Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological data have revealed that the progestogen in oral contraceptives (OCs) is involved in hypertension, ischemic heart diseases, and stroke. Atherosclerotic lesions were implicated owing to the androgenic properties of progestogens. However, atherosclerosis did not develop despite reduced high density lipoprotein (HDL) and elevated low density lipoprotein (LDL), presumably because of the strong effect of ethinyl estradiol (EE) upon induction of hepatic LDL- and remnant-receptors. A series of findings indicate that vasospasms caused by the effect of progestogens are involved in arterial thromboses. In postmenopausal women, the addition of progestogens to the estrogen treatment may trigger ischemic diseases. Estrogens exert a vasodilatory effect and stabilize the vascular tonus through the responsiveness of the endothelium, neurotransmitter release, and direct blocking of calcium channels. Progestogens increase the sensitivity of arteries to vasoconstrictory compounds and reduce blood flow. In women treated with ovulation inhibitors, and EE-induced activation of the renin-angiotensin-aldosterone system was observed. Aldosterone acts vasodilatorily, while progestogens with high affinity to the aldosterone receptor may exert a strong vasoconstrictory effect. If vascular lesions are present, the vasoconstrictory action of progestogens may cause acute ischemic attacks. Therefore, the lowest effective dose of the progestogen has to be used for replacement therapy. In hysterectomized women, the extra administration of progestogens should be avoided and in women with arterial diseases they should be prescribed with discretion. Additional progestogens given for 14 days 3 months apart may suffice for the prevention of endometrial hyperplasia. Both the EE and progestogen doses in OCs should be reduced. Progestogen-dominant ovulation inhibitors should be restricted to cases with an additional indication.
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PMID:[Hormonal contraception and substitution therapy: the importance of progestogen for cardiovascular diseases]. 145

Oocyte depletion and ovarian aging results in profound alterations at the biological level. The reduction in numbers of follicles leads to reduction of circulating inhibin and increased serum FSH, characteristic marker of ovarian failure. The remaining follicles are overstimulated and premature ovulation may ensue. This, leads to luteal deficiency and reduction in progesterone production and relative hyperestrogenemia. The above changes characterize the premenopausal period. In a second phase, anovulatory cycles interchange with premature and occasionally normal ovulatory cycles. This phase is characterized by increased FSH and LH and decreased progesterone/estradiol ratio resulting in irregular bleeding, endometrial hyperplasia, polyps, fibromas, mammary dystrophies, disturbance of mood, appetite and thermoregulation. Lastly, the sensitivity of ovarian follicles to FSH and LH is lost with a decline of E2 below 20 pg/ml produced almost exclusively from peripheral conversion from circulating androgens. The beneficial effects of E2 are lost resulting in atrophy of the sensitive tissues, decreased calcium absorption, increased bone resorption, accelerated bone loss and osteoporosis, rise in serum triglycerides, increased VLDL and LDL lipoproteins, increased LDL/HDL cholesterol, a profile which favors atherosclerosis.
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PMID:Endocrine aspects of menopause. 266 71

Unopposed estrogens, both exogenous and endogenous, increase the risk of endometrial cancer although the magnitude of the association between estrogen replacement therapy and adenocarcinoma has been exaggerated by the epidemiologic case-control studies. Not all postmenopausal women need estrogen replacement therapy since some produce sufficient endogenous estrogens to remain asymptomatic and prevent atrophic vaginitis, osteoporosis and atherosclerosis. However, within this group may be those at risk for endometrial cancer, so they need to be identified and treated with cyclic progestogens. Sequential oral contraceptives did not protect young women from adenocarcinoma of the endometrium because of too little progestogen for too short a duration in view of the relatively high dosage of estrogen. However, combination birth control pills significantly decrease the risk for endometrial carcinoma. Endometrial hyperplasia is a precancerous lesion in some women and can be effectively reversed with 10-13 days of progestogen monthly in at least 98% of patients. The progestogen challenge test has been devised to identify postmenopausal women at greatest risk for adenocarcinoma. It should be administered to all postmenopausal women with an intact uterus. This includes asymptomatic women, patients receiving estrogen replacement therapy and women being evaluated for hormone therapy. If there is a positive response to the progestogen challenge, as manifested by withdrawal bleeding, then the progestogen should be continued for 13 days each month for as long as withdrawal bleeding results. If there is no response then the progestogen challenge test should be repeated at each annual examination. Universal use of the progestogen challenge test should prevent nearly all endometrial cancers.
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PMID:The role of hormones in the etiology and prevention of endometrial cancer. 379 26

Progestogens are clearly useful to balance the proliferative effects of estrogens on the endometrium; however, some progestogens have been shown to attenuate the cardiovascular benefits of estrogen, and this has been the subject of considerable debate. Accumulating evidence confirms the deleterious effects of medroxyprogesterone acetate on estrogen's cardioprotective effects and provides new and compelling evidence that not all progestogens are alike in this regard. Maintaining estrogen's cardioprotective effects is strongly dependent upon the type of progestogen and route and method of administration. Numerous periclinical studies conducted on nonhuman primates and other models have demonstrated that certain progestogens, such as micronized progesterone, can be administered concurrently with estrogen replacement therapy, providing protection against endometrial hyperplasia without significantly affecting the beneficial effects of estrogen on lipid profiles, atherosclerosis and vascular reactivity.
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PMID:Rationale for hormone replacement therapy in atherosclerosis prevention. 1075 6

Although progestational hormones are clearly beneficial in preventing estrogen-induced endometrial hyperplasia and cancer, their effect on other areas is far less clear. Of particular interest is the attenuating effect medroxyprogesterone acetate (MPA) has on the cardiovascular benefits of postmenopausal estrogen treatment. MPA reduces the dilatory effect of estrogens on coronary arteries, increases the progression of coronary artery atherosclerosis, accelerates low-density lipoprotein uptake in plaque, increases the thrombogenic potential of atherosclerotic plaques and promotes insulin resistance and its consequent hyperglycemia. These effects may be largely limited to MPA and not shared with other progestogens.
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PMID:Progestogens and cardiovascular disease. A critical review. 1139 29

The general benefits of the use of methods of contraception are the documented decrease of maternal and fetal mortality and morbidity, the diminution of the rate of prematurity and low birth weight, the decrease in induced abortion and sexually transmitted diseases (STDs) and certain gynecological cancer types. Natural methods of contraception pose the benefit of lacking effects on the organs and not introducing any external factors into the body. Barrier methods provide protection against STDs (a 50% reduction) and against cervical cancer (human papilloma virus), especially for adolescents and those with multiple sex partners. The chemical methods provide local antiseptic and antibiotic action that can be beneficial for vaginal and cervical infections. Hormonal methods, namely the oral contraceptive (OC) pill, also possess noncontraceptive benefits: regulation of the menstrual cycle, including diminution of dysmenorrhea, menstrual pain, menstrual flow, and anemia; reduced risk of pelvic inflammatory disease, endometrial and ovarian cancer, benign breast pathology, acne, and hirsutism; in addition to the therapy of polycystic ovarian syndrome, hypothalamic amenorrhea, and dysfunctional hemorrhage. Further benefits include the decrease of the risk of osteoporosis, rheumatoid arthritis by 60% in families at risk, ectopic pregnancy, atherosclerosis, uterine myomas by up to 31%, and ovarian cysts. Contraceptives that contain progestational hormones (oral, injectable, implant, or IUD forms) are also beneficial for endometrial hyperplasia and uterine polyps. IUDs (except for progestational IUDs) have local effect without the potential side effects of hormones. Terminal methods of contraception (tubal ligation and ligation of the vas deferens) are reliable without causing alterations in the physiology of the organs.
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PMID:[Non-contraceptive benefits of contraception]. 1217 57