Table 1.

Pharmacological treatment options for SHGT

Treatment modality	Mechanism of action	Comments	Limitations
Fibrates	Increase of LPL level, decrease in hepatic TG synthesis by induction of hepatic FFA oxidation, and stimulation of reverse cholesterol transport	Considered drugs of first choice	Slow onset of TG lowering
Nicotinic acid	Reducing VLDL secretion via receptor	Reliable long-term effect on TG level	Prominent side effects such as facial flushing, slow onset of TG lowering
HMG-CoA reductase inhibitors	Inhibition of cholesterol synthesis	Only of use in combination with other drugs such as fibrates in order to achieve synergistic effects	Higher risk of myositis or myopathy, no drug of first choice
Omega-3-FA	Reduced hepatic TG synthesis, enhanced peroxisomal b-oxidation, increased LPL activity and adipose tissue LPL expression	Potent drug with no side effects, immediate onset of action	No limitations
MCT	No chylomicron formation, no chylomyicron synthesis, induction of michondrial b-oxidation of FA	Immediate onset of action on TG levels	No limitations
Insulin	Activation of LPL (acceleration of chylomicron degradation)	Useful especially in the treatment of poorly controlled diabetic subjects with HTG	Only of limited efficiency
Heparin	Stimulation of release of endothelial LPL	Not recommended as a monotherapy	Cave: increased LPL degradation and depletion of LPL plasma stores

Note carefully that conventional treatment of any comorbidity, e.g., pancreatitis is imperative as well as screening for secondary causes of HTG and treatment of the underlying disease

LPL lipoprotein lipase;TG triglycerides;FA fatty acids;FFA free fatty acid;VLDL very low density lipoproteins;HMG-CoA hydroxy-methylglutaryl-coenzyme-A;MCT medium-chain triglycerides;HTG hypertriglyceridemia