid improvement in triglyceride levels (3578 → 1739 → 1244 mg/dL) and resolution of metabolic acidosis. Broad-spectrum antimicrobials were started due to immunosuppressed status and discontinued when infectious workup was negative. Echocardiography demonstrated preserved graft function. Transplant cardiology recommended maintaining and escalating immunosuppression due to prior rejection history, despite metabolic toxicity risk. The patient transitioned to a basal-bolus insulin regimen and was initiated on fenofibrate for persistent hypertriglyceridemia. He was discharged on tacrolimus 1.5 mg twice daily, sirolimus 1 mg daily, prednisone 5 mg daily, fenofibrate, and subcutaneous insulin with close endocrinology and transplant cardiology follow-up. Discussion This case highlights the complex interplay between immunosuppressive therapy and metabolic complications in transplant recipients. Tacrolimus and sirolimus impair pancreatic beta-cell function and increase insulin resistance, while corticosteroids worsen hyperglycemia and promote dyslipidemia. In transplant patients, modification of immunosuppression may not be feasible due to the risk of graft rejection, requiring aggressive metabolic management and multidisciplinary coordination. Early recognition of hypertriglyceridemic DKA, careful fluid management in cardiac transplant recipients, and prompt insulin therapy are essential for optimal outcomes. This abstract is funded by: None
Urooj et al. (Fri,) studied this question.
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