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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abnormalities in coagulation and haemostasis represent a well-known link between obesity and thrombosis (both arterial and venous). Several studies have shown that obese patients have higher plasma concentrations of all pro-thrombotic factors (fibrinogen, vonWillebrand factor (vWF), and factor VII), as compared to non-obese controls, with a positive association with central fat. Similarly, plasma concentrations of plasminogen activator inhibitor-1 (PAI-1) have been shown to be higher in obese patients as compared to non-obese controls and to be directly correlated with visceral fat. Furthermore, obesity is characterized by higher plasma concentrations of anti-thrombotic factors, such as tissue-type plasminogen activator (t-PA) and protein C, as compared to non-obese controls, the increase in these factors being likely to represent a protective response partly counteracting the increase in pro-thrombotic factors. The issue of whether adipose tissue contributes directly to plasma PAI-1, its products stimulating other cells to produce PAI-1, or whether it primarily contributes indirectly has not yet been resolved. It has been proposed that the secretion of interleukin-6 (IL-6) by adipose tissue, combined with the actions of adipose tissue-expressed TNF-alpha in obesity, could underlie the association of insulin resistance with endothelial dysfunction, coagulopathy, and coronary heart disease. The role of leptin in impairing haemostasis and promoting thrombosis has been recently reported. Finally, some hormonal abnormalities (androgen, F, catecholamines) associated with the accumulation of body fat may contribute to the impairment of coagulative pathway in obesity. As to intervention strategies, dietary (i.e., low-fat high-fiber diet) and lifestyle (i.e., physical activity) measures have been demonstrated to be effective in improving the obesity-associated pro-thrombotic risk profile.
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PMID:Coagulation and fibrinolysis abnormalities in obesity. 1250 53

Hepatotoxicity is a serious complication in patients taking HAART. Coinfection with hepatitis viruses increases the risk of liver toxicity while taking antiretroviral therapy. Baseline transaminases should be checked before beginning antiretorviral therapy and all patients should be screened for pre-existing liver disease, most notably hepatitis B and C infections. Regular monitoring of transaminases is mandatory when commencing antiretroviral therapy. In patients with normal liver function, transaminases may be checked monthly after commencing HAART for the first 3 months. If stable this can be broadened to 3 month intervals. In patients with pre-existing liver disease monitoring should be performed more frequently (every 2 weeks) when initiating therapy. Once stable liver enzymes should be checked monthly. The less hepatotoxic drugs such as lamivudine and abacavir should be preferred in patients at high risk for hepatotoxicity. Risks include co-infection with hepatitis B and C viruses, a previous record of hepatotoxicity, cirrhosis, obesity and female gender. Minor enzyme elevations (< 5-fold upper normal limit) are generally safe to tolerate and usually resolve. Patients must be closely observed with regular liver function tests and a hypersensitivity type drug reaction should be excluded. The onset of clinical symptoms, elevated serum lactate or evidence of severe hepatic dysfunction (coagulopathy or elevation of ammonia levels) are suggestive of severe toxicity and HAART should be withheld. Treatment of suspected HAART related hepatotoxicity should first involve withdrawal of therapy. Hypersensitivity reactions may be treated with corticosteroids. Nucleoside-induced mitochondrial damage may improve with riboflavin or thiamine therapy.
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PMID:Hepatotoxicity of antiretroviral therapy. 1287 6

The direct correlation between glucose levels and cardiovascular disease in individuals with type 2 diabetes can now be applied to individuals that share an abnormal metabolic milieu similar to that found in central obesity, the metabolic syndrome, and type 2 diabetes. Premature macrovascular complications with a very high morbidity and mortality rate can be found in these nondiabetic populations. The typical phenotype has visceral or central obesity, excess of free fatty acids, insulin resistance, increased insulin secretion, and hypertension. A more complex metabolic-cardiovascular syndrome develops that includes dyslipidemia, abnormal production of cytokines, chronic inflammatory state, and abnormal coagulation. The interplay of all these cardiovascular risk factors is responsible for the accelerated atherosclerotic process. The different terminologies used for populations sharing this common ground for premature cardiovascular disease now generally accepted as the metabolic syndrome, are also discussed. Aggressive insulin treatment during acute illness in individuals with the abnormal metabolic milieu is beneficial. Insulin treatment is changing from using insulin as a hormone to treat only severe hyperglycemia, to a new paradigm using insulin in high doses as a drug. Aggressive insulin regimens should be used to treat only minimal elevations of blood glucose or to prevent hyperglycemia. The newly observed properties of insulin are reviewed which include suppression of inflammatory cytokines and adhesion molecules, improved hemostasis, and other cardiac beneficial effects. The concomitant administration of intravenous glucose and insulin permits the administration of higher insulin doses that can result in improved outcome due to its nonglycemic-related benefits. The use of aggressive insulin therapy requires both better and more cost-effective algorithms to successfully treat this high-risk population during acute illness.
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PMID:Using insulin as a drug rather than as a replacement hormone during acute illness: a new paradigm. 1450 30

THE PREGNANT PATIENT: Age; maternal disease; prophylactic antibiotics; gastroesophageal reflux; obesity; starvation; genotyping; coagulopathy; infection; substance abuse; altered drug responses in pregnancy; physiological changes of pregnancy. THE FETUS: Fetal monitoring; intrauterine surgery. THE NEWBORN: Breastfeeding; maternal infection, fever, and neonatal sepsis evaluation. OBSTETRIC COMPLICATIONS: Embolic phenomena; hemorrhage; preeclampsia; preterm delivery. OBSTETRIC MANAGEMENT: External cephalic version and cervical cerclage; elective cesarean delivery; fetal malpresentation; vaginal birth after cesarean delivery; termination of pregnancy. OBSTETRIC ANESTHESIA: Analgesia for labor and delivery; anesthesia for cesarean delivery; anesthesia for short obstetric operations; complications of anesthesia. MISCELLANEOUS: Consent; ethics; history; labor support; websites/books/leaflets/journal announcements.
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PMID:What's new and novel in obstetric anesthesia? Contributions from the 2003 scientific literature. 1579 48

Glicocorticosteroids (GS) are widely used for the treatment of nephrotic syndrome (NS), even though this form of therapy is associated with a spate of early and late side effects. The present study assessed physical development and function of vital organs in adults who were treated with GS for NS of childhood. 96 patients were compared with 15 controls. History-taking and anthropometric measurements were done in all patients. Kidney function, lipid and carbohydrate metabolism, water-electrolyte balance and clotting factors were studied in 29 cases. Reference values for lithium clearance and fractional lithium excretion were calculated using results obtained in controls. Physical development of individuals with NS diagnosed in childhood did not differ from controls. However, their growth rate was greater than expected. The risk of overweight and obesity in this group was not higher than in the general population. However, disturbances of lipid and carbohydrate metabolism, as well as impaired kidney function were more frequent in this group. Females appear to be at greater risk of coagulopathy as compared with males. Taking these findings into account, former NS patients treated with GS in childhood should be regularly examined with laboratory tests even if cured of the disease.
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PMID:[Distant effects of steroid therapy in the nephrotic syndrome of childhood]. 1652 62

Considerable evidence is available in support of an independent association between obstructive sleep apnoea syndrome (OSAS) and cardiovascular disease, which is particularly strong for systemic arterial hypertension and growing for ischaemic heart disease, stroke, heart failure, atrial fibrillation and cardiac sudden death. The pathogenesis of cardiovascular disease in OSAS is not completely understood but likely to be multifactorial, involving a diverse range of mechanisms including sympathetic nervous system overactivity, selective activation of inflammatory molecular pathways, endothelial dysfunction, abnormal coagulation and metabolic dysregulation, the latter particularly involving insulin resistance and disordered lipid metabolism. The present report, which arose out of a European Union Cooperation in the field of Scientific and Technical Research (COST) action on OSAS (COST B26), reviews the current evidence for an independent association and proposes research priorities to identify the underlying mechanisms involved, with a view to identifying novel therapeutic strategies. Large-scale collaborative studies of carefully defined patient populations with obstructive sleep apnoea syndrome, adequately controlled for potential confounders, are needed. Such studies carry the prospect of evaluating potential interactions between different basic mechanisms operating in obstructive sleep apnoea syndrome and cardiovascular disease, and interactions with other related disorders, such as obesity, diabetes and dyslipidaemia. Furthermore, translational studies involving cell culture and animal models linked to studies of obstructive sleep apnoea syndrome patients are necessary to integrate basic mechanisms with the clinical disorder.
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PMID:Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. 1719 82

A frequent condition affecting patients with stroke is venous thromboembolism (VTE), which consists of two components: deep vein thrombosis, and pulmonary embolism as its complication The main risk factors of VTE are: age over 65 years, motor deficit with immobilisation, heart failure, infection, obesity and coagulopathy Typical symptoms of deep vein thrombosis (pain, tenderness, swelling of calf and increased skin temperature) can be masked by sensory and autonomic deficits following brain ischaemia Diagnosis of VTE is based on clinical symptoms confirmed by biochemical and radiological findings The treatment of VTE consists of anticoagulation; prevention of VTE in stroke patients is based on use of low-molecular heparins and non-pharmacological methods.
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PMID:[Deep vein thrombosis in patients with stroke]. 1762 19

Serial venous duplex scans (VDS) were done in 507 trauma patients with at least one risk factor (RF) for venous thromboembolism (VTE) during a 2-year study period. Deep vein thrombosis (DVT) was detected in 31 (6.1%) patients. This incidence was 3.1 per cent in low (1-2 RFs), 3.4 per cent in moderate (3-5 RFs), and 7.7 per cent in high (> or =6 RFs) VTE scores (P = 0.172). Incidence was statistically different (3% vs. 7.2%, P = 0.048) on reanalyzing patients in two risk categories, low-risk (1-4 RFs) and high-risk (> or =5 RFs). Only 4 of 16 RFs had statistically higher incidence of DVT in patients with or without RFs: previous VTE (27.3% vs. 5.6%, odds ratio (OR) 6.628, P = 0.024), spinal cord injury (22.6% vs. 5%, OR 5.493, P = 0.001), pelvic fractures (11.4% vs. 5.1%, OR 2.373, P = 0.042), and head injury with a greater than two Abbreviated Injury Score (10.5% vs. 4.2%, OR 2.639, P = 0.014). On reanalyzing patients with > or =5 RFs vs. <5RFs, obesity (14.3 vs. 6.1%, P = 0.007), malignancy (5.6% vs. 0.6%, P = 0.006), coagulopathy (10.8% vs. 1.8%, P = 0.000), and previous VTE (3.2% vs. 0%, P = 0.019) were significant on univariate analysis. Patients with DVT had 3.70 +/- 1.75 RFs and a 9.61 +/- 4.93 VTE score, whereas, patients without DVT had 2.66 +/- 1.50 RFs and a 6.83 +/- 3.91 VTE score (P = 0.000). DVTs had a direct positive relationship with higher VTE scores, length of stay, and number of VDS (>1 r, P < or = 0.001). Increasing age was a weak risk factor (0.03 r, P = 0.5). First two VDS diagnosed 77 per cent of DVTs. Patients with injury severity score of > or =15 and 25 had higher DVTs compared with the ones with lower injury severity score levels (P < or = 0.05). Pulmonary embolism was silent in 63 per cent and DVTs were asymptomatic in 68 per cent.
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PMID:Venous thromboembolism in trauma patients. 1809 58

Intrauterine or fetal growth restriction is best defined by using customised birth weight percentiles based upon the growth potential for an individual infant. Growth restriction in utero may be classified as asymmetric or symmetric depending upon the duration of the process. Asymmetric growth restriction is caused by placental insufficiency, maternal hypertensive conditions, long-standing maternal diabetes, smoking, living at altitude or multiple gestation. Symmetric growth restriction may be due to congenital infections, chromosomal or other abnormalities, fetal alcohol syndrome, low socioeconomic status or be constitutional. The underlying cause of growth restriction often predicts the potential adverse effects on the foetus and newborn and later effects in childhood and adulthood. With placental insufficiency, there may be chronic or acute on chronic fetal hypoxia with birth asphyxia and hypothermia, neonatal hypoglycaemia, polycythaemia and coagulopathy. Management is directed at prevention or early treatment of these conditions. In contrast, symmetrically growth-restricted infants should be examined carefully to look for congenital infections and malformations that may need specific interventions. Infants with constitutional short stature generally do not need any specific management. Feeding of growth-restricted infants is important to overcome deficiencies incurred in utero. Most infants show catch-up growth although about 10% do not. Those with excessive catch-up growth may be at greatest risk of developing insulin resistance in adulthood leading to diabetes, obesity and heart disease. The so-called fetal origins of disease may actually have a postnatal onset related more to excessive weight gain in infancy. There is still controversy over the indications for growth hormone treatment in growth-restricted infants who remain of short stature in early childhood. Intrauterine growth restriction is also associated with a five- to seven-fold increased risk of cerebral palsy probably due to chronic placental insufficiency.
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PMID:Neonatal management and long-term sequelae. 1963 99

Adhesion molecules play a significant role in leukocyte migration across the endothelium and are also involved in regulating immune system. It is shown that diabetic patients have an increase of soluble adhesion molecules (sICAM-1, sICAM-2, sVCAM-1, sE-selectin, sL-selectin, sP-selectin) considered an integral part of inflammatory state. This inflammation is responsible for the increased cardiovascular risk of these patients. There is a close link between hyperglycemia, oxidative stress, coagulopathy and inflammation and between these factors and the vascular damage. Various studies have showed the potential role of adhesion molecules in the pathogenesis of diabetic vasculopathy. They promote leukocyte recruitment, which is one of the initial steps in the genesis of atherosclerotic plaque. Adhesion molecules are also involved in the pathogenesis of diabetes mellitus type 1; sICAM-1 would have a particular immunomodulatory role in the process of destroying beta-cells and could be used as a subclinical marker of insulitis. Plasma levels of soluble adhesion molecules correlate with hyperglycemia, insulin resistance, dyslipidemia and obesity; they are associated with the development of nephropathy, retinopathy, myocardial infarction, stroke and obliterant peripheral arterial disease in diabetic type 1 and 2. Given the role of these molecules in endothelial dysfunction genesis and tissue damage associated with diabetes, they could constitute a therapeutic target for the prevention of genesis and progression of chronic complications of diabetic disease.
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PMID:[Adhesion molecules and diabetes mellitus]. 2054 49


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