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PubMed · 9564230

[How I study hypertriglyceridemia].

Abstract

The strategy for the diagnosis of hypertriglyceridaemia comprises three successive steps. First, the physician should confirm the biological abnormality by at least one additional blood sample taken after an overnight fast; recent data, however, suggest that postprandial hypertriglyceridaemia may also represent a cardiovascular risk factor. Second, the phenotype of hypertriglyceridaemia should be considered as either isolated high triglyceride levels or hypertriglyceridaemia combined with hypercholesterolemia may be present; the combination of hypertriglyceridaemia with a low HDL cholesterol concentration or its association with the metabolic or insulin resistance syndrome should also be investigated. Third, all should be done in order to find the etiology of the hypertriglyceridaemia (by determining its genetic or nutritional origin, by excluding possible underlying pathologies, by looking for drugs able to increase serum triglyceride levels). These various steps should help the physician to take the final decision of treating one particular patient as well as to chose the most appropriate, nutritional or pharmacological, treatment.

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BibTeXRIS

A J Scheen. 1998. [How I study hypertriglyceridemia].. https://pubmed.ncbi.nlm.nih.gov/9564230/

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Changes in normal lipid profile of menopausal women with combined hormone replacement therapy. Comparative clinical trial of two hormonal combinations (conjugated estrogens/medroxyprogesterone acetate versus estradiol valerate/cyproterone acetate).

OBJECTIVES: To compare the effect on plasma lipids of conjugated estrogens/medroxyprogesterone acetate (CE/MPA) and estradiol valerate/cyproterone acetate (EV/CPA) in healthy peri and postmenopausal women during 1 year. METHODS: Multicentric, controlled, single blinded Phase III clinical trial. Women were randomized to two treatment groups: Group A (n = 49 women): CE 0.625 mg/day for 21 days and MPA 5 mg from day 12 to 21. Group B (n = 55 women): EV 2 mg/day for 21 days and CPA 1 mg from day 12 to 21. Total cholesterol (TC), high density cholesterol (HDL-C), low density cholesterol (LDL-C), triglycerides, aminotransferases and alkaline phosphatase were measured before starting therapy, and after 3, 6, 9 and 12 months of hormone replacement therapy (HRT). TC/HDL-C and LDL-C/HDL-C ratios were determined. RESULTS: There were no changes in TC levels. HDL-C increased and LDL-C decreased significantly, with no differences between groups but within each group. Triglycerides increased significantly but remained within normal values, with no differences between groups. TC/HDL-C ratio showed a slight and steady decrease in both groups. LDL-C/HDL-C ratio decreased in both treatment groups. CONCLUSION: Both cyclic sequential preparations used in HRT showed a favorable effect on plasma lipids in healthy peri and postmenopausal women, with an increase in HDL-C and a decrease in LDL-C levels, as well as in the LDL-C/HDL-C and TC/HDL-C ratios. Our study confirms the positive effect of estrogens on lipids, which does not seem to be adversely affected by the addition of progestogens derived from pregnanes.

Cholesterol, HDL