Hypertriglyceridemia

Background

• ~5% of acute pancreatitis caused by high triglycerides
• Etiologies
  • Familial hypertriglyceridemia, autosomal dominant with variable penetrance
  • Secondary forms
    • DM, obesity, EtOH, estrogen therapy
    • Hypothyroidism, ESRD, nephrotic syndrome, HIV, anti-HIV meds
• TG levels > 2000mg/dL almost always have both secondary and genetic form
• 1.7% of US estimated to have [TG] between 500-2000

• May present with normal serum lipase levels

Pathophysiology

• Excess TG hydrolyzed by increased concentration of pancreatic lipase
• Produces increased concentration of free fatty acids that exceeds binding capacity of albumin
• Micelles are formed that attack platelets, vascular endothelium and acinar cells
• Ischemia and pancreatic injury result
• An acidic environment potentiates free fatty acid toxicity

Management

Management of acute pancreatitis in the setting of hypertriglyceridemia

• Evidence for management based on case series and reports
• Insulin drip - most dramatic and rapid intervention, with reduction within 24 hrs
  • 5-10 units/hr with or without dextrose infusion to maintain BSs ~150mg/dL
  • May require higher dosages for diabetics, 0.1–0.3 U/kg/hr
  • Titrate to BS 140–180mg/dL
• Treat concurrent hypothyroidism if present
• Pain control
• Niacin 500mg QD
• Gemfibrozil or fenofibrate
• Max dose statin, 81mg ASA
• Heparin q8 SC, effect short-lived
• NPO initially
• May advance diet starting at TG level < 1000mg/dL with resolution of abdominal pain/pancreatitis symptoms
  • No fat diet
  • Low calorie diet
• Follow TG levels, goal < 500-1000mg/dL by discharge

Plasma exchange

• Therapeutic plasma exchange, for 1-3 days (sickest patients)
• For euglycemic patients, not routine first line
• Requires central venous access

Disposition

• Asymptomatic hypertriglyceridemia is treated as an outpatient
• For acute pancreatitis, ICU or step-down for frequent labs, insulin drip

See Also

• Acute pancreatitis