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Part 1 Hormone replacement therapy and general medical practice
Appropriate management of HRT in the primary care setting Part 2 Hormone replacement therapy, cardiovascular health and bone density
Hormone replacement therapy and the postmenopausal cardiovascular system: metabolic basis and clinical implications Fracture reduction and bone density protection – maximising the impact of HRT Part 3 Hormone replacement therapy, the endometrium and haematological
Thrombophilia, thromboembolism and hormone replacement therapy: an exposition of current knowledge Part 4 Hormone replacement therapy, ‘neuroprotection’ and chemoprevention
of colorectal malignancy
Dene Robertson, Jacqueline Compton and Declan Murphy Hormone replacement therapy and its putative protective effect in colorectal cancer: aetiological basis and clinical significance Part 5 The menopause, treatment options and patient education
Increasing adherence to appropriate therapy: strategies for effective patient education on the use of conventional and alternative therapies Part 6 Effectiveness and efficiency of menopause services
The structure of an effective service: the theoretical basis and practical organisation of a multidisciplinary menopause clinic vi Contents
Cost-effectiveness of HRT for menopausal symptoms and fracture prevention Rachael L Fleurence and David J Torgeson Appropriate management of HRT in the primary care setting 13
Hormone replacement therapy and the postmenopausal cardiovascular system 25
synthesis of apolipoprotein AI, the main protein component of HDL and HDL .
Transdermal estradiol appears to have a less marked effect on HDL-cholesterol thanoral oestrogen (Crook et al. 1992). However, it does increase HDL , and also causes a reduction in HDL . HDL contains a significant amount of apolipoprotein AII, increased levels of which are associated with vascular lesions in animal models.
Thus, a reduction in HDL could theoretically be a beneficial effect for CHD risk. The type and route of administration of oestrogen determine its effects on triglycerides. As triglycerides may be a particular risk factor for CHD in women, thisis of potential importance. Increased endogenous triglyceride levels are associatedwith low HDL and HDL -cholesterol, insulin resistance and adverse changes in haemostatic parameters. Increased intake of exogenous triglycerides results in increased chylomicron remnants, which themselves are atherogenic. However, oestrogens primarily affect endogenous triglyceride concentrations.
Conjugated equine oestrogens cause an increase in triglycerides (Crook et al. 1992),an effect that is pharmacological, resulting from the hepatic first-pass effect of thissteroid. Orally administered estradiol has a smaller effect on raising triglycerides,although transdermal estradiol causes a reduction in triglycerides (Crook et al. 1992),which is a physiological effect of oestrogen. Progestogens have differing effects on lipids and lipoproteins, depending on their androgenicity and perhaps on their overall dosage (Stevenson 1997). The addition ofprogestogens to oestrogen therapy has no adverse effect in terms of lowering LDLbecause, although they increase LDL production, they also increase its clearance.
Androgenic progestogens, such as norgestrel, reverse the HDL-raising effect ofoestrogen (Crook et al. 1992) because they increase hepatic lipase activity. It is notknown whether this reduction in HDL reflects any impairment in remnant clearanceor in reverse cholesterol transport, so the clinical significance of lowering HDLremains to be determined. In contrast, certain non-androgenic progestogens, such asdydrogesterone, have little negative impact on oestrogen-induced increases in HDLand HDL (Crook et al. 1997), whereas others, such as medroxyprogesterone acetate, clearly attenuate the increases. Testosterone-derived progestogens, such as levonorgestrel, decrease triglyceride levels by reducing secretion of very-low-density lipoprotein (VLDL). C-21 progestogens do not prevent the increase intriglycerides induced by oral oestrogens. Thus, combined oestrogen/progestogenHRT may lead to an increase in HDL, but at the expense of an increase in triglycerides, or lead to a decrease in triglycerides at the expense of a decrease, or noincrease, in HDL. Which change is more important in terms of CHD benefit remainsunknown. When all these changes in lipids and lipoproteins are considered together,however, the various changes seen with most HRT combinations are likely to be beneficial overall, although, in certain situations, some HRT regimens will be potentially more beneficial than others.
Insulin resistance is considered to be a pivotal metabolic disturbance in the pathogenesis of CHD (Godsland & Stevenson 1995). Women with diabetes have a 34 John C Stevenson
Proudler AJ, Felton CV, Stevenson JC (1992). Ageing and the response of plasma insulin, glucose and C-peptide concentrations to intravenous glucose in postmenopausal women.
Clinical Science 83, 489–494
Proudler AJ, Ahmed AIH, Crook D, Fogelman I, Rymer JM, Stevenson JC (1995). Hormone replacement therapy and serum angiotensin-converting enzyme activity in postmenopausal
women. The Lancet 346, 89–90
Psaty BM, Heckbert SR, Atkins D et al. (1994). The risk of myocardial infarction associated with the combined use of estrogens and progestins in postmenopausal women. Archives of
Internal Medicine
154, 1333–1339
Roque M, Heras M, Roig E et al. (1998). Short-term effects of transdermal estrogen replacement therapy on coronary vascular reactivity in postmenopausal women with
angina pectoris and normal results on coronary angiograms. Journal of the American
College of Cardiologists
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Rosano GMC, Sarrel PM, Poole-Wilson PA, Collins P (1993). Beneficial effect of oestrogen on exercise-induced myocardial ischaemia in women with coronary artery disease. The
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Rosano GM, Caixeta AM, Chierchia S et al. (1997). Short-term anti-ischemic effect of 17β- estradiol in postmenopausal women with coronary artery disease. Circulation 96,
Sack MN, Rader DJ, Cannon RO (1994). Oestrogen and inhibition of oxidation of low- density lipoproteins in postmenopausal women. The Lancet 343, 269–270
Schuster H, Wienker TF, Stremmler U, Noll B, Steinmetz A, Luft FC (1995). An angiotensin- converting enzyme gene variant is associated with acute myocardial infarction in women
but not in men. American Journal of Cardiology 76, 601–603
Shibata M, Lees B, Collins P, Stevenson J, Mister R, Flather M (2001). Prevention of cardiovascular disease in women: evidence for the use of hormone replacement therapy.
Journal of the British Menopause Society 17, 33–37
Spellacy WN, Buhi WC, Birk SA (1972). The effects of estrogens on carbohydrate metabolism: glucose, insulin and growth hormone studies on one hundred and seventy one
women ingesting Premarin, mestranol and ethinyl estradiol for six months. American
Journal of Obstetrics and Gynecology
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Spencer CP, Godsland IF, Cooper AJ, Ross D, Whitehead MI, Stevenson JC (2000). Effects of oral and transdermal 17β-estradiol with cyclical oral norethindrone actetate on insulin
sensitivity, secretion, and elimination in postmenopausal women. Metabolism 49, 742–747
Stampfer MJ & Colditz GA (1991). Estrogen replacement therapy and coronary heart disease: a quantitative assessment of the epidemiologic evidence. Preventative Medicine 20, 47–63
Stampfer MJ & Grodstein F (1994). Role of hormone replacement in cardiovascular disease.
In: Lobo RA, ed. Treatment of the Postmenopausal Woman: Basic and clinical aspects.
New York: Raven Press, pp 223–233 Stefano GB, Prevot V, Beauvillain JC et al. (2000). Cell-surface estrogen receptors mediate calcium-dependent nitric oxide release in human endothelia. Circulation 101, 1594–1597
Stevenson JC (1996). Metabolic effects of the menopause and oestrogen replacement. In: Barlow DH (ed.) Baillière’s Clinical Obstetrics and Gynaecology. The menopause: keyissues. London: Ballière Tindall, pp 449–467 Stevenson JC (1997). Hormone replacement therapy and lipids. Menopause Review 2, 15–20
Stevenson JC (2000). Cardiovascular effects of estrogens. Journal of Steroid Biochemistry and
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