Effect of oestrogen replacement therapy on serum lipid profile

Abstract

Oestrogen replacement therapy either via oral or transdermal route has a beneficial effect on serum lipid profile of menopausal women. Whereas the oral route is more effective in increasing HDL cholesterol levels, the transdermal route is better for reducing the serum triglyceride level; hence, the latter should be the route of choice in women with high serum triglyceride levels.

Effects of raloxifene, hormone therapy, and soy isoflavone on serum high-sensitive C-reactive protein in postmenopausal women

“…The oral administration of estrogens for HT causes an increase in serum triglyceride concentrations [24]. However, the type of estrogen given with or without progesterone, and/or the type of progesterone associated with the estrogen, may also affect the total effects of HT.…”

The Role of Sex Hormones in Diabetic Retinopathy

“…Some controversy has arisen over the delivery method of HRT. Nanda et al found that HRT transdermal therapy (estrogen 50 µg/day) had the advantage of lowering triglyceride levels as opposed to oral (conjugated equine estrogens 0.625mg/day) (Nanda et al 2003). The Women's Health Initiative (WHI) trial and the Heart and Estrogen/Progestin Replacement Study (HERS) found that a favorable lipid profile developed using exogenous estrogens, but also found using estrogen with progestin was associated with elevated levels of CVD.…”

Effect of sexual steroids on the calcium content of aortic atherosclerotic plaque of oophorectomized rabbits

“…First, the women studied were older (average, 63.3 years), a period of time when tromboembolic events are more frequent; second, the control group used statins to a greater extent, and third the doses of steroids prescribed were high. In fact, regarding the steroid doses, it is known that estrogens, depending on the type, dose and method of administration increase high density lipoprotein (14) and reduce low density lipoprotein (15), while progestagens, depending on the type and dosage, can antagonize the beneficial effects of estrogen.…”

“…In the present study, this relation was also expected but, in fact, it did not occur. Possible explanations for this outcome include the antioxidant effects of estrogens and other effects such as alterations in the catabolism of low density lipoprotein (14), increase in high density lipoprotein (15), disturbance in the production of nitric oxide (16,17) and the antiatherogenic effects of estrogens, like those related to cellular proliferation of the neointima (18,19).…”