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

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

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

Due to increases in life expectancy, women are living 30 years or more beyond menopause. This has led to an increasing interest in the association between postmenopausal estrogen deficiency and degenerative diseases associated with aging such as cardiovascular disease, osteoporosis and dementia. Women are two times more likely to develop late-onset Alzheimer's disease (AD) than age-matched men. A large number of observational reports and a few randomized clinical trials have indicated that estrogen replacement therapy (ERT) may retard the development and severity of dementia in postmenopausal women. The mechanism underlying the protective action of estrogen in AD is under active investigation. A chronic inflammatory reaction mediated by abnormal deposition of proteins such as amyloid-beta (A beta) is central to the pathology of AD. We investigated the effect of low doses of conjugated estrogen (Premarin) in an animal model of A beta-induced vascular disruption and inflammatory reaction. This rodent model allows live videomicroscopic recording and electron microscopic analysis of peripheral vascular disruption and inflammatory reaction triggered by A beta. Estrogen prevented vascular deposition of A beta, endothelial and vessel wall disruption with plasma leakage, platelet and mast cell activation, and characteristic features of an inflammatory reaction: adhesion and transmigration of leukocytes. The beneficial effect was lost when estrogen treatment was discontinued. Estrogen also protected the cerebral blood vessels from endothelial dysfunction induced by A beta. This novel protective effect of estrogen against A beta cytotoxicity in peripheral and cerebral vasculature may contribute to the therapeutic efficacy of estrogen in AD and coronary vascular disease.
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PMID:Estrogen protects peripheral and cerebral blood vessels from toxicity of Alzheimer peptide amyloid-beta and inflammatory reaction. 1068 97

Women are two to three times more likely to develop late-onset Alzheimer's disease (AD) than age-matched men. A large number of observational reports and a few randomized clinical trials have indicated that estrogen replacement therapy (ERT) may retard the development and severity of dementia in postmenopausal women. A chronic inflammatory reaction mediated by abnormal deposition of proteins such as amyloid-beta (A beta) is central to the pathology of AD. We investigated the effect of low doses of conjugated estrogen (Premarin) in an animal model of A beta-induced vascular disruption and inflammatory reaction. Estrogen prevented vascular deposition of A beta, endothelial and vessel wall disruption with plasma leakage, platelet and mast cell activation, and characteristic features of an inflammatory reaction: adhesion and transmigration of leukocytes. The beneficial effect was lost when estrogen treatment was discontinued. This novel protective effect of estrogen against A beta-induced vascular dysfunction may contribute to the therapeutic efficacy of estrogen in AD and coronary vascular disease.
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PMID:Vascular actions of estrogen and Alzheimer's disease. 1081 45

Estrogen is important for the primary prevention of vascular disease in young women, but the mechanisms of protection at the vascular cell are still largely unknown. Although traditionally thought of as a nuclear transcription factor, the estrogen receptor has also been identified in the cell plasma membrane to signal but serve largely undefined roles. Here we show that estradiol (E2) rapidly activates p38beta mitogen-activated protein kinase in endothelial cells (EC), which activates the mitogen-activated protein kinase-activated protein kinase-2 and the phosphorylation of heat shock protein 27. The sex steroid preserves the EC stress fiber formation and actin and membrane integrity in the setting of metabolic insult. E2 also prevents hypoxia-induced apoptosis and induces both the migration of EC and the formation of primitive capillary tubes. These effects are reversed by the inhibition of p38beta, by the expression of a dominant-negative mitogen-activated protein kinase-activated protein kinase-2 protein, or by the expression of a phosphorylation site mutant heat shock protein 27. E2 signaling from the membrane helps preserve the EC structure and function, defining potentially important vascular-protective effects of this sex steroid.
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PMID:Estrogen signals to the preservation of endothelial cell form and function. 1098 97

Multiple factors appear to contribute to the expression of Alzheimer's disease (AD). About 30% of cases of dementia of the Alzheimer's type (DAT) 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 of 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 the repair of neurons damaged by the 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. Given the distressingly high prevalence of AD among older women and the exorbitant social and economic costs associated with this disorder, a true risk reduction on the order of one-third to one-half, as suggested by several recent analytical studies, would be of tremendous public health importance.
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PMID:The role of estrogen replacement therapy in Alzheimer's disease. 1126 26


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