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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The abuse of anabolic-androgenic steroids by athletes has recently been associated with the development of myocardial infarction and stroke. Because platelets play a pathogenic role in these disorders, the authors hypothesized that androgenic steroid abuse among weight lifters was associated with increased platelet aggregation as measured in vitro. Twenty-eight study participants were recruited. Twelve denied current androgen use. However, 8 of these 12 tested positive for urinary androgens. Nonsignificant trends toward increased platelet counts and increased platelet aggregation to adenosine diphosphate were noted when androgen users were compared to nonusers. However, when stratified by age, older (greater than 22 years) androgen users required lower concentrations of collagen to produce 50% aggregation of test platelets than did younger (less than or equal to 22 years) androgen users (1.47 versus 3.35 micrograms/ml; p = .01). Further subgroup analysis revealed nonsignificant trends toward increased adenosine diphosphate-induced aggregability and nonsignificant trends in the platelet count in older weight lifters. Subsequent studies using collagen threshold aggregometry revealed no age-dependent effect in 17 other men (aged 18 to 46 years) not specifically selected for activity (r = .17). This study suggests an association between androgen use, age, and increased platelet sensitivity to collagen in weight lifters and may be helpful in explaining recent thrombotic disease in androgen users. It additionally calls into question the validity of subjective reporting when assessing androgen use among weight lifters.
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PMID:Androgenic-anabolic steroid abuse and platelet aggregation: a pilot study in weight lifters. 153 13

Anabolic/androgenic steroid abuse is an increasing medical and public health problem. The uncontrolled use of these agents has been associated with numerous toxic side-effects including deleterious cardiovascular changes. The most widely reported to these latter changes include the development of adverse lipid profiles and hypertension. Acute thrombosis has only recently been linked to androgen abuse. Such a causative link has been proposed in reports of acute myocardial infarction and stroke in several athletes using androgens. Unfortunately, there exists no direct evidence that androgens are thrombogenic in humans. However, indirect experimental data suggests that androgens affect platelet aggregation, coagulation proteins and the vascular system in ways that facilitate thrombosis. Androgens also increase several anticoagulant and fibrinolytic proteins. However, they have not been shown to protect from thrombosis in high risk patients. Existing data supports a possible thrombogenic effect of exogenous androgens. Further studies are needed to clarify the hemostatic influence associated with androgen abuse in weightlifters. The abuse of these agents may diminish if acute thrombosis becomes clearly and scientifically associated with their uncontrolled use.
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PMID:Anabolic/androgenic steroid abuse and thrombosis: is there a connection? 192 73

Steroids reduce permeability of the blood-brain barrier and inhibit active sodium transport by brain capillaries in vitro. Since the rate of edema formation during the early stages of ischemia is related to the rate of sodium transport from blood to brain, this study was designed to determine whether steroids reduce ischemic edema formation by inhibiting blood-brain barrier sodium transport. Dexamethasone was compared with progesterone since the latter is a more potent inhibitor of sodium transport in isolated capillaries. Sprague-Dawley rats were treated with vehicle (n = 22) or 2 mg/kg of either dexamethasone (n = 22) or progesterone (n = 17) 1 hour before occlusion of the middle cerebral artery. After 4 hours of ischemia, brain water content and blood-brain barrier permeability to [3H] alpha-aminoisobutyric acid and sodium-22 were determined. In controls, mean +/- SEM water content of tissue in the center of the ischemic zone was 82.4 +/- 0.2%. Brain edema was significantly reduced following pretreatment with either dexamethasone (80.6 +/- 0.1%, p less than 0.001) or progesterone (81.5 +/- 0.3%, p less than 0.05). There was also a significant reduction in blood-brain barrier permeability to alpha-aminoisobutyric acid in normal brain following either treatment (e.g., 2.21 +/- 0.19 and 1.37 +/- 0.10 microliters/g/min, p less than 0.001, for control and dexamethasone treatments, respectively), but no effect on the permeability to sodium (e.g., 1.19 +/- 0.05 and 1.12 +/- 0.11 microliters/g/min for control and dexamethasone treatments, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1990 Aug
PMID:Effect of steroids on edema and sodium uptake of the brain during focal ischemia in rats. 238 1

19-Noraldosterone, which was recently shown to be synthesized and produced in the human adrenal gland, possesses potent mineralocorticoid and hypertensinogenic activities. 18,19-Dihydroxycorticosterone (18,19-(OH)2-B) and 18-hydroxy-19-norcorticosterone (18-OH-19-nor-B), a possible precursor of 19-noraldosterone, have been identified in human urine. These mineralocorticoid hormones are regulated by the renin-angiotensin system and synthesized in adrenal glomerulosa cells. Urinary 19-noraldosterone correlated with urinary 18,19-(OH)2-B, 18-OH-19-nor-B, 18-hydroxycorticosterone (18-OH-B), and aldosterone. Urinary excretion of 19-noraldosterone, 18,19-(OH)2-B, and 18-OH-19-nor-B were increased in patients with aldosterone-producing adenoma (APA) and in those with idiopathic hyperaldosteronism (IHA), but the two did not differ significantly. Urinary 18-OH-B and 18-hydroxycortisol (18-OH-F) were significantly higher in APA compared with IHA. Though urinary 18-OH-F and 18-OH-B concentrations were useful markers, urinary 19-noraldosterone, 18,19-(OH)2-B, and 18-OH-19-nor-B could not be used to distinguish the two subsets of primary aldosteronism. Urinary 19-noraldosterone did not differ in hypertensive and normotensive patients. However, urinary 19-noraldosterone was increased in some hypertensive patients. In spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP), urinary 19-noraldosterone was increased at the prehypertensive stage compared with Wistar-Kyoto (WKY) rats. Urinary 19-noraldosterone was decreased in 9-week-old SHR and SHRSP compared with WKY rats. However urinary 19-noraldosterone was higher in SHRSP than in SHR. These elevated levels of 19-noraldosterone may contribute to hypertension in some individuals and in experimental hypertensive rats.
Steroids 1995 Jan
PMID:Significance of 19-noraldosterone, a new mineralocorticoid, in clinical and experimental hypertension. 779 99

Anabolic steroid use is widespread and has been associated with a variety of pathological conditions. The subject of this case is a 22 years old man with cerebral ischaemic stroke. He had no previous medical complaints but had a history of anabolic steroid abuse. This case presents a side effect of long term abuse of these drugs.
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PMID:[Ischemic cerebral stroke and anabolic steroids (case report)]. 1110 78

Estrogenic compounds have been shown to protect neurons from a variety of toxic stimuli in vitro and in vivo and depletion of estrogen at menopause has been associated with increased risk of neurodegenerative diseases. Genistein is an isoflavone soy derivative that binds to estrogen receptors with selective estrogen receptor modulator (SERM) properties. Recent FDA recommendations of soy intake for cholesterol reduction have prompted investigation into the potentially estrogenic role of dietary soy phytochemicals in the brain. In this study, we have shown that 50nM genistein significantly reduces neuronal apoptosis in an estrogen receptor-dependent manner. The importance of apoptosis in the brain has been recognized with regard to organization of the developing brain as well as degeneration in response to disease or stroke; however, the effects of estrogenic compounds on neuronal apoptosis have not been thoroughly examined. We developed a model of apoptotic toxicity in primary cortical neurons by using the endoplasmic reticulum (ER) calcium-ATPase inhibitor, thapsigargin, to test potential anti-apoptotic effects of 17beta-estradiol and genistein. Estrogen receptor beta, but not estrogen receptor alpha, was detected in our primary neuron cultures. Thapsigargin-induced apoptosis was confirmed by loss of mitochondrial function, DNA laddering, nuclear condensation and fragmentation, and caspase activation. Both 17beta-estradiol and genistein reduced the number of apoptotic neurons and reduced the number of neurons containing active caspase-3. This effect was blocked by co-addition of ICI 182780. Our results demonstrate that genistein and 17beta-estradiol have comparable anti-apoptotic properties in primary cortical neurons and that these properties are mediated through estrogen receptors.
Steroids 2002 Dec
PMID:17beta-Estradiol and the phytoestrogen genistein attenuate neuronal apoptosis induced by the endoplasmic reticulum calcium-ATPase inhibitor thapsigargin. 1244 Nov 88

Hashimoto's autoimmune thyroiditis is a common cause of thyroid disease. Neurological dysfunction related to thyroid hypo or hyperfunction is well known. Not so is autoimmune thyroid disease-associated or Hashimoto's encephalopathy, which includes different neurological manifestations appearing in the context of autoimmune thyroiditis with normal hormone levels. Around fifty cases have been reported since the first description by Brain in 1966. Pathogenesis is unknown, although the most accepted theory points out to an autoimmune cerebral dysfunction. There are two different clinical presentations. The vasculitic type is characterized by relapsing-remitting stroke-like episodes. The diffuse-progressive type shows insidious cognitive impairment, confusion, psychosis, somnolence and coma. Cerebrospinal fluid is abnormal in more than 80% of patients, with high protein levels and mononuclear pleocytosis. Steroids are the treatment of choice, although favourable evolution have been reported spontaneously or after thyroxine treatment.
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PMID:[Hashimoto's encephalopathy]. 1248 58

Abuse of anabolic steroids is an increasing problem not only among athletes but also body-builders and teenagers. A fast-developing black market has been established since the opening of the borders to eastern Europe. Medico-legal aspects of doping are addressed with particular reference to toxicology and pathology. Constituents of anabolic steroids bought on the black market were identified using gas chromatography/mass spectrometry; the products did not contain the expected ingredients in 35% of cases. Long-term effects and fatalities because of anabolic steroid abuse are reported here based on our own case material and a literature review. In our own cases, severe cardiovascular side-effects developed after long-term abuse of Dianabol (methandrostenolone) and Oral-Turinabol (chlordehydromethyltestosterone), i.e. myocardial infarction, stroke, organomegaly and/or severe atherosclerosis. The pathogenesis of cardiovascular complications (cardiotoxic effect, risk of atherosclerosis, thrombogenic risk) is discussed based on the available literature reports following fatal outcome after the abuse of anabolic steroids.
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PMID:Medico-legal aspects of doping. 1533 51

The cerebral vasculature is a target tissue for sex steroid hormones. Estrogens, androgens, and progestins all influence the function and pathophysiology of the cerebral circulation. Estrogen decreases cerebral vascular tone and increases cerebral blood flow by enhancing endothelial-derived nitric oxide and prostacyclin pathways. Testosterone has opposite effects, increasing cerebral artery tone. Cerebrovascular inflammation is suppressed by estrogen but increased by testosterone and progesterone. Evidence suggests that sex steroids also modulate blood-brain barrier permeability. Estrogen has important protective effects on cerebral endothelial cells by increasing mitochondrial efficiency, decreasing free radical production, promoting cell survival, and stimulating angiogenesis. Although much has been learned regarding hormonal effects on brain blood vessels, most studies involve young, healthy animals. It is becoming apparent that hormonal effects may be modified by aging or disease states such as diabetes. Furthermore, effects of testosterone are complicated because this steroid is also converted to estrogen, systemically and possibly within the vessels themselves. Elucidating the impact of sex steroids on the cerebral vasculature is important for understanding male-female differences in stroke and conditions such as menstrual migraine and preeclampsia-related cerebral edema in pregnancy. Cerebrovascular effects of sex steroids also need to be considered in untangling current controversies regarding consequences of hormone replacement therapies and steroid abuse.
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PMID:Influence of sex steroid hormones on cerebrovascular function. 1679 20

Estrogen is an important hormone signal that regulates multiple tissues and functions in the body. This review focuses on the neurotrophic and neuroprotective actions of estrogen in the brain, with particular emphasis on estrogen actions in the hippocampus, cerebral cortex and striatum. Sex differences in the risk, onset and severity of neurodegenerative disease such as Alzheimer's disease, Parkinson's disease and stroke are well known, and the potential role of estrogen as a neuroprotective factor is discussed in this context. The review assimilates a complex literature that spans research in humans, non-human primates and rodent animal models and attempts to contrast and compare the findings across species where possible. Current controversies regarding the Women's Health Initiative (WHI) study, its ramifications, concerns and the new studies needed to address these concerns are also addressed. Signaling mechanisms underlying estrogen-induced neuroprotection and synaptic plasticity are reviewed, including the important concepts of genomic versus nongenomic mechanisms, types of estrogen receptor involved and their subcellular targeting, and implicated downstream signaling pathways and mediators. Finally, a multicellular mode of estrogen action in the regulation of neuronal survival and neurotrophism is discussed, as are potential future directions for the field.
Steroids 2007 May
PMID:Neurotrophic and neuroprotective actions of estrogen: basic mechanisms and clinical implications. 1737 65


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