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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper deals with hemorrhagic stroke (HS) pathogenesis and diagnosis in young people. Among cerebrovascular diseases in the young acute hemorrhagic strokes take noticeable place. Arterial hypertension, diabetes mellitus, smoking, alcoholism are among risk factors of subarachnoidal hemorrhage (SAH). Massive hemorrhages occur in the rupture of arterial aneurysms and arteriovenous malformations. HS in the young may be caused by blood diseases, i.e. leukemias, hemophilias, idiopathic thrombocytopenic purpura, coagulopathies; vasculitis in diffuse diseases of the connective tissue; non-inflammatory arteriopathies; drug addiction. Genetic predisposition to HS development is discussed with focus to such diseases as a family form of moya-moya disease, glucocorticoid-depressed hyperaldosteronism, elastic pseudoxanthoma, Marfan's syndrome, renal olycystosis, Sturge-Veber syndrome. It is recommended to use wider updated methods of neurovisualization (CT, MRT, angiography) in diagnosis of HS. The conclusion is made that HS diagnosis, especially in the young, needs a multidisciplinary approach with active participation of neurologist, neurosurgeon, therapist, endocrinologist, hematologist.
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PMID:[Specific features of pathogenesis and diagnosis of hemorrhagic stroke in young patients]. 1511 67

Primary aldosteronism is associated with glucose intolerance and diabetes, which is due in part to impaired insulin release caused by reduction of potassium, although other possibilities remain to be elucidated. To evaluate the in vivo effects of aldosterone on glucose metabolism, a single dose of aldosterone was administered to mice, which resulted in elevation of the blood glucose level. In primary cultured mouse hepatocytes, the gene expression of gluconeogenic enzymes such as glucose-6-phosphatase (G6Pase), fructose-1,6-bisphosphatase and phosphoenolpyruvate carboxykinase increased in response to aldosterone in a dose-dependent manner even at a concentration similar to a physiological condition (10(-9) M). The inhibitory effect of insulin on G6Pase gene expression was partially suppressed by aldosterone. Furthermore, aldosterone enhanced G6Pase promoter activity in human hepatoma cell line HepG2, which was prevented by co-treatment with a glucocorticoid antagonist RU-486, but not a mineralocorticoid antagonist spironolactone. In contrast, aldosterone had no effects on major insulin signaling pathways including insulin receptor substrate-1, protein kinase B, and forkhead transcription factor. These results suggest that aldosterone may affect the inhibitory effect of insulin on hepatic gluconeogenesis through the glucocorticoid receptor, which may be one of the causes of impaired glucose metabolism in primary aldosteronism.
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PMID:Aldosterone stimulates gene expression of hepatic gluconeogenic enzymes through the glucocorticoid receptor in a manner independent of the protein kinase B cascade. 1511 77

Kearns-Sayre syndrome, first described by Kearns and Sayre in 1958, is a rare disorder consisting of ptosis, limited movement of both eyes and atypical retinal pigmentary change (salt-pepper like appearance). Most cases have shown an increase in the concentration of mitochondria and ragged-red fiber under Gomori-trichrome staining on muscle biopsy. Occasionally, it is combined with other neurologic and endocrinologic symptoms such as ataxia, dementia, diabetes, and hyperaldosteronism. We recently experienced three cases of male teenaged patients who expressed the clinical features of Kearns-Sayre syndrome.
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PMID:Kearns-Sayre syndrome -3 case reports and review of clinical feature. 1534 17

Herpes simplex virus type 2 (HSV-2), which has been recognized as a potential cardiovascular pathogen and implicated in carotid atherosclerosis and coronary artery disease, is independently associated with the future risk of cardiovascular death. Investigations have demonstrated that hypertension may be related to inflammation, and inflammation is one of the symptoms of HSV-2 infection. This cross-sectional study investigated the correlation between HSV-2 infection and essential hypertension. One thousand two hundred and forty four inpatients (488 patients with essential hypertension and 756 normotensives) were investigated serologically for the specific immunoglobulin G (IgG) to HSV-2 by enzyme-linked immunosorbent assay. Patients diagnosed with pheochromocytoma, primary aldosteronism, aorto-arteritis or renal artery stenosis were excluded. The prevalence of HSV-2 IgG seropositivity was significantly higher in the hypertensive group than in the normotensive group (38.3% vs. 29.8%, p =0.002). After adjustment for confounding factors, an association of HSV-2 IgG seropositivity with essential hypertension was found on binary logistic regression analysis. The adjusted odds ratio of essential hypertension was 1.4 (95% confidence intervals, 1.1 to 1.8; p =0.005) for HSV-2 infection; the adjusted covariates included age, male sex, smoking, body mass index, dyslipidemia, diabetes and coronary artery disease. The results of this study indicated that HSV-2 infection might be an independent risk factor for essential hypertension.
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PMID:Herpes simplex virus type 2 infection is a risk factor for hypertension. 1549 72

This paper presents a signpost for hypertension research, emphasizing areas most likely to yield major clinical and public health benefits. Specific questions are posed in the context of fetal and maternal precursors of cardiovascular disease, vascular biology, resistant hypertension, antihypertensive drugs, primary aldosteronism, lifestyle and genetic interactions and translational research. Worldwide increasing rates of obesity and diabetes demonstrate the need for a global approach to cardiovascular risk and the need for more effective use of existing knowledge. Equal emphasis is given to the critical importance of the fundamental research required to defeat hypertensive cardiovascular disease in the long run.
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PMID:Hypertension research in the 21st century: where is the gold? 1561 14

We report a rare case of primary aldosteronism due to an adrenocortical carcinoma. A 61-year-old woman with a history of hypertension and hypokalemia was referred for evaluation of a 4.2 cm measuring adrenal mass without secondary signs of malignancy. Endocrinological testing was consistent with primary aldosteronism. The patient underwent surgical resection of the adrenal mass; histology revealed an adrenocortical carcinoma. Postoperatively blood pressure, serum potassium, and aldosterone returned to normal. Four months after adrenalectomy, the patient presented again with hypokalemic hypertension and was found to have metastatic disease. Endocrinological investigation revealed primary aldosteronism and subclinical autonomous glucocorticoid hypersecretion. Careful hormonal investigation should be obtained in patients with adrenal masses causing excessive aldosterone secretion. In uncertain cases of primary aldosteronism, we would suggest to measure 18-hydroxycortisol levels, as excessive amounts may indicate adrenocortical carcinoma.
Exp Clin Endocrinol Diabetes 2005 Apr
PMID:Steroid profile in an adrenocortical carcinoma producing aldosterone. 1589 61

Diabetes mellitus is associated with natriuresis, whereas estrogen has been shown to be renoprotective in diabetic nephropathy and may independently regulate renal sodium reabsorption. The aim of this study was to determine the effects of 17-beta estradiol (E(2)) replacement to diabetic, ovariectomized (OVX) female rats on the expression of major renal sodium transporters. Female, Sprague-Dawley rats (210 g) were randomized into four groups: (1) OVX; (2) OVX+E(2); (3) diabetic+ovariectomized (D+OVX); and (4) diabetic+ovariectomized+estrogen (D+OVX+E(2)). Diabetes was induced by a single intraperitoneal injection of streptozotocin (55 mg/kg.body weight (bw)). Rats received phytoestrogen-free diet and water ad libitum for 12 weeks. E(2) attenuated hyperglycemia, hyperalbuminuria, and hyperaldosteronism in D rats, as well as the diabetes-induced changes in renal protein abundances for the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), and the alpha- and beta-subunits of the epithelial sodium channel (ENaC), that is, E(2) decreased NKCC2, but increased alpha- and beta-ENaC abundances. In nondiabetic rats, E(2) decreased plasma K(+) and increased urine K(+)/Na(+) ratio, as well as decreased the abundance of NKCC2, beta-ENaC, and alpha-1-Na-K-adenosine triphosphate (ATP)ase in the outer medulla. Finally, the diabetic, E(2) rats had measurably lower final circulating levels of E(2) than the nondiabetic E(2) rats, despite an identical replacement protocol, suggesting a shorter biological half-life of E(2) with diabetes. Therefore, E(2) attenuated diabetes and preserved renal sodium handling and related transporter expression levels. In addition, E(2) had diabetes-independent effects on renal electrolyte handling and associated proteins.
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PMID:17-beta Estradiol attenuates streptozotocin-induced diabetes and regulates the expression of renal sodium transporters. 1651 30

Increased plasma aldosterone concentrations (PACs) are associated with higher cardiovascular risk and target organ damage (TOD). Hyperglycemia can potentiate the cellular effects of aldosterone, and the prevalence of diabetes in primary aldosteronism (PA) is 7%-59%. The prevalence of PA in hypertensive individuals is estimated to be 10%-14%. This study of 61 hypertensive diabetic patients not taking spironolactone and with serum creatinine values <2.5 mg/dL sought to establish the prevalence of PA in hypertensive diabetics and compare the prevalence of PA in patients with TOD with those patients without TOD. PA was suspected if PACs were >15 ng/dL and plasma renin activity was <1 ng/dL/h (ratio >30). Although 14 patients had suppressed renin with PACs >8 ng/dL (including two with PACs >11 ng/dL), none met our criteria for PA. There was no correlation between PAC and TOD. This study indicates that routine screening for PA in hypertensive diabetic patients is not justified and that PAC does not correlate with TOD. Further study is needed.
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PMID:The prevalence of primary aldosteronism in diabetic patients. 1659 27

Although there are some case reports of combined aldosterone and cortisol producing adrenal tumor, overt diabetes mellitus has been rarely described. A 55-year-old hypertensive woman had hypokalemia and overt hyperglycemia without Cushingoid clinical features. The body mass index was 18.2 kg/m2, fasting blood glucose was 302 mg/dl and hemoglobin A1c was 11.6%. Endogenous insulin secretion was well preserved, whereas insulin sensitivity measured by short insulin tolerance test was markedly impaired. A solitary left aldosterone- and cortisol-producing adrenal tumor was diagnosed. We described a rare case of overt diabetes mellitus in a patient with combined primary aldosteronism and Cushing's syndrome.
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PMID:Overt diabetes mellitus in a patient with combined primary aldosteronism and Cushing's syndrome. 1713 25

Hormonal regulation is not possible without the cardiovascular system, and thus the heart plays a special role not only in the action and synthesis, but also in the distribution of hormones. Severe endocrine disorders with cardiac involvement are often threatening for the patient. The impact of aberrant thyroid function, the sympathetic-adrenal symptoms of which predominantly affect the heart, is well known. Diabetes mellitus and the associated metabolic syndrome are major causes of cardiovascular disease and determine its morbidity and lethality rates. Acromegaly causes a complex cardiomyopathy that may result in cardiac failure refractive to conventional treatment. The excessive production of adrenal hormones in Cushing's syndrome, hyperaldosteronism and pheochromocytoma primarily harms the heart by causing severe hypertension. The same holds true for long-standing hyperparathyroidism. Recent prospective studies did not confirm the protective effect of hormone replacement therapy on cardiovascular disease.
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PMID:[Endocrine disorders and the heart]. 1733 54


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