High triglyceride levels are commonly seen in clinical practice. It can increase the risk of cardiovascular disease, and when extremely high, it can cause acute pancreatitis.
Please find below NLA recommendations on how to manage hypertriglyceridemia. Guidelines were published on April 2015. The text has been slightly modified for easier and succinct reading.
GT
Also see:
Journal of Clinical Lipidology
Guidelines
April 2015
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
- The atherogenicity of smaller species of triglyceride-rich remnant lipoprotein particles that may enter the subendothelial space;
- Elevated triglycerides may act a marker of increased concentrations of atherogenic particles (apo B–containing, apo C3–containing, small dense LDL particles); and
- 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 an increased risk of acute pancreatitis. Although significant CHYLOMICRONEMIA generally does not occur until the fasting triglyceride level is substantial >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 the risk of pancreatitis.