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 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevalence of hypogonadism has been found to be increased in certain chronic illnesses, especially diabetes, hypertension and obesity. Recently, the prevalence of hypogonadism in primary care practices mirrored that in our population of men with erectile dysfunction (ED). In this study, the prevalence of hypogonadism in nearly 1000 men with ED was tabulated, using a retrospective chart review, and analyzed for association with the various contributing medical and psychological factors. The prevalence of hypogonadism was determined in men with a variety of chronic illnesses, and was further characterized by decade. We observed an association between hypertension (P=0.025), tobacco abuse (P=0.0059), sleep apnea (P=0.0001), work stress (P=0.041) and hypogonadism. These data were further analyzed for the odds ratio and confidence interval (Forest plot), which showed strong association for sleep apnea and work stress. We did not observe any significant association between diabetes, atherosclerosis, alcohol abuse, multiple medications, asthma, seizure disorder, anxiety/depression and hypogonadism (P values for Cochran-Mantel-Haenszel general association were 0.48, 0.97, 0.25, 0.69, 0.22, 0.76 and 0.98, respectively). We suggest that a host of chronic illnesses have a high prevalence of secondary hypogonadism. Men who have chronic medical or psychological illnesses should have their testosterone level checked, especially when sexual dysfunction symptoms or signs are present.
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PMID:Hypogonadism in men with erectile dysfunction may be related to a host of chronic illnesses. 1979 59

Obstructive sleep apnea (OSA) is characterized by recurrent apnea during sleep that may unbalance oxidative stress, increasing atherosclerosis. Among oxidative stress markers, 15-F(2t)-isoprostane is considered one of the most sensitive and specific metabolites of lipid peroxidation. To explore the relationship between urinary 15-F(2t)-isoprostane with sleep apnea severity and carotid modifications in nonobese OSA patients, 31 nonobese sleep apnea patients were studied, along with 10 lean subjects without OSA. Patients were assessed by polysomnography, blood pressure measurement, and ultrasonography to determine the carotid intima-media thickness (IMT). Urinary 15-F(2t)-isoprostanes were measured by liquid chromatography-tandem mass spectrometry. Urinary 15-F(2t)-isoprostane concentrations were increased in severe OSA patients compared to control subjects (20.2+/-7.3 vs 12.3+/-2.8 ng/mmol creatinine; P=0.020). Mean carotid IMT was correlated with 15-F(2t)-isoprostane (r=0.532; P<0.001) and with the apnea-hypopnea index (r=0.345; P=0.029). 15-F(2t)-Isoprostane level was related to the night time spent at SaO(2)<90% (r=0.478; P=0.002), the apnea-hypopnea index (r=0.465; P=0.003), and the mean nocturnal SaO(2) (r=-0.424; P=0.007). These results showed a relationship between lipid peroxidation, carotid intima-media thickness, and intermittent hypoxia in nonobese OSA patients, thus reinforcing the hypothesis that oxidative stress could be involved in the early atherosclerotic process.
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PMID:Association of urinary 15-F2t-isoprostane level with oxygen desaturation and carotid intima-media thickness in nonobese sleep apnea patients. 2002 64

Analysis of the Framingham data has shown that the risk of heart failure is increased substantially among diabetic patients, while persons with the metabolic syndrome have an increased risk of both atherosclerosis and diabetes mellitus. Sleep apnea may be related to the metabolic syndrome and systemic inflammation through hypoxia, which might also cause the cardiac remodeling by increased oxidative stress. On the other hand, the renin-angiotensin system is activated in diabetes, and local angiotensin II production may lead to oxidative damage via the angiotensin II type 1 receptor. Basic and clinical data indicate that angiotensin II receptor blockers have the potential to preserve left ventricular function and prevent cardiac remodeling that is exaggerated by oxidative stress in patients with diabetes. Thus, alleviation of oxidative stress might be one possible strategy in the treatment of diabetic patients associated with sleep apnea.
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PMID:Regulation of oxidative stress and cardioprotection in diabetes mellitus. 2006 32

Sleep is an essential part of our daily living, and sleep disturbances may intervene with the biological and physiological processes in human body leading to the development of metabolic dysfunction. Short sleep duration and poor sleep quality have adverse effects on metabolism and hormonal processes, contributing to increased cardiovascular risk. Obstructive sleep apnoea is a chronic condition characterized by repetitive upper airway collapse during sleep, causing intermittent hypoxaemia, recurrent arousals and sleep fragmentation. Sleep disturbances can increase sympathetic activity, provoke systemic inflammation and oxidative stress, and impair vascular endothelial function. Obstructive sleep apnoea is increasingly recognized to be an independent cardiovascular risk factor. There is intense research interest in the association between obstructive sleep apnoea and the metabolic syndrome - the constellation of inter-related metabolic derangements including central obesity, hypertension, insulin resistance and dyslipidaemia, which appears to directly promote the development of atherosclerosis. The underlying pathophysiologic pathways or mechanistic links between obstructive sleep apnoea and metabolic syndrome have not been well delineated. This article reviews the current knowledge of the relationship between sleep disturbances, sleep-disordered breathing and the metabolic syndrome in adults.
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PMID:Sleep & the metabolic syndrome. 2030 46

Childhood obesity is a global epidemic and is associated with medical consequences. These consequences of childhood obesity include its association with cardiovascular risk factors, notably impaired glucose tolerance, hypertension, atherogenic dyslipidemia, micro inflammation, and comorbidities including nonalcoholic fatty liver disease (NAFLD), sleep apnoea, and early atherosclerosis. This article aims to demonstrate and review the local clinical evidences in Hong Kong Chinese children and adolescents in exploring the epidemiology and medical consequences associated with obesity in the youth population and highlighting the research direction in searching the etiology of these associations.
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PMID:Medical consequences of childhood obesity: a Hong Kong perspective. 2039 Dec 43

Obstructive sleep apnea, a breathing disorder in sleep characterized by intermittent and recurrent pauses in respiration, is also a major risk factor for cardiovascular morbidity and mortality. Accumulated evidence implicates the apnea-related multiple cycles of hypoxia/reoxygenation in promoting the formation of reactive oxygen species that oxidize and damage macromolecules and activate critical redox-sensitive signaling pathways and transcription factors. This activation facilitates the expression of sets of genes encoding proteins in various pathways, including inflammatory and lipogenic, as well as proteins essential to adaptation to hypoxia. Consequently, inflammatory and immune responses are activated, thus resulting in the activation of endothelial cells/leukocytes/platelets. These activated cells express adhesion molecules and proinflammatory cytokines that in turn may further exacerbate inflammatory responses and cause endothelial cell injury and dysfunction, promoting the development of cardiovascular morbidities in sleep apnea. No less important in activating such inflammatory cascades is the hyperlipidemia that is another characteristic of obstructive sleep apnea. Evidence supporting the existence of endothelial dysfunction and early clinical signs of atherosclerosis in these patients provides a firm support to the above chain of events. If left untreated, this cascade of events may eventually lead to overt cardiovascular morbidity.
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PMID:Intermittent hypoxia: the culprit of oxidative stress, vascular inflammation and dyslipidemia in obstructive sleep apnea. 2047 24

The endothelin (ET)-system is composed of three endothelins, two receptors and two enzymes. The study of this system presents a great interest to understand the cardiovascular physiopathology. The ET-system is involved in cardiac organogenesis, angiogenesis and vascular tone homeostasis. Its role in arterial pulmonary hypertension, arterial hypertension and atherosclerosis has been shown. The numerous ET-system's targets suggest that it could be involved in pathologies which bring together various cardiovascular disorders such as the obstructive sleep apnoea syndrome. Thus, the ET-system generates today a lively interest for experimental and clinical trials.
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PMID:[The endothelin system: its involvement in the cardiovascular system]. 2057 Apr 18

Aldosterone is present and active all along the cardiovascular continuum. Excessive tissue production occurs in cardiovascular diseases including myocardial infarction (MI) and heart failure, resulting in a multitude of adverse effects in the cardiovascular system necessitating pharmacologic blockade of this neurohormone. Both human and animal studies have consistently proven the beneficial effects of antialdosteronics in the improvement of: 1) endothelial function, 2) modulation of inflammatory mechanisms between blood and the vascular wall and 3) reduction of tissue proliferation and cardiovascular remodeling leading to different severities of cardiovascular damage. These basic mechanisms of anti-aldosterone therapy strongly support the promising data observed in major clinical trials with aldosterone blockers in cardiovascular diseases, specially in heart failure patients. Whereas aldosterone receptor blockers were initially viewed as potassium-sparing diuretics there has been a clear change of concept in the past 10 years, mainly following the positive results of RALES with spironolactone in chronic heart failure, followed by EPHESUS using eplerenone in patients with systolic dysfunction post MI. The significant positive results in both studies were a clear support for the inclusion of this pharmacologic intervention as first line treatment in most international guidelines for the management of heart failure. More recent and ongoing studies are exploring the usefulness of this type of intervention in preventing vascular and myocardial hypertrophy and remodeling in refractory hypertensive and some hyperfibrotic syndromes. There are also provocative studies investigating in the possibility of inhibiting atherosclerosis. More recently, some studies are suggesting the benefit of aldosterone blockade in sleep apnea. In addition, two large multicentric trials, TOPCAT and EMPHASIS are analyzing the potential use of antialdosteronics in patients with cardiac insufficiency and preserved systolic function and the possibility of extending their indication in systolic heart failure to Phase II respectively. New compounds, blocking the synthesis of aldosterone instead of blocking its receptor are being developed, and initial Phase 2 studies are positive. All of the above results are very interesting, show an optimistic future and are consolidating and enlarging the spectrum of aldosterone blockade in cardiovascular disorders every day.
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PMID:Aldosterone inhibition and cardiovascular protection: more important than it once appeared. 2067 26

Although the majority of patients with glaucoma have elevated intraocular pressure as the presumed etiology for their resultant neuropathy, it is well known that approximately 25% of patients with glaucoma have intraocular pressure within the normal range for their race. These patients may have conditions that facilitate non-pressure related stress to the retina and optic nerve that might directly contribute to their glaucomatous neuropathy and include chronic or intermittent ischemia (i.e atherosclerosis, heart disease, vasospasm, migraine, sleep apnea), altered scleral/optic nerve head morphology that predisposes to glaucomatous stress (i.e myopia); genetic mutations that predispose to glaucoma damage at normal IOP (OPA-1,optineurin, myocilin) and evidence of aberrant immunity that suggests that their glaucoma might be a form of an autoimmune neuropathy (i.e. presumed autoimmune glaucoma). This review provides a critical assessment of the potential role for autoimmunity as an initiating or exacerbating etiology in some patients with glaucoma.
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PMID:The case for autoimmunity in glaucoma. 2080 Nov 14

Hypoxia-inducible factor-1 (HIF-1) is a nuclear transcription factor that is upregulated in hypoxia and co-ordinates the adaptive response to hypoxia by driving the expression of over 100 genes. In facilitating tissues to adapt to hypoxia, HIF-1 may have a role in reducing the cellular damage induced by ischaemia, such as that seen in peripheral arterial disease (PAD), or following acute ischaemic insults such as stroke and myocardial infarction. This therefore raises the possibility of HIF-1 modulation in such contexts to reduce the consequences of ischaemic injury. HIF1 has further been implicated in the pathogenesis of atherosclerosis, abdominal aortic aneurysm (AAA) formation, pulmonary hypertension and systemic hypertension associated with obstructive sleep apnoea. Through a better understanding of the role of HIF-1 in these disease processes, novel treatments which target HIF-1 pathway may be considered. This review summarises the role of HIF-1 in arterial disease, specifically its role in atherosclerosis, ischaemic heart disease, in-stent restenosis following coronary revascularisation, stroke, PAD, AAA formation, pulmonary artery hypertension and systemic hypertension. The potential for exploiting the HIF-1 signalling pathway in developing therapeutics for these conditions is discussed, including progress made so far, with attention given to studies looking into the use of prolyl-hydroxylase inhibitors.
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PMID:Hypoxia-inducible factor-1 in arterial disease: a putative therapeutic target. 2080 88


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