@2024 Afarand., IRAN
ISSN: 2251-8215 Sarem Journal of Reproductive Medicine 2017;1(2):55-58
ISSN: 2251-8215 Sarem Journal of Reproductive Medicine 2017;1(2):55-58
Postmenopausal Hormone Therapy Effect on Atherogenic Factors and Chylomicrons Levels
ARTICLE INFO
Article Type
Original ResearchAuthors
Saremi A.T. (*)Fasihi F. (1)
Safavi M. (2)
Hakak N. (2)
Ghanbari Torshaki F. (2)
(*) “Sarem Fertility & Infertility Research Center (SAFIR)” and “Sarem Cell Research Center (SCRC)”, Sarem Women’s Hospital, Tehran, Iran
(1) “Sarem Fertility & Infertility Research Center (SAFIR)” and “Sarem Cell Research Center (SCRC)”, , Sarem Women’s Hospital, Tehran, Iran
(2) Sarem Fertility & Infertility Research Center (SAFIR), Sarem Women’s Hospital, Tehran, Iran
Correspondence
Article History
Received: February 4, 2016Accepted: May 14, 2016
ePublished: June 15, 2017
BRIEF TEXT
Cardiovascular diseases are the most important cause of death in the United States that more than 50,000 deaths per year is due to this disease [1].
A large number of cardiovascular diseases occur in postmenopausal women, so that heart diseases appear in women 10 years earlier than men [2]. Menopause is part of a woman's life, that due to reduced ovarian capacity, permanent menstrual cessation occur. The average age of menopause is between 50 and 52 years old. After menopause, the amount of estrogen production by the ovaries is very small and this deficiency is associated with complications such as hot flashes, psychiatric complications, atrophic complications, osteoporosis, and cardiovascular complications [3]. The cause of most cardiovascular diseases is atherosclerosis of the large arteries [4]. Postmenopausal hormone replacement therapy is one of the major issues in women's health care. According to studies, estrogen is the key hormone in women that affects almost all cells of the body [5]. Also, estrogen has a major impact on heart disease [6]; so that prevention of cardiovascular disease is considered as the main benefit of hormone therapy [7]. Undoubtedly, cardiovascular disease is multifactor and many studies have identified the relationship between fatty factors such as triglyceride and HDL cholesterol with heart disease [8]. In fact, triglyceride levels above 150 mg / dl have a strong correlation with atherogenic changes in LDL particles, which increases the risk of coronary heart disease by 3 times [9]. In an epidemiological study, there has been an inverse association between the amount of HDL and the incidence of atherosclerosis [10]. The main anti- atherogenic property of HDL is HDL2, and there is a strong reverse relationship between HDL2 and coronary artery disease [11]. Chylomicron clearance and chylomicron residues are increased by hormone therapy, which is the protective effect of estrogen against cardiovascular disease [12]. The ratio of total cholesterol to heavy lipoprotein cholesterol is a very promising factor for coronary heart disease and suggests an increase in the risk of coronary heart disease in people between 50 and 95 years of age by increasing this ratio [13].
Considering that serum lipids are largely dependent on nutrition status, genetic status and lifestyle, and also according to researches carried out in Western countries, and in Iran there is no significant research in this field, this research was conducted with the aim of determining the effect of hormone therapy on serum lipids by educating women about the symptoms and complications of menopause and highlighting the natural points and abnormalities of the disease.
In this study, all postmenopausal women who referred to Sarem Medical Center due to complications of menopause or women's problems between the years of 1998-1997 were interviewed while receiving consent.
In the initial visit with 44 postmenopausal women, interviews and pre-treatment tests were performed on them, of which only 18 returned 6 months after treatment, 20 of whom refused to continue the study, and 5 of them only repeated second-line trials without treatment; one who was treated was excluded from the study because of the use of lipid lowering drugs.
The data was collected by a questionnaire, which included demographic characteristics (age, menopause age), blood pressure, weight, height, premenopausal disease or pre-menopausal factors, smoking, and so on. Patients had not been treated with hormone therapy for at least 3-6 months and did not use lipid lowering drugs and had a blood pressure higher than 160.95. During the examinations performed by a gynecologist, they were asked in a questionnaire about history of liver disease, thyroid disease, history of breast or endometrial cancer, and abnormal uterine bleeding, and their examination was performed that they were healthy. Also, the results of cholesterol, triglyceride, AI, RF, HDL, LDL tests and hormonal tests were recorded before and after treatment. The instrument for measuring variables were instruments for measuring height, weight, blood pressure and specific kits for measuring the level of cholesterol, triglyceride, HDL-C, LDL-C calculations using the Friedwald formula, calculating RF, AI and also the spectrophotometric apparatus Cecil 1010 for the purpose of reading blood lipid tests. One measure of lipid and lipoprotein factors RF and AI was performed before treatment, and then it was performed at least 6 months after hormonal treatment. These subjects were treated with conjugated estrogen and medroxyprogesterone daily for 6 months. Data were analyzed using T-test and Wilcoxon tests for serum total cholesterol level before and after treatment.
The mean weight of patients was 66.1 ± 13.3; mean BMI was 26 .3± 5; mean age was 48.51 ± 4.95 and the mean age of menopause was 45.10 ± 4.70. The referral was 72% due to menopause and 28% due to women's problems. The mean systolic blood pressure was 12.8 ± 1.89 and the mean diastolic blood pressure was 8.7 ± 1.1. The mean FSH in these women was 54.4 ± 3.33 and the mean LH was 26.4 ± 1.19. The mean of estradiol was 76.6 ± 24.3. T-test (p = 0.350) and non-parametric Wilcoxon test (p = 0.140) did not show a significant difference in serum total cholesterol level before and after treatment. No significant correlation was found between the replacement hormone therapy and triglyceride levels (p = 0.690), while there was a significant correlation between replacement hormone therapy and the level of triglyceride (p = 0.0001). There was a significant relationship between replacement hormone therapy and serum LDL-C (p = 0.027). Also, there was a significant correlation between alternative hormone therapy and reduction of RF (p = 0.0001) and also reduction of atherogenic index (AI) (p = 0.0001; Table 1; Figure 1).
... [14]. Sack et al. did not find any significant changes in serum cholesterol level after 3 weeks of subcutaneous hormone therapy in 18 postmenopausal women. However, other studies found contradictory results [15]. In a study conducted by Dunk in the United States in 1995, after 3 months of hormone therapy for 32 hyper-cholesterolemic postmenopausal women, mean serum cholesterol reached from 261 mg / dl to 233 mg / dl. In another study, conducted by Cressman in Sweden in 1997, after 2 months of hormone therapy for 25 postmenopausal women, serum HDL levels changed from 5.0+1.1 to 6.0 ± 1.32 mg after treatment (p<0.001) [16]. In a study conducted by Crook in London in 1997, after 6 months of hormone therapy for 29 postmenopausal women, total serum total cholesterol levels decreased by 7.3%, but their triglyceride levels did not change in comparison to the pretreatment status. The results of this study were consistent with the study of Crook and with the results of the Dank research.
HRT consumption which increases HDL and reduces LDL as one of the risk decreasing factors for coronary heart disease is suggested for postmenopausal women.
Hormone therapy increases HDLC and decreases LDLC, RF, and AI, thereby reduces the risk of cardiovascular disease in postmenopausal women.
TABLES and CHARTS
Show attach fileCITIATION LINKS
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[2]Kannel, WB, Wilson PW. Risk factors that attenuate the female coronary disease advantage. Arch Intern Med. 1995;155(1):57-61.
[3]Santoro N, Randolph JF Jr. Reproductive hormones and the menopause transition. Obstet Gynecol Clin North Am. 2011;38(3):455-66.
[4]Hodis HN, Mack WJ. Coronary heart disease and hormone replacement therapy after the menopause. Climacteric. 2009;12(Suppl 1):71-5.
[5]Alexandersen P, Karsdal MA, Christiansen c. Long-term prevention with hormone-replacement therapy after the menopause: Which women should be targeted?. Womens Health (Lond). 2009;5(6):637-47.
[6]Mendelsohn ME. Protective effects of estrogen on the cardiovascular system. Am J Cardiol. 2002;89(12A):12E-17E.
[7]Kuttenn F, Gerson M. Hormone replacement therapy of menopause, heart and blood vessels. Arch Mal Coeur Vaiss. 2001;94(7):685-9. [French]
[8]Schaefer EJ, Genest JJ Jr, Ordovas JM, Salem DN, Wilson PW. Familial lipoprotein disorders and premature coronary artery disease. Atherosclerosis. 1994;108 Suppl:S41-S54.
[9]Gofman JW, Delalla O, Glazier F, Freeman NK, Lindgren FT, Nichols AV, et al. The serum lipoprotein transport system in health, metabolic disorders, atherosclerosis and coronary heart disease. J Clin Lipidol. 2007;1(2):104-41.
[10]Jonas HA, Kronmal RA, Psaty BM, Manolio TA, Meilahn EN, Tell GS, et al. Current estrogen-progestin and estrogen replacement therapy in elderly women: Association with carotid atherosclerosis, CHS Collaborative Research Group, Cardiovascular Health Study. Ann Epidemiol. 1996;6(4):314-23.
[11]Cziraky MJ, Watson KE, Talbert RL. Targeting low HDLcholesterol to decrease residual cardiovascular risk in the managed care setting. J Manag Care Pharm. 2008;14(8 Suppl):S3-28.
[12]Suk Danik J, Rifai N, Buring JE, Ridker PM. Lipoprotein(a), hormone replacement therapy, and risk of future cardiovascular events. J Am Coll Cardiol. 2008;52(2):124-31.
[13]Urabe M, Yamamoto T, Kashiwagi T, Okubo T, Tsuchiya H, Iwasa K, et al. Effect of estrogen replacement therapy on hepatic triglyceride lipase, lipoprotein lipase and lipids including apolipoprotein E in climacteric and elderly women. Endocr J. 1996;43(6):737-42.
[14]Wagner JD, Martino MA, Jayo MJ, Anthony MS, Clarkson TB, Cefalu WT. The effects of hormone replacement therapy on carbohydrate metabolism and cardiovascular risk factors in surgically postmenopausal cynomolgus monkeys. Metabolism, 1996;45(10):1254-62.
[15]Sack MN, Rader DJ, Cannon RO 3rd. Oestrogen and inhibition of oxidation of low-density lipoproteins in postmenopausal women. Lancet, 1994;343(8892):269-70.
[16]Cressman MD, Heyka RJ, Paganini EP, O’Neil J, Skibinski CI, Hoff HF. Lipoprotein(a) is an independent risk factor for cardiovascular disease in hemodialysis patients. Circulation. 1992;86(2):475-82.
[2]Kannel, WB, Wilson PW. Risk factors that attenuate the female coronary disease advantage. Arch Intern Med. 1995;155(1):57-61.
[3]Santoro N, Randolph JF Jr. Reproductive hormones and the menopause transition. Obstet Gynecol Clin North Am. 2011;38(3):455-66.
[4]Hodis HN, Mack WJ. Coronary heart disease and hormone replacement therapy after the menopause. Climacteric. 2009;12(Suppl 1):71-5.
[5]Alexandersen P, Karsdal MA, Christiansen c. Long-term prevention with hormone-replacement therapy after the menopause: Which women should be targeted?. Womens Health (Lond). 2009;5(6):637-47.
[6]Mendelsohn ME. Protective effects of estrogen on the cardiovascular system. Am J Cardiol. 2002;89(12A):12E-17E.
[7]Kuttenn F, Gerson M. Hormone replacement therapy of menopause, heart and blood vessels. Arch Mal Coeur Vaiss. 2001;94(7):685-9. [French]
[8]Schaefer EJ, Genest JJ Jr, Ordovas JM, Salem DN, Wilson PW. Familial lipoprotein disorders and premature coronary artery disease. Atherosclerosis. 1994;108 Suppl:S41-S54.
[9]Gofman JW, Delalla O, Glazier F, Freeman NK, Lindgren FT, Nichols AV, et al. The serum lipoprotein transport system in health, metabolic disorders, atherosclerosis and coronary heart disease. J Clin Lipidol. 2007;1(2):104-41.
[10]Jonas HA, Kronmal RA, Psaty BM, Manolio TA, Meilahn EN, Tell GS, et al. Current estrogen-progestin and estrogen replacement therapy in elderly women: Association with carotid atherosclerosis, CHS Collaborative Research Group, Cardiovascular Health Study. Ann Epidemiol. 1996;6(4):314-23.
[11]Cziraky MJ, Watson KE, Talbert RL. Targeting low HDLcholesterol to decrease residual cardiovascular risk in the managed care setting. J Manag Care Pharm. 2008;14(8 Suppl):S3-28.
[12]Suk Danik J, Rifai N, Buring JE, Ridker PM. Lipoprotein(a), hormone replacement therapy, and risk of future cardiovascular events. J Am Coll Cardiol. 2008;52(2):124-31.
[13]Urabe M, Yamamoto T, Kashiwagi T, Okubo T, Tsuchiya H, Iwasa K, et al. Effect of estrogen replacement therapy on hepatic triglyceride lipase, lipoprotein lipase and lipids including apolipoprotein E in climacteric and elderly women. Endocr J. 1996;43(6):737-42.
[14]Wagner JD, Martino MA, Jayo MJ, Anthony MS, Clarkson TB, Cefalu WT. The effects of hormone replacement therapy on carbohydrate metabolism and cardiovascular risk factors in surgically postmenopausal cynomolgus monkeys. Metabolism, 1996;45(10):1254-62.
[15]Sack MN, Rader DJ, Cannon RO 3rd. Oestrogen and inhibition of oxidation of low-density lipoproteins in postmenopausal women. Lancet, 1994;343(8892):269-70.
[16]Cressman MD, Heyka RJ, Paganini EP, O’Neil J, Skibinski CI, Hoff HF. Lipoprotein(a) is an independent risk factor for cardiovascular disease in hemodialysis patients. Circulation. 1992;86(2):475-82.