In this case, insulin therapy effectively reduced triglycerides from 65 mmol/L, preventing the need for plasmapheresis in a patient with severe hypertriglyceridaemia-induced pancreatitis.
Intravenous insulin therapy can be highly effective as first-line treatment for severe hypertriglyceridemia-induced acute pancreatitis complicated by non-cardiogenic pulmonary edema, avoiding the need for plasmapheresis.
Absolute Event Rate: 0% vs 0%
Abstract Introduction Hypertriglyceridaemia-induced acute pancreatitis (HTG-AP) accounts for up 4% of pancreatitis cases. Risk rises significantly when triglycerides exceed 11 mmol/L, though values above 50 mmol/L are rare and usually associated with severe systemic complications and multi-organ dysfunction. Pulmonary oedema, especially non-cardiogenic in origin, is an unusual and life-threatening complication that complicates acute management. Clinical Case A 30-year-old Indian man with no prior medical history presented with sudden severe epigastric pain, recurrent vomiting, and acute dyspnoea. Investigations revealed newly diagnosed diabetes mellitus (HbA1c 78 mmol/mol), acute pancreatitis (CT - showing peripancreatic inflammation), triglycerides (65 mmol/L). Despite initial resuscitation, he developed acute hypoxia with bilateral pulmonary infiltrates on chest X-ray, consistent with non-cardiogenic pulmonary oedema. Echocardiography confirmed preserved left ventricular systolic function, effectively excluding a cardiogenic cause. He was transferred to intensive care for ventilatory support. Management included variable-rate intravenous insulin infusion, and electrolyte monitoring. Insulin played a dual role: achieving glycaemic control and lowering triglycerides by enhancing lipoprotein lipase activity and accelerating clearance of chylomicrons. Over several days, triglycerides progressively declined, avoiding the need for plasmapheresis. Once stabilised, a basal-bolus subcutaneous insulin regimen was initiated, commenced on a low-fat diabetic diet, and provided with a continuous glucose monitor to support ongoing glycaemic management. Long-term therapy was planned with rosuvastatin 10 mg, lifestyle modification, and diabetes clinic follow-up. This case is remarkable for three key reasons:Severity of hypertriglyceridemia – at 65 mmol/L, far above the threshold for pancreatitis.Dual acute complications – concurrent pancreatitis and non-cardiogenic pulmonary oedema.Underlying risk factors – strong family history and South Asian ethnicity raising suspicion of familial combined hyperlipidaemia or other inherited metabolic disorder. Although plasmapheresis has been advocated in severe HTG-AP, insulin therapy proved highly effective here, emphasising its role as first-line therapy in resource-limited and urgent settings. Long-term management requires a comprehensive approach integrating lipid control, diabetes management, dietary modification, and family risk assessment. Conclusion This case illustrates an unusual and life-threatening initial presentation of diabetes with severe hypertriglyceridemia, acute pancreatitis, and non-cardiogenic pulmonary oedema. It reinforces the importance of high clinical suspicion, urgent ITU support, and early triglyceride-lowering strategies. The integration of digital glucose monitoring and specialist lipid evaluation supports recovery and optimises long-term control.
Virgo et al. (Thu,) reported a other. In this case, insulin therapy effectively reduced triglycerides from 65 mmol/L, preventing the need for plasmapheresis in a patient with severe hypertriglyceridaemia-induced pancreatitis.
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