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 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hospitalized patients with acute medical conditions are at significant risk of venous thromboembolism (VTE): approximately 10-30% of general medical patients may develop deep-vein thrombosis or pulmonary embolism, and the latter is a leading contributor to deaths in hospital. Despite consensus-group recommendations that at-risk medical patients should receive thromboprophylaxis, there is currently no consensus as to which patients are at risk, and many patients may not receive appropriate thromboprophylaxis. This paper reviews evidence for the risk of VTE associated with different medical conditions and risk factors, and presents a risk-assessment model for risk stratification in medical patients. Medical conditions associated with a moderate to high risk of VTE include cardiac disease, cancer, respiratory disease, inflammatory bowel disease, and infectious diseases. Importantly, analyses of data from the MEDENOX study show that thromboprophylaxis significantly reduces the risk of VTE in these patient subgroups. Risk factors in medical patients include a history of VTE, history of malignancy, increasing age, thrombophilia, prolonged immobility, and obesity. These medical conditions and risk factors are included in a risk-assessment model which is hoped will provide a simple means of assisting clinicians in deciding whether thromboprophylaxis should be used in an individual patient.
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PMID:Assessment of venous thromboembolism risk and the benefits of thromboprophylaxis in medical patients. 1627 Jun 26

Obesity is a chronic disease and prevalence and incidence are progressively increasing. Treatment of obesity is important to reduce mortality and associated diseases, like diabetes mellitus, hypertension, abnormal blood lipid levels, coronary heart disease, thromboembolic disease, cancer (endometrial, gallbladder, cervical, ovarian, breast, prostate and colorectal), polycystic ovary syndrome (PCOS), gallbladder disease, respiratory disease, arthritis, gout. Most of these pathologies profits by a modest weight loss (5-10%). A correct management of obesity should include integration of therapeutic strategies, that we have actually at disposal: diet, physical training, behaviour therapy, pharmacologic therapy and surgery. We should get together low-calorie and low-fat diet with behaviour change and physical training. Physical training induces a significant weight loss and reduces cardiovascular risks and insulin resistance. Orlistat, that reduces up to 30% lipid adsorption, is a valid remedy if with an adequate diet. A new drug, sibutramine, shows efficacy: it increases satiety and energy expenditure caused by thermogenesis in brown adipose tissue. Surgical approaches including some procedures, are indicated for great obesity (BMI >40).
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PMID:[Management of overweight and obese patient. New acquisition]. 1648 74

While the functions of many of the proteins located in or associated with the photoreceptor cilia are poorly understood, disruption of the function of these proteins may result in a wide variety of phenotypes ranging from isolated retinal degeneration to more pleiotropic phenotypes. Systemic findings include neurosensory hearing loss, developmental delay, situs-inversus, infertility, disorders of limb and digit development, obesity, kidney disease, liver disease, and respiratory disease. The concept of "retinal ciliopathies" brings to attention the importance of further molecular analysis of this organelle as well as provides a potential common target for therapies for these disorders. The retinal ciliopathies include retinitis pigmentosa, macular degeneration, cone-dystrophy, cone-rod dystrophy, Leber congenital amaurosis, as well as retinal degenerations associated with Usher syndrome, primary ciliary dyskinesia, Senior-Loken syndrome, Joubert syndrome, Bardet-Biedl syndrome, Laurence-Moon syndrome, McKusick-Kaufman syndrome, and Biemond syndrome. Mutations for these disorders have been found in retinitis pigmentosa-1 (RP1), retinitis pigmentosa GTPase regulator (RPGR), retinitis pigmentosa GTPase regulator interacting protein (RPGR-IP), as well as the Usher, Bardet-Biedl, and nephronophthisis genes. Other systemic disorders associated with retinal degenerations that may also involve ciliary abnormalities include: Alstrom, Edwards-Sethi, Ellis-van Creveld, Jeune, Meckel-Gruber, Orofaciodigital Type 9, and Gurrieri syndromes. Understanding these conditions as ciliopathies may help the ophthalmologist to recognize associations between seemingly unrelated diseases and have a high degree of suspicion that a systemic finding may be present.
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PMID:The retinal ciliopathies. 1789 9

During 2007, the human species became predominantly urban. Australia is highly urbanised, and health varies within Australian cities. Australian urban life is characterised by sedentariness, excess food intake, reliance on cars for transport, a high level of exposure to media and marketing messages, and a consumer culture. These characteristics are linked to obesity, diabetes, heart disease, some cancers, chronic respiratory disease, injury, depression and anxiety. The evolution of cities has been characterised as a four-stage process: poverty, industrial, consumption and eco-city. Each stage but the last has defining health disorders. Transition to healthy and sustainable cities requires infrastructure investment in new urban areas (including mass transit, education and health services), better conditions for walking and cycling, access to healthy food and encouragement of suburban economic development. There is a role for everyone in the transition to healthy and sustainable cities.
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PMID:The way we live in our cities. 1807 10

Previous studies of leptin with cardiovascular disease (CVD) risk factors have been limited by clinical samples or lack of representation of the general population. This cross-sectional study, designed to examine whether leptin or insulin may mediate the endogenous relation of obesity with metabolic, inflammatory, and thrombogenic cardiovascular risk factors, included 522 men and 514 women aged >or=40 years who completed a physical examination during the third National Health and Nutrition Examination Survey. Participants were free of existing CVD, cancer (except non-melanoma skin cancer), diabetes, or respiratory disease. In multivariable analyses adjusted for race/ethnicity and lifestyle factors, waist circumference (WC) was positively associated with blood pressure, triglyceride, LDL cholesterol, total cholesterol:HDL ratio, apolipoprotein B, C-reactive protein (CRP), and fibrinogen concentrations, and negatively associated with HDL cholesterol and apolipoprotein A1 levels. The associations of WC with the metabolic CVD risk factors were largely attenuated after adjustment for insulin levels, while the associations of WC with the inflammatory and thrombogenic factors (CRP and fibrinogen, respectively) were largely explained by adjustment for leptin concentrations. However, leptin levels were not independently associated with CRP and fibrinogen in men and CRP in women when adjusted for WC. Positive associations of leptin and insulin with fibrinogen in women, independent of WC, were noted. These results suggest that insulin may be an important mediator of the association of obesity with metabolic but not inflammatory or thrombogenic CVD risk factors, while leptin does not appear to influence cardiovascular risk through a shared association with these risk factors. However, we cannot rule out the possibility that leptin and insulin influence cardiovascular risk in women through independent effects on fibrinogen concentrations.
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PMID:The relation of leptin and insulin with obesity-related cardiovascular risk factors in US adults. 1816 70

Acutely ill medical patients are at moderate to high risk of venous thromboembolism: ~10 to 30% of general medical patients may develop deep vein thrombosis or pulmonary embolism, and the latter is a leading contributor to deaths in hospital. Medical conditions associated with a high risk of venous thromboembolism include cardiac disease, cancer, respiratory disease, inflammatory bowel disease, and infectious diseases. Predisposing risk factors in medical patients include a history of venous thromboembolism, history of malignancy, complicating infections, increasing age, thrombophilia, prolonged immobility, and obesity. Heparins, including unfractionated and low molecular weight, as well as fondaparinux have been shown to be effective agents in prevention of VTE in this setting. However, it has not yet been possible to demonstrate a significant effect on mortality rates in this population. In medical patients, unfractionated heparin has a higher rate of bleeding complications than low molecular weight heparin. There is no evidence for the use of aspirin, warfarin, or mechanical methods. We recommend either low molecular weight heparin or fondaparinux as safe and effective agents in the thromboprophylaxis of medical patients.
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PMID:Venous thromboembolism prophylaxis for the medical patient: where do we stand? 1830 89

Respiratory function is impaired in obesity but there are limitations with body mass index and skin-fold thickness in assessing this effect. The present authors hypothesised that the regional distribution of body fat and lean mass, as measured by dual-energy X-ray absorptiometry (DXA), might be more informative than conventional measurements of total body fat. In total, 107 subjects (55 female, 51.4%) aged 20-50 yrs with no respiratory disease were recruited. Respiratory function tests, anthropometric measurements and a DXA scan were performed. Partial correlation and linear regression analyses were used to explore the effect of adiposity and lean body mass on respiratory function. The majority of respiratory function parameters were significantly correlated with DXA and non-DXA measurements of body fat. Neither thoracic nor abdominal fat had a greater effect. There were some differences in the effect of adiposity between the sexes. Respiratory function was negatively associated with lean body mass in females but positively associated in males. This disappeared after adjustment in females but remained in males. The effects of thoracic and abdominal body fat on respiratory function are comparable but cannot be separated from one another.
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PMID:The effect of adiposity measured by dual-energy X-ray absorptiometry on lung function. 1835 55

Obesity is the most common metabolic disease in the world and its prevalence has been increasing over several decades. The World Health Organization (WHO) predicts that, by 2015, around 700 million adults will be obese (at least 10% of the projected global population). This will be a huge health and economic burden with associated increases in diabetes, cardiovascular and musculoskeletal disease, and malignancy. While there has been little focus on the impact of obesity on respiratory disease, there are clear effects on pulmonary function and inflammation which will increase the prevalence and morbidity of lung disease. There is an inverse relationship between body mass index and forced expiratory volume in 1 s. Increases in body weight lead to worsening of pulmonary function. The reasons for this include the mechanical effects of truncal obesity and the metabolic effects of adipose tissue. Obesity is linked to a wide range of respiratory conditions including chronic obstructive pulmonary disease, asthma, obstructive sleep apnoea, pulmonary embolic disease and aspiration pneumonia. It is important for those providing care for people with respiratory disease to appreciate the impact of obesity and to provide appropriate advice for weight reduction. Healthcare planners should consider the impact of obesity for future resources in respiratory care.
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PMID:Obesity and the lung: 1. Epidemiology. 1858 31

Sleep-disordered breathing and sleep apnoea are conditions frequently associated with comorbidity, including obesity, diabetes, hypertension, insulin resistance (metabolic syndrome) and cardiovascular disease. The diabetic state (type 1 and type 2 diabetes) may be associated to diminished lung function and, in particular, decreased vital capacity, and the association between chronic obstructive pulmonary disease (COPD) and type 2 diabetes may be due to a shared inflammatory process. Also, the alteration in circulating endothelial progenitor cells found in respiratory disease, the metabolic syndrome and cardiovascular disease reflect a common condition of endothelial dysfunction.
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PMID:The metabolic syndrome, diabetes and lung dysfunction. 1882 64

Local airway inflammation in chronic respiratory disease is well described. Recently it has been recognised that chronic obstructive respiratory disease, asthma and obstructive sleep apnoea, all involve a systemic inflammatory component. Overspill of airway inflammation, as well as direct metabolic effects, are potential contributors to systemic inflammation. This review will discuss the role of certain types of fatty acids in promoting systemic inflammation, via the innate immune response. Fatty acids are necessary as the key energy source in the body. However, they can be detrimental if present in excess. Various features of respiratory disease lead to altered lipid metabolism, and notably an increase in circulating levels of non-esterified fatty acids (NEFA). Dietary intake, obesity, hypoxia and smoking, will be discussed as factors promoting an increase in circulating NEFA. While n-3 polyunsaturated and monounsaturated fatty acids may be non-(or anti-)inflammatory, saturated and n-6 polyunsaturated fatty acids have been shown to stimulate the innate immune response. Thus, increased circulating NEFA may be directly contributing to systemic inflammation, thereby increasing susceptibility of individuals to chronic inflammatory diseases, including respiratory disease, cardiovascular disease and diabetes. Finally, the review will discuss how the recognition of NEFA as important inflammatory stimulants in respiratory disease, leads to the possibility that pathways involved in lipid metabolism may provide therapeutic targets.
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PMID:Innate immune mechanisms linking non-esterified fatty acids and respiratory disease. 1901 34


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