Discussion
High triglyceride levels can stem from primary factors in fewer than 5% of cases, often linked to genetic reasons. More commonly, however, hypertriglyceridemia is secondary to various factors such as diabetes, obesity, pregnancy, excessive carbohydrate intake, hypothyroidism, alcohol consumption, hepatitis, sepsis, renal failure, and specific medications, including estrogen, glucocorticoids, β blockers, bile acid binding resins, thiazides, tamoxifen, cyclosporine, protease inhibitors, and isotretinoin (8). Hypertriglyceridemia is the third most common cause of acute pancreatitis, following alcohol and gallstones, and is classically considered a risk factor only when its levels are higher than 1000 mg/dl. (1,9) However, the case described above alerts us to the possibility of acute pancreatitis as a sequela of moderate hypertriglyceridemia.
Pancreatitis secondary to hypertriglyceridemia can sometimes be suspected during physical examination by detecting eruptive xanthomas or lipemia retinalis. Significant increases in triglyceride levels can lead to falsely low serum amylase and lipase, potentially necessitating reliance on pancreatic CT scans for diagnosis. (3)
Early management of acute pancreatitis and prevention of its complications are the mainstay of treatment. Initiation of conservative treatment, including aggressive intravenous hydration, initial bowel rest, and pain control, needs to be done soon after the diagnosis is suspected. In addition, several treatment modalities like insulin and heparin, plasmapheresis, combined blood purification therapy (CBPT), High-Volume Hemofiltration (HVHF), and Hemoperfusion (HP) have been described for the targeted treatment of hypertriglyceridemic pancreatitis. (10)
An observational study published by Nawaz et al. prospectively enrolled acute pancreatitis patients and categorized them into mild, moderate, and severe based on serum triglyceride levels. The study concluded that elevated serum triglycerides are independently associated with the development of complications like persistent organ failure, regardless of the underlying etiology of acute pancreatitis. Thus, targeting triglyceride-induced lipotoxicity could present an appealing approach for creating new interventions to treat acute pancreatitis.(11)