Lipoprotein (a) concentrations in postmenopausal women taking norethisterone.

Farish, E; Rolton, Hilary A.; Barnes, Judith; Hart, D.M.

doi:10.1136/bmj.303.6804.694

Cited by 114 publications

(34 citation statements)

References 4 publications

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“…13 However, nonspecific receptor pathways have also been suggested. 5 -6 centrations increase in early pregnancy 15 and decrease after administration of norethisterone 16 or anabolic steroids. 17 A role for gonadal steroids in the regulation of Lp(a) has recently been emphasized by the marked effect of estrogen treatment and orchidectomy on Lp(a) concentrations in men with prostatic carcinoma.…”

mentioning

confidence: 99%

Growth hormone treatment of growth hormone-deficient adults results in a marked increase in Lp(a) and HDL cholesterol concentrations.

Edén

Wiklund

Oscarsson

et al. 1993

Arterioscler Thromb

208

108

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The effects of growth hormone treatment of adults with adult-onset pituitary insufficiency on lipoproteins and apolipoproteins were investigated. Nine patients, one women and eight men (age range, 34-58 years), who had been treated for pituitary tumors were studied. They had complete pituitary insufficiency with a duration of at least 1 year. All patients received replacement therapy with thyroid hormones, glucocorticoids, and gonadal steroids. The study had a double-blind, placebo-controlled, crossover design for active treatment with recombinant human growth hormone (0.25-0.5 units/kg per week s.c given each evening) for 6 months. Fasting serum levels of cholesterol; triglycerides; high density lipoprotein and low density lipoprotein cholesterol; apolipoproteins A-I, B, and E; and lipoprotein (a) were measured before and after 6 and 26 weeks of treatment Lipoprotein (a) concentrations increased markedly during treatment and were about twice as high compared with pretreatment levels. Serum cholesterol and low density lipoprotein cholesterol concentrations were decreased after 6 weeks of treatment, but levels had returned to pretreatment levels after 26 weeks. High density lipoprotein cholesterol concentrations increased during treatment and were significantly higher than pretreatment levels after 26 weeks of treatment Serum trigiyceride concentrations did not change significantly, but in two patients with marked hypertriglyceridemia, growth hormone treatment resulted in a marked decrease. Serum concentrations of apolipoproteins A-I, B, and E did not change significantly, but changes in apolipoprotein A-I and B concentrations were in parallel to those observed for high density lipoprotein cholesterol and low density lipoprotein cholesterol, respectively. These results suggest that growth hormone is a major regulator of lipoprotein metabolism and also demonstrate that lipoprotein (a) concentrations are regulated by growth hormone. (Arteriosclerosis and Thrombosis 1993;13:296-301) KEY WORDS • lipoproteins • growth hormone • hypopituitarism F ew human studies have been performed on the effects of growth hormone (GH) on the different lipoprotein fractions and apolipoprotein levels. Moreover, studies on the effects of GH on the regulation of serum lipid levels have given conflicting results. However, both GH excess, as in acromegaly, 1 and deficiency 2 result in an increased risk of death due to cardiovascular disorders, which might indicate a role for GH in the control of lipoprotein metabolism in humans.Several recent publications have reviewed the genetics, biochemistry, and possible role in arteriosclerosis and thrombogenesis of lipoprotein (a) (Lp[a]). 3~6 The plasma concentration of Lp(a) is mainly genetically From the Department of Physiology (S.E., J.O.), the

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confidence: 99%

Growth hormone treatment of growth hormone-deficient adults results in a marked increase in Lp(a) and HDL cholesterol concentrations.

Edén

Wiklund

Oscarsson

et al. 1993

Arterioscler Thromb

208

108

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“…1318 Recently, epidemiological investigations have reported that concentrations of Lp(a) are higher in postmenopausal women than in premenopausal women 19 and that postmenopausal women taking female sex hormones have lower Lp(a) levels than those not taking such medication. 20 Small-sized studies 21 - 22 also show that hormone replacement therapy (HRT) in postmenopausal women lowers the concentration of Lp(a) markedly.…”

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confidence: 99%

Effects of hormone replacement therapy on lipoprotein(a) and lipids in postmenopausal women.

Kim¹,

Jang²,

Cho³

et al. 1994

Arterioscler Thromb

112

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High concentrations of lipoprotein(a) [Lp(a)], an independent risk factor for atherosclerosis, cannot be managed by the usual lipid-lowering agents. It has been suggested that Lp(a) levels are related to female sex hormones. Estrogen replacement therapy makes the lipid profiles favorable for delaying atherosclerosis in postmenopausal women. The effects of the combination therapy of estrogen and progesterone on lipids are controversial. This study was designed to evaluate the effect of female sex hormones on the concentration of Lp(a) and to clarify the influence of progesterone on the effect of estrogen in postmenopausal women. Postmenopausal women (n=184) were divided into four groups: control; 0.625 mg conjugated equine estrogen (CEE) plus 10 mg medroxyprogesterone acetate (MPA); 0.625 mg CEE plus 5 mg MPA; and 0.625 mg CEE only. Medication for 2 months lowered the concentrations of Lp(a) by 20% in all treated groups. The decrease was more pronounced in subjects with a relatively higher basal Lp(a) concentration. Estrogen replacement therapy raised the concentration of high-density lipoprotein cholesterol and decreased low-density lipoprotein cholesterol without changing total cholesterol. The combination therapy of estrogen and progesterone abolished the effect of estrogen on highdensity lipoprotein cholesterol. Hormone replacement therapy lowered Lp(a) levels in postmenopausal women. The effect was prominent in subjects with high basal Lp(a) levels. This decrease may be one of the mechanisms of the cardioprotective effects of estrogen. The cardioprotective effect of estrogen cannot be applied to the combination therapy due to the adverse effect of progesterone on high-density lipoprotein cholesterol. Premenopausal women have lower cardiovascular morbidity and mortality than men of a similar age. After menopause, the incidence of cardiovascular diseases increases and no difference is noticed during the eighth decade between men and women. 23 Female sex hormones have been used for the alleviation of postmenopausal symptoms and the treatment of osteoporosis. Most but not all reports have shown that estrogen replacement therapy in postmenopausal women re-

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“…Use of norethisterone, a synthetic gestagen, is associated with a decreased concentration of serum Lp(a) in postmenopausal women (33). These findings suggest that hormones in breast milk may at least to some extent account for its Lp(a) lowering effects.…”

Section: Relative Change (%)mentioning

confidence: 89%