Hypertriglyceridemia (HTG) is a well established but underestimated cause of acute (AP) and recurrent AP (RAP). The clinical presentation of HTG-induced pancreatitis (HTG pancreatitis) is similar to other causes. Pancreatitis secondary to HTG is typically seen in the presence of one or more secondary factors (uncontrolled diabetes, alcoholism, medications, pregnancy) in a patient with an underlying common genetic abnormality of lipoprotein metabolism (Familial combined hyperlipidemia or Familial HTG). Less commonly, a patient with rare genetic abnormality (Familial chylomicronemic syndrome) with or without an additional secondary factor is encountered. The risk of AP in patients with serum triglycerides >1000 mg/dl and >2000 mg/dl is ∼5% and 10-20% respectively. It is not clear whether HTG pancreatitis is more severe than when it is due to other causes. Clinical management of HTG pancreatitis is similar to that of other causes. Insulin infusion in diabetic patients with HTG can rapidly reduce triglyceride levels. Use of apheresis is still experimental and better designed studies are needed to clarify its role in management of HTG pancreatitis. Diet, lifestyle changes, control of secondary factors are key to the treatment and medications are useful adjuncts to long term management of triglyceride levels. Control of triglyceride levels to well below 500 mg/dl can effectively prevent recurrences of pancreatitis.

Hypertriglyceridemia (HTG) is a rare cause of pancreatitis. Pancreatitis secondary to HTG, presents typically as an episode of acute pancreatitis (AP) or recurrent AP, rarely as chronic pancreatitis. A serum triglyceride (TG) level of more than 1,000 to 2,000 mg/dL in patients with type I, IV, or V hyperlipidemia (Fredrickson's classification) is an identifiable risk factor. The typical clinical profile of hyperlipidemic pancreatitis (HLP) is a patient with a preexisting lipid abnormality along with the presence of a secondary factor (e.g., poorly controlled diabetes, alcohol use, or a medication) that can induce HTG. Less commonly, a patient with isolated hyperlipidemia (type V or I) without a precipitating factor presents with pancreatitis. Interestingly, serum pancreatic enzymes may be normal or only minimally elevated, even in the presence of severe pancreatitis diagnosed by imaging studies. The clinical course in HLP is not different from that of pancreatitis of other causes. Routine management of AP caused by hyperlipidemia should be similar to that of other causes. A thorough family history of lipid abnormalities should be obtained, and an attempt to identify secondary causes should be made. Reduction of TG levels to well below 1,000 mg/dL effectively prevents further episodes of pancreatitis. The mainstay of treatment includes dietary restriction of fat and lipid-lowering medications (mainly fibric acid derivatives). Experiences with plasmapheresis, lipid pheresis, and extracorporeal lipid elimination are limited.

Among adverse drug reactions, pancreatitis is often-ignored because of the difficulty in implicating a drug as its cause. The physician should have a high index of suspicion for DIP, especially in specific subpopulations such as geriatric patients who may be on multiple medications, HIV+ patients, cancer patients, and patients receiving immunomodulating agents.