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[Treatment of hypertriglyceridemia. Current aspects]
M Malaguarnera1, I Giugno, P Ruello
1Istituto di Medicina Interna e Geriatria, Università, Catania. malaguar@mbox.unict.it
Insights
Hypertriglyceridemia contributes to atherosclerosis through various mechanisms. Effective treatments include lifestyle changes and medications like statins, fibrates, and omega-3 fatty acids, particularly for resistant cases.
Area of Science:
- Cardiology
- Metabolic Disorders
- Pharmacology
Background:
- Hypertriglyceridemia is linked to atherosclerosis via low HDL-c, altered LDL-c quality, hemostasis changes, and comorbidities like obesity and hypertension.
- It presents as primary (genetic) or secondary (metabolic disease consequence), necessitating tailored treatment approaches.
Purpose of the Study:
- To review the physiopathology of hypertriglyceridemia in atherosclerosis.
- To outline treatment strategies, including diet and pharmacotherapy.
- To discuss the roles of various drugs in managing hypertriglyceridemia.
Main Methods:
- Literature review of hypertriglyceridemia's role in atherosclerosis.
- Analysis of treatment guidelines and pharmacological interventions.
- Comparison of drug efficacy in reducing triglyceride levels.
Main Results:
- Hypertriglyceridemia involves multiple atherothrombotic pathways.
- Treatment is recommended for diet-resistant cases and those with additional risk factors.
- Key drugs include omega-3 fatty acids, nicotinic acid, fibrates, and statins.
Conclusions:
- Pharmacological therapy for hypertriglyceridemia is reserved for resistant cases and high-risk individuals.
- Specific drugs like acarbose, atorvastatin, and cerivastatin show efficacy in reducing triglycerides and VLDL synthesis.
Abstract:
The hypertriglyceridemia attends the physiopathology of the atherosclerosis by various mechanisms: association of low levels of high density lipoprotein-cholesterol (HDL-c), modification of quality of low density lipoprotein-cholesterol (LDL-c), influence on hemostatic processes, association with other hazard's factors (obesity, hypertension, etc.). The hypertriglyceridemia distinguishes in primary and secondary. In primary forms the origin is essentially genetic, while the secondary ones are metabolic consequence of various pathologies (renal, thyroid, diabetes mellitus etc.). The hypertriglyceridemia's treatment is founded on a correct feeding and/or on eventual use of drugs. Apart from the secondary forms, in which is obligatory to treat at first the basal disease, the pharmacological therapy of the hypertriglyceridemia is suggested only in resistant cases to alone dietetic therapy and overall in presence of other factors of atherothrombotic hazard. The most utilized drugs are: omega-3 fatty acids, the nicotinic acid and its derivatives, the fibrates and the statins. The stronghold of alpha-glucosidases inhibitors is the acarbose. It reduces the biosynthesis of very low density lipoproteins (VLDL) by the reduction of substrata with an improvement of glucidic metabolism. Atorvastatin and cerivastatin develop a greater action to reduce serum levels of triglycerides as to the foregoing ones because of the better selectivity of receptor binding, the greater halflife and inhibition of the apolipoprotein's B100 synthesis.