Triglycerides

High triglycerides are commonly seen in clinical practice. It can increase the risk of cardiovascular disease and certainly cause pancreatitis at extreme levels.

Please find below NLA recommendations on how to approach hypertriglyceridemia. Guidelines were published in April 2015. Text has been slightly modified for easier and succinct reading.

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EXCERPTS FROM THE GUIDELINES:

Prospective epidemiologic studies and meta-analyses have demonstrated a positive relationship between serum triglyceride levels and incidence of ASCVD, although the mechanisms responsible for this association are not fully understood. Possible pathophysiological links include (1) the atherogenicity of smaller species of triglyceride-rich remnant lipoprotein particles that may enter the subendothelial space; (2) elevated triglycerides may act a marker of increased concentrations of atherogenic particles (apo B–containing, apo C3–containing, small dense LDL particles); and (3) triglycerides are associated with other metabolic disturbances (insulin resistance, inflammation, endothelial dysfunction, hypercoagulation, and lower reverse cholesterol transport). An elevated triglyceride concentration is also a component of the metabolic syndrome.

The NLA Expert Panel agreed that an elevated triglyceride level is not a target of therapy per se, except when very high >500 mg/dL. When triglycerides are between 200-500 mg/dL, the targets of therapy are non–HDL and LDL. Fasting triglyceride levels of >500 mg/dL (and especially >1000 mg/dL) are associated with increased risk of acute pancreatitis. Although significant CHYLOMICRONEMIA generally does not occur until the fasting triglyceride level is substantially >500 mg/dL (~750 mg/dL), there is no single threshold of triglyceride concentration above which pancreatitis may occur, and it can be exacerbated by other risk factors.

A threshold of >500 mg/dL was selected to define very high triglycerides because the triglyceride level fluctuates markedly and such individuals are at risk for developing more severe hypertriglyceridemia. A cohort study that examined the risk for acute pancreatitis according to the degree of hypertriglyceridemia (triglycerides <150, 150–499, >500 mg/dL) in >65,000 subjects found a significant dose-response relationship between triglyceride concentration and incident acute pancreatitis during 15 years of follow-up.

The risk increased 4% for each 100 mg/dL increase in triglyceride level (after adjustment for covariates and removal of patients hospitalized for gallstones, chronic pancreatitis, alcohol-related comorbidities, renal failure, and other biliary diseases). Thus, when the triglyceride concentration is very high (>500 mg/dL, and especially if >1000 mg/dL), reducing the concentration to <500 mg/dL to prevent pancreatitis becomes the primary goal of therapy. There are limited clinical trial data to support the benefits of triglyceride-lowering therapy for reducing risk for pancreatitis.

 

NLA Guidelines, Part 1

Journal of Clinical Lipidology

April 2015