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

The role of circulatory congestion in the cardiorespiratory dysfunction of massive obesity was investigated in 18 patients. They were hypervolemic and had increased cardiac outputs proportionate to their weight. The average resting left ventricular filling pressure was within the upper limits of normal, but it increased to abnormally high levels with increased venous return of passive leg raising, and further during exercise. The elevations in pressure were associated with high resting central blood volumes which increased significantly with exertion. These findings are consistent with reduced distensibility of the central circulation in these congested patients. Weight reduction was accompanied by a decrease in central blood volumes and restoration of a normal left ventricular response in three of four patients and a return toward normal in one. The improvement in ventricular function with relief of edema and dyspnea. In 14 patients with normal or only minimal alveolar hypoventilation, there were no significant transpulmonary diastolic pressure gradients despite a marked increase in left ventricular end-diastolic pressures. One patient, after regaining weight, subsequently had an abnormal gas exchange and an increased pulmonary vascular resistance. He and two others with severe alveolar hypoventilation demonstrated cor pulmonale on a background of left ventricular dysfunction and congestion of the circulation. Two other patients, the least obese of the group, had hypoventilation and cor pulmonale with normal left ventricular pressures. Hypervolemia and a hyperdynamic state are common features of the obese patients. High cardiac output is maintained despite marked circulatory congestion which may result in generalized anasarca and increased ventricular filling pressures. This clinical syndrome may be present in obese patients without intrinsic heart disease and may be reversible with weight reduction. The central circulatory congestion may contribute to the development of the alveolar hypoventilation syndrome in certain obese patients.
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PMID:Role of circulatory congestion in the cardiorespiratory failure of obesity. 102 Jul 53

Many epidemiological and clinical studies show a strong association between arterial hypertension and obesity. The underlying pathophysiological mechanism is unknown. It is thought that the etiopathogenesis of obesity hypertension is exceptional and in that view hormonal, neural, volume and hemodynamic properties of obesity, as well as salt and/or caloric consumption, are outlined. In this article all these factors are discussed. According to the current hypothesis, hyperinsulinemia which is probably a physiologic adaptation to obesity, plays a key role in the pathogenesis of arterial hypertension. Insulin increases the reabsorption of sodium by means of an immediate effect on the kidney tubules. An increase of sodium in the body leads to hypervolemia and to the elevated blood pressure. Chronic hyperinsulinemia perhaps increases the blood pressure indirectly also by means of the central nervous system, namely, by stimulating the activity of the sympathetics.
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PMID:[Arterial hypertension in the obese--aspects of etiopathogenesis]. 823 16

While the prevalence of hypertension is clearly increased among the overweight persons, the pathophysiological mechanisms underlying this frequent association of obesity and hypertension are still poorly understood. The expansion of extracellular volume, inducing hypervolaemia and increased cardiac output, represents the characteristic haemodynamic feature of the obesity-related hypertension. The maintenance of hypervolemia in the face of elevated blood pressure, indicates a resetting of pressor natriuresis toward higher blood pressure. The development of hypertension also indicates an increase in peripheral vascular resistance, thus the lack of physiological adaptation of peripheral resistance to increased cardiac output. The mechanisms underlying these changes in renal function and vascular reactivity can no longer be attributed to hyperinsulinaemia as such, but might be related to insulin resistance responsible for the enhancement in pressor activity of noradrenaline and angiotensin II. This increased reactivity to pressor factors may be due to an inadequate nitric oxide generation by vascular endothelium and to increased sodium and calcium concentration in vascular smooth muscle cells. The role of increased neuropeptide Y (NPY) activity, may also be involved. As to enhancement of tubular sodium reabsorption, it could be related to histological changes within the renal medulla, leading to compression of tubules and vasa recta, hence a more efficient sodium reabsorption. As to the therapeutic approach, the low-energy sodium-restricted diet associated with increased physical activity, represents the cornerstones of treatment for the obesity-related hypertension. If this approach fails, the pharmacological treatment becomes necessary, and the use of the converting enzyme inhibitors seems to be the most appropriate choice of drug therapy for hypertensive obese patients.
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PMID:Obesity and hypertension: from pathophysiology to treatment. 1019 61

A retrospective review of dengue patients admitted to Queen Sirikit National Institute of Child Health (previously known as Children's Hospital) from 1995 to 1999 revealed 4,532 confirmed cases of dengue infection; 80.9% were dengue hemorrhagic fever (DHF) and 19.1% were dengue fever cases (DF). Among the DHF patients; 30.6% had shock. The majority of them, 66.6%, had a normal nutritional status, while 9.3% were malnourished and 24.2% had obesity as classified by weight for age. Compared with control patients with other diagnoses (excluding HIV/AIDS patients), malnourished children had a lower risk of contracting dengue infection (odds ratio = 0.48, 95% Cl = 0.39-0.60, p = 0.000) while obese children had a greater risk of infection with dengue viruses (odds ratio = 1.96, 95% Cl = 1.55-2.5, p = 0.000). The clinical signs, symptoms and laboratory findings of dengue were almost the same among the 3 groups of malnourished, normal, and obese patients. The minor differences observed were that in obese children liver enlargement was found less often; maculopapular/convalescence rash and elevations of alanine aminotransferase were found more often. Malnourished patients had a higher risk of developing shock (37.8%) than normal (29.9%) and obese patients (30.2%) (p = 0.000). Obese patients had more unusual presentations: encephalopathy (1.3%) and associated infections (4.8%), than normal (0.5% and 2.7%) and malnourished patients (1.2% and 3.1%). Complications of fluid overload were found more in obese patients (6.5%) compared to normal (3.2%) and malnourished patients (2.1%) (p = 0.000). The case-fatality rates (CFR) in malnourished patients and obese patients were 0.5% and 0.4%, respectively, while in normal patients the CFR was 0.07%. Under and over nutrition DHF patients had either a greater risk of shock or unusual presentations and complications, which can lead to severe disease or complications and probably a higher CFR.
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PMID:Is dengue severity related to nutritional status? 1591 44

Overweight and obesity is the most common chronic disease in the United States and is associated with an increased risk for morbidity and mortality. For the hospitalized patient, the mechanical, metabolic, and inflammatory physiologic changes induced by obesity necessitate additional considerations for care. Calculation of nutritional requirements is problematic and challenging due to difficulty in measuring body composition and energy expenditure. Provision of selective hypocaloric feeding in this population may be particularly beneficial in reducing complications of hyperglycemia, fluid overload, and reduction in fat mass. Clinical care should incorporate a team approach that addresses the special nutritional and metabolic needs of this population.
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PMID:Nutritional support of the obese patient. 1604 19

The metabolic syndrome, defined as a cluster of visceral obesity, insulin resistance, dyslipidemia and elevated blood pressure, is associated with pro-thrombotic, pro-atherogenic and inflammatory risk factors that predispose to cardiovascular disease. Although activators of the peroxisome proliferator-activated receptors (PPARalpha,gamma,delta) in various combinations are under development for treating the metabolic syndrome, they are hampered by adverse effects related to increased adipogenesis, weight gain, fluid overload and carcinogenesis. The recent discovery that telmisartan and irbesartan, antihypertensive angiotensin II type 1 receptor (AT1-R) blockers (ARBs), were uniquely capable of activating PPARgamma, has provided a novel approach to addressing the multifactorial components of the metabolic syndrome. Both drugs have established favorable safety profiles and can activate PPARgamma at concentrations potentially achievable at therapeutic doses. Emerging studies have revealed that both these drugs have beneficial metabolic profiles. This information provides a strategic rationale and pharmacological platform for the development of novel dual ARB/PPARgamma agonists to target the metabolic syndrome and its cardiovascular sequelae, for which therapy is presently insufficient or non-existent. Beneficial effects of these agents include increased energy expenditure, improved lipid profile, increased insulin sensitivity, blood pressure reduction, and amelioration of the associated pro-inflammatory and pro-atherogenic risk profiles. The potential benefit for treatment of the metabolic syndrome, cardiovascular protection, and prevention of related end-organ complications could be of immense clinical value.
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PMID:Treating the metabolic syndrome using angiotensin receptor antagonists that selectively modulate peroxisome proliferator-activated receptor-gamma. 1629 56

The incidence of resistant hypertension remains to be clarified. In this article, three categories of resistance are distinguished: resistant patient, resistant clinician and refractory hypertension. Inadequate compliance, which in case of antihypertensive treatment means taking fewer doses of medications than prescribed, remains a significant cause of poor blood pressure control. Among most frequent physician-related causes of resistant hypertension, there are measurement errors, pseudohypertension, white coat hypertension and therapy errors. Careful elimination of patient- and physician-related reasons of inadequate blood pressure control should lead to the diagnosis of truly resistant hypertension. One of the causes of refractory hypertension may be concomitant use of other medications that are known to reduce antihypertensive effect of main drugs. Resistance may be associated with increased intravascular volume or fluid overload or with sympathetic activation. Modifiable contributing factors responsible for resistant hypertension include obesity often coexisting with insulin resistance and metabolic syndrome as well as excessive alcohol use and cigarette smoking. Another potential cause of refractory hypertension is the presence of secondary hypertension. Certain therapeutic modifications are essential in resistant hypertension.
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PMID:Resistant hypertension. 1642 42

The metabolic syndrome consists of a combination of cardiovascular risk factors that include hyperglycemia with or without type 2 diabetes mellitus, visceral obesity, elevated blood pressure, and atherogenic dyslipidemia. These interrelated disorders and their associated lipotoxicity, oxidative stress, and inflammatory state predispose to a constellation of cardiovascular conditions leading to high risk of heart attack, stroke, renal failure, blindness, and lower extremity amputation. Visceral obesity, a prime risk factor for type 2 diabetes and a major component of the metabolic syndrome, potentiates atherogenesis, atherosclerosis, organ lipotoxicity, and oxidative tissue damage.Peroxisome proliferator-activated receptors (PPARs) are relatively recently discovered nuclear transcription factors that are modulated by dietary fatty acids, including the essential polyunsaturated fatty acids, arachidonic acid and its metabolites, and are essential to the control of energy metabolism. Of the three PPAR isoforms (alpha, gamma, and delta), synthetic pharmaceutical ligands that activate PPARalpha (the antidyslipidemic fibric acid derivatives ['fibrates']) and PPARgamma (the antidiabetic thiazolidinediones) have been studied extensively. Recently developed dual PPARalpha/gamma agonists may combine the therapeutic effects of these drugs, creating the expectation of greater efficacy, and perhaps other advantages in the treatment of type 2 diabetes and the metabolic syndrome. However, thiazolidinediones are hampered by adverse effects related to increased weight gain and fluid overload. It remains to be seen whether the dual PPARalpha/gamma agonists currently under development have similar limitations. Nevertheless, existing clinical data imply that the combined effects of thiazolidinediones and fibrates are likely to be emulated by dual PPARalpha/gamma agonists, providing superior efficacy to these classes for the treatment of type 2 diabetes, the metabolic syndrome, and their cardiovascular and other end-organ complications.
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PMID:Dual Peroxisome Proliferator-Activated Receptor-alpha/gamma Agonists : In the Treatment of Type 2 Diabetes Mellitus and the Metabolic Syndrome. 1654 49

Peritoneal dialysis (PD) patients present an extremely high mortality rate, but the mechanisms mediating the increased risk of mortality observed in this group of patients are still largely unknown, which limits the perspective of effective therapeutic strategies. The leading hypothesis that tries to explain this high mortality risk is that PD patients are exposed to a number of traditional risk factors for cardiovascular disease (CVD) already at the onset of their chronic kidney disease (CKD), since many of these risk factors are common to both CVD and CKD. Of particular importance, chronic inflammation recently emerged as an important novel risk factor related to multiple complications of CKD. There are many stimuli of the inflammatory response in CKD patients, such as fluid overload, decreased cytokine clearance, presence of uremia-modified proteins, presence of chronic infections, metabolic disturbances (including hyperglycemia), obesity. Many of these factors are related to PD. Latin America has made some progress in economic issues; however, a large portion of the population is still living in poverty, in poor sanitary conditions, and with many health-related issues, such as an increasing elderly population, low birth weights, and increasingly high energy intake in the adult population, which, in combination with changes in lifestyle, has provoked an increase in the prevalence of obesity, diabetes, and CVD. Therefore, in Latin America, there seems to be a peculiar situation combining high prevalence of low education level, poor sanitary conditions, and poverty with increases in obesity, diabetes, and sedentary lifestyle. Since inflammation and mortality risk are intimately related to both sides of those health issues, in this review we aim to analyze the peculiarities of inflammation and mortality risk in the Latin-American PD population.
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PMID:Inflammation in peritoneal dialysis: a Latin-American perspective. 1746 89

Obesity shows a strong association with hypertension, primarily due to secretion of an abundance of para- and endocrine peptides by the visceral adipose tissue that play a key role in the pathogenesis of high blood pressure and are responsible for the accelerated atherothrombosis encountered in overweight individuals. Increased activity of the RAAS and the sympathetic nerve system are the main pathophysiologic factors; hypertension in obese subjects is characterized by increased peripheral arterial resistance, high cardiac output, hypervolemia and salt sensitivity. Medical therapy sees blockade of the RAAS in front. Priority in treatment should be given to improvements in life style, primarily in increasing physical activity and decreasing caloric intake, and to medical treatment of associated risk factors according to the modern concept of global risk management.
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PMID:[Hypertension and overweight]. 1867 87


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