Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen treatment of postmenopausal women is effective in relieving the symptoms of vasomotor instability and urogenital atrophy; estrogen treatment is effective in preventing accelerated bone loss and osteoporosis in young women following castration, but in postmenopausal women aging is a more important determinant of accelerated bone loss than is decreased estrogen secretion. Low-dose estrogen treatment of postmenopausal women neither prevents nor increases the risk of arteriosclerotic cardiovascular disease or cerebral vascular disease. It cannot be definitively established that estrogen treatment of postmenopausal women causes an increased incidence of breast tumors, but it is clear that such treatment does not prevent these tumors. It is established that estrogen treatment of postmenopausal women increases the risk ratio of endometrial carcinoma.
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PMID:Estrogen treatment of postmenopausal women. Benefits and risks. 57 21

In addition to oral contraceptives (OCs), the morning-after pill, the minipill, and depot preparations also belong to hormonal contraceptives. The latter two contraceptives have not become established among young women because of inadequate cycle control. For postcoital contraception in Austria, Neogynon and Stediril-D, consisting of 0.05 mg of ethinyl estradiol (EE) + 0.25 mg of levonorgestrel, are used within 48 hours of unprotected intercourse. Lower dose OCs have considerably reduced the risks of side effects. Micropills are the optimal OCs with EE under 50 mcg combined with the new generation of gestagens. The beneficial effects include menstrual regularity and the prevention of anemia, ovarian cysts, and fibrocystic mastopathy. Nausea, headache, spotting, and weight gain do occur in individual cases, even among young people. The potential risk of thromboembolism is the most important, although arterial cardiovascular risk is minimal in young age. The probability of postpill amenorrhea is less than 1%. Micropills can be used by young diabetics provided the disease is not beyond 10 years' duration and there is no angiopathy. Acne, seborrhea, and hirsutism are beneficially influenced by a combination of 0.035 mg of EE with 2 mg of cyproterone acetate. The relative risk of endometrial and ovarian cancer are only about half as high among OC users as among nonusers. The risk of breast cancer in young OC users has not been conclusively explained. Regular colposcopy and cytology is recommended for young OC users to preclude the risk of malignancies of the genital tract. Sex education and the use of OCs that are the most suitable and effective for young people can reduce the number of unwanted pregnancies and abortion. The comparison of two 5-year periods in the 1970s and 1980s at the University Obstetrical-Gynecological Clinic in Graz showed that the incidence of births among women under 18 years of age decreased from 3.6% (778) to 1.6% (353).
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PMID:[Benefits and risks of hormonal contraception]. 146 64

Serum level of the amino acid homocysteine, and vitamins folate, B12 and pyridoxal phosphate, and red blood cell folate levels were determined on Cycle days 3 and 21 in 26 women using the oral contraceptive Marvelon (30 mcg ethinyl estradiol and 150 mcg desogestrel), compared with 15 menstruating women. The 26 pill users had taken Marvelon for mean 3.7 years. Fasting homocysteine was assayed with an amino acid autoanalyzer; folate and B12 by radioimmunoassay; pyridoxal by high-performance liquid chromatography. The pill users had significantly higher homocysteine on Day 3 than controls (p0.01), levels comparable to those in heterozygote carriers of homocystinuria. Homocysteine levels were significantly lower in pill users on Day 21 compared to their levels on Day 3. Pyridoxal levels were significantly lower in Marvelon users on both days tested (p0.05). Homocysteine, folate and B12 were not significantly different in pill users and non-users on Day 21. The data indicate a cycle of high and low homocysteine levels in users of Marvelon. High homocysteine has been implicated in vascular disease, and may be a causative factor in the risk for thrombosis in pill users.
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PMID:Effects of sub-50 oral contraceptives on homocysteine metabolism: a preliminary study. 153 73

A historical review of the 28-year history of oral contraceptives from the viewpoint of correlation or lack thereof between drug toxic and pathologic effects seen in laboratory animals and those seen clinically is presented. Early high dose pills were expected to cause growth of uterine fibroids, but instead they had the unexpected effect of an estrogen dose-related venous thrombosis risk. Work on rats predicted that pills would cause liver cancers, but instead to slightly increase the incidence of being liver adenomas in women. Similarly, rat research predicted pituitary microadenomas. Pituitary effects in women, while rare, are thought to be due to prescription of pills to women with irregular cycles of pituitary origin. Progestins of the 17-acetoxy series were considered likely to produce breast cancers, as they had in beagle dogs. They apparently have not done so in women. They were reports in the mid-1970s that sequential pills containing 100 mcg ethinyl estradiol cause endometrial carcinoma. These pills have been discontinued. Recent evidence has been accumulating that low-dose pills containing levonorgestrel increase blood pressure and possible LDL-cholesterol. Risk of death from vascular disease, however, seems to be concentrated in women who smoke, especially those over 35.
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PMID:Oral contraceptives: significance of their effects in man and relationship to findings in animal models. 267 91

Estrogen-progestogen oral contraceptives (OCs) have been shown in numerous studies to increase the risk of venous thromboembolic disease, myocardial infarction, and thrombotic stroke. Until recently, it has been assumed that the increased risk of vascular disease was attributable to the estrogen component of the OC. However, available evidence suggests that venous thromboembolic complications are determined by the estrogen component, whereas arterial complications may be due to both the estrogenic and progestogenic components. The authors investigated the comparative effect of different low-dose combined OCs on the hemostatic system. The effects of ethinyl estradiol on coagulation fibrinolysis and platelet function were found to be dose-related: 50 mcg of ethinyl estradiol produced significantly greater changes than 30 mcg, and the effects of 30 mcg ethinyl estradiol were modified by the progestogen used. Further studies compared 50 mcg and 30 mcg estrogen contraceptives and a triphasic formulation containing levonorgestrel. Again, changes in coagulation activity and fibrinolysis were related to the dose of estrogen and progestogen. The absence of significant changes in antithrombin III with monophasic and triphasic levonorgestrel suggests that levonorgestrel counteracts the action of estrogen in depressing this coagulation inhibitor. The fewest changes in coagulation factors and inhibitors occurred among women taking low-dose estrogen combined with levonorgestrel, indicating that progestogen used in combination modifies the estrogenic effects on the coagulation system. Current research is aimed at finding estrogen-progestogen combinations that produce fewer changes in the hemostatic system and in other metabolic processes. The combination of low-dose ethinyl estradiol with levonorgestrel in a triphasic preparation should reduce the risk of vascular complications and contribute to the safety of OCs.
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PMID:Oral contraceptives and blood coagulation. 294 71

A large-scale prospective study of 23,000 current oral contraceptive users and a similar number of matched nonusers (controls) was conducted to evaluate the effects of 2 types of progestogens (norethindrone acetate of NEA and levonorgestrel) on the rate of reporting of arterial diseases. 3 NEA pills contained 50 mcg of ethinyl estradiol combined with 1, 3, and 4 mg of NEA. 2 levonorgestrel pills contained 30 mcg ethinyl estradiol combined with 150 and 250 mcg respectively of levonorgestrel. All 3 categories of arterial diseases (ischemic heart disease, cerebrovascular, and peripheral vascular diseases) exhibited a clear association of higher rates of reporting with larger doses of progestogens. In cerebrovascular diseases specifically, and arterial diseases in general, the trend with the NEA dose is statistically significant (P0.05). Pills with 250 mcg levonorgestrel are also significantly associated with a higher rate of total arterial disease than those with 150 mcg of progestogen. A striking inverse relationship is observed between high density lipoprotein cholesterol and the progestogen dose and rate of reporting of arterial disease, confirming previous observations. This study does not provide evidence that progestogens administered alone would have the same effects, nor does it assume that estrogens do not contribute to the increased risk of vascular disease in pill users. The need to develop a contraceptive risk of vascular disease in pill users. The need to develop a contraceptive pill with the lowest activity of both steroids consistent with contraceptive effectiveness and high menstrual cycle control is indicated.
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PMID:Progestogens and arterial disease--evidence from the Royal College of General Practitioners' study. 680 81

The effect of hormone replacement therapy on carbohydrate metabolism in menopausal women is briefly reviewed. Estrogen treatment has bi-phasic effect; abnormal glucose tolerance with a normal insulin level is commonly found within 3 months of treatment, followed by normalization of the glycemia when treatment is extended beyond one year. Normal tolerance usually occurs once treatment is stopped. Estrogens may therefore be regarded as being glucogenic (reversible blood glucose elevation) rather than diabetogenic (permanent hyperglycemia). With some exceptions, progestogens have little effect on glucose tolerance within the first 3-6 months of treatment; thereafter progressive hyperglycemia and hyperinsulinemia occur. Postulated mechanisms for the hormonal effect on carbohydrate metabolism are noted, including the possible synergistic effect of estrogens on progestogen glucogenic activity. The significance of chronic hyperglycemia and vascular disease is commented upon.
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PMID:Carbohydrate metabolism in relation to hormonal replacement therapy. 704 37

Multiple factors appear to contribute to the expression of Alzheimer's disease (AD). About 30 percent of cases of dementia of the Alzheimer's type can be attributed to genetic factors. These observations raise the possibility of identifying multiple interventions that may modify the disease process and, therefore, the clinical expression of the dementia. Prominent among factors that may contribute to dementia and, specifically, to dementia of the Alzheimer's type is cerebral vascular disease. Estrogen is a potent factor that not only prevents vascular disease but also improves blood flow in diseased vessels, including blood flow in regions on the brain affected by AD. Estrogen also has direct effects on neuronal function that may play an important role not only in the preservation of neurons but in repair of neurons damaged by disease process. These effects of estrogen on the CNS suggest that the hormone may be effective not only in the prevention of dementia but also in its treatment. The results of clinical trials, reviewed in this presentation, are very promising but are limited by the paucity of subjects and often the lack of adequate controls. Larger, randomized, placebo-controlled trials are needed to definitively establish the efficacy of estrogen in the treatment of dementia of the Alzheimer's type.
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PMID:The role of estrogen in the treatment of Alzheimer's disease. 915 65

Although ischemic colitis is often considered a condition of elderly persons or persons with vascular disease, it also occurs in healthy adults under age 60. While some patients may have gangrenous forms of ischemic colitis, others may have a benign, self-limited form of the disorder. In these cases, the condition is termed "transient ischemic colitis." This disorder should be included in the differential diagnosis in patients presenting with abdominal pain and hematochezia or bloody diarrhea. Estrogen or oral contraceptive therapy is associated with transient ischemic colitis, so its use should further raise suspicion. The effectiveness of discontinuation of estrogen therapy is controversial, but this measure should be considered. Conservative management includes repeated careful assessment, pain management and fluid replacement. Complications are rare and the prognosis is excellent. Occasionally, patients have recurrences.
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PMID:Transient ischemic colitis in young adults. 931 62

Although the incidence of vascular disease increases progressively with age, the increment observed in women between 50 and 60 years old does not seem to be directly correlated to the menopause. On the other hand, significant modifications of some risk factors, particularly those related to lipid metabolism and the hemostatic system have been observed in postmenopausal women. It should be stressed that the results of these studies, although generally concordant, cannot be applied directly to the entire population: the majority of women studied were well-educated and from the upper-middle social and economic classes and thus more prone to comply with behavioral and therapeutic precepts. Moreover, non-white women were excluded from these studies. At present, numerous data attest to the beneficial effect of hormone replacement therapy on cardiovascular disease in postmenopausal women. The presently running National Institutes of Health 9-year randomized primary prevention study (Women's Health Initiative) and the secondary prevention "Heart Estrogen/Progestin Replacement Study" should, within a few years, provide further and, it is hoped, definitive information concerning the utility of hormone replacement therapy for the primary and secondary prevention of cardiovascular disease.
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PMID:[Hormone replacement therapy and cardiovascular pathology in menopause]. 964 41


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