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)