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

The frequent concurrence of other cardiovascular risk factors in hypertensive patients, such as obesity and diabetes mellitus, suggests that overlapping genetic and environmental factors may contribute to the common metabolic and cardiovascular derangements observed in these populations. Hypertension and hyperglycemia accelerate atherosclerosis in diabetics, and play an important role in associated morbidity and mortality. Several abnormalities in blood pressure regulatory systems such as the renin-angiotensin system, the sympathetic nervous system, and sodium/volume control have been described in diabetes mellitus. Sodium retention and cardiovascular hyperreactivity appear to occur early in the course of diabetes mellitus, even at normal blood pressure levels and before onset of renal failure, and could set the stage for the development of hypertension. The relationship between obesity and hypertension is also well-established, and may reflect metabolic and cardiovascular adaptations in obese subjects which predispose to blood pressure elevations. Obese subjects display changes in sympathetic nervous system activity, sodium metabolism, and vascular hemodynamics. Sodium-sensitive blood pressure responses in the obese may be secondary to increased cardiac output or fluid volume, and are directly related to circulating insulin levels. Certain metabolic and vascular characteristics of obesity and diabetes mellitus are found in patients with essential hypertension. It has been suggested that insulin and insulin resistance may be the common link between these risk factors. Improved understanding of metabolic considerations in the treatment of obese and diabetic hypertensives should lead to more careful selection of medications that avoid metabolic complications. Although diuretics and beta-blockers may be useful in some patients, there are several reasons not to recommend their use as initial therapy in obese and diabetic hypertensives. On the other hand, calcium channel blockers and angiotensin converting enzyme inhibitors are highly effective, with minimal effects on metabolic parameters, and are well-suited as first-line therapy in the treatment of obese and diabetic hypertensives.
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PMID:Metabolic considerations in hypertension. 207 23

A 3-year-old boy presented with decreased renal function, hypertension, obesity and developmental delay. Evaluation of his kidneys revealed blunting of the calyces and multiple renal cortical cysts. Ophthalmologic evaluation showed no abnormalities on examination but electroretinography showed reduced retinal function suggesting a diffuse retinal disorder. Based on the clinical presentation with the associated abnormalities, the diagnosis of Bardet-Biedl syndrome, a form of the Laurence-Moon-Biedl syndrome was made. This syndrome should be considered and specific diagnostic efforts should be made in pediatric patients who present with renal failure and obesity.
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PMID:Early diagnosis of Bardet-Biedl syndrome. 240 Jun 55

Hepatic steatosis and steatonecrosis occur in nonalcoholic individuals, usually in a setting of obesity, type II diabetes mellitus, and after jejunoileal bypass. We propose an hypothesis for the pathogenesis of these hepatic lesions based on an observation in peritoneal dialysis patients. Hepatic histology was examined at autopsy in 11 patients with type I diabetes mellitus and renal failure who had received i.p. insulin in conjunction with continuous ambulatory peritoneal dialysis (CAPD). Steatosis in a unique subcapsular distribution occurred in 10 of 11 patients treated with i.p. insulin and in 0 of 9 controls receiving CAPD without insulin. Three of the 11 had steatonecrosis, 2 of whom had Mallory bodies. We suggest that insulin has an important role in the pathogenesis of steatosis and steatonecrosis. In CAPD patients the lesions occurred only under the capsule where concentrations of insulin are high secondary to its i.p. administration. In obese patients the lesions occur throughout the liver where insulin concentrations are high because of elevated levels in the portal vein. Free fatty acids (FFA) are oxidized in the liver by a pathway that is blocked by insulin. In the presence of insulin, FFA are preferentially esterified into triglycerides which accumulate in large quantities leading to steatosis; small amounts of FFA escaping local control may lead to membrane injury and steatonecrosis. Steatosis and/or steatonecrosis will occur when there is insulin secretion sufficient to block FFA oxidation but not sufficient to block FFA mobilization from adipose tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subcapsular steatonecrosis in response to peritoneal insulin delivery: a clue to the pathogenesis of steatonecrosis in obesity. 265 21

We present a case of granulomatous interstitial nephritis and renal failure after a jejunoileal bypass for obesity. Improvement of the renal function occurred after reversal of the intestinal bypass. The renal biopsy showed an interstitial nephritis, oxalate crystal deposition and several aggregates of multinucleated giant cells related to the crystal material (granulomatous reaction). By ultrastructural and histochemical studies we demonstrated mitochondrial alterations in the tubular epithelial cells, and we suggested the proximal tubule origin of the giant cells. The association of the oxalate crystals with damaged tubules and giant cells suggests that the oxalate crystals are responsible for these alterations. The possibility of an associated immunological process as the cause of the interstitial nephritis cannot be excluded.
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PMID:Granulomatous interstitial nephritis after a jejunoileal bypass: an ultrastructural and histochemical study. 271 63

To determine the interfamilial and intrafamilial variation in the expression of the Bardet-Biedl syndrome (a form of Laurence-Moon-Biedl syndrome), we looked for the five recognized features of the disorder (retinal dystrophy, obesity, polydactyly, mental retardation, and hypogonadism), plus possible renal manifestations, in some or all of 32 patients with this disorder. All 28 patients examined had severe retinal dystrophy, but only 2 had typical retinitis pigmentosa. Polydactyly was present in 18 of 31 patients, but syndactyly, brachydactyly, or both were present in all. Obesity was present in all but 1 of 25 patients. Only 13 of 32 patients were considered mentally retarded. Scores on verbal subtests of intelligence were usually lower than scores on performance tasks. Seven of eight men had small testes and genitalia, which was not due to hypogonadotropism. All 12 women studied had menstrual irregularities, and 3 had low serum estrogen levels (1 of these had hypogonadotropism, and 2 had primary gonadal failure). The remaining women who were of reproductive age had endocrinologic evidence of reproductive dysfunction. Diabetes mellitus was present in 9 of 20 patients. Renal structural or functional abnormalities were universal (n = 21), and three patients had end-stage renal failure. We conclude that the characteristic features of Bardet-Biedl syndrome are severe retinal dystrophy, dysmorphic extremities, obesity, renal abnormalities, and (in male patients only) hypogenitalism. Mental retardation, polydactyly, and hypogonadism in female patients are not necessarily present.
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PMID:The cardinal manifestations of Bardet-Biedl syndrome, a form of Laurence-Moon-Biedl syndrome. 277 27

The conventional "stepped-care" approach to the treatment of hypertension deserves revision. Rational therapy considers a variety of factors to obtain maximum efficacy, safety, tolerability, compliance, and neutralization of neural tone for the prevention of sudden death. The patient's age, gender, race, behavior profile, hemodynamic and neurohumoral status (plasma renin activity, norepinephrine/epinephrine ratio), and quality of life will help determine the choice of antihypertensive agent. Concomitant risk factors (smoking, obesity, diabetes, hypercholesterolemia), the presence of sequelae (left ventricular hypertrophy and/or failure, renal failure), and the existence of other disorders (mitral valve prolapse, depression, anxiety) must also be considered when initiating treatment. In addition, the cost of ancillary expenses (laboratory tests, hospitalizations, and emergency room visits) must be weighed against the potential benefits of therapy. Beta blockers are effective, well tolerated, and versatile for the treatment of concomitant cardiovascular disorders and as behavior modifiers. Calcium channel blockers and angiotensin converting enzyme inhibitors also show promise and merit consideration as therapy for specific groups of hypertensive patients.
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PMID:The 1980s: a patient-specific therapeutic approach in hypertension. 288 36

Data from several epidemiologic studies have suggested that the prevalence of hypertension in patients with diabetes mellitus is approximately 1.5-2.0 times greater than in an appropriately matched nondiabetic population. In patients with insulin-dependent diabetes mellitus (IDDM), hypertension is generally not present at the time of diagnosis. As renal insufficiency develops, blood pressure rises and may exacerbate the progression to end-stage renal failure. In non-insulin-dependent diabetes mellitus (NIDDM), many patients are hypertensive at the time of diagnosis. The incidence of hypertension in NIDDM is related to the degree of obesity, advanced age, and extensive atherosclerosis that is typically present, and it probably includes many patients with essential hypertension. Several other pathophysiologic mechanisms also contribute to the genesis and maintenance of hypertension in the patient with diabetes. Hyperglycemia and increases in total-body exchangeable sodium may lead to extracellular fluid accumulation and expansion of the plasma volume. In some patients, alterations in the function of the renin-angiotensin-aldosterone system and vascular sensitivity to vasoactive hormones may also play a role. It has recently been suggested that hyperinsulinemia and insulin resistance may also contribute to the maintenance of an elevated blood pressure because insulin is known to promote sodium retention and enhance sympathetic nervous system activity. The evidence for these hypotheses and their respective contributions to the etiology of hypertension in IDDM and NIDDM are discussed.
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PMID:Etiology and prevalence of hypertension in diabetic patients. 307 72

Isolated non inflammatory lesions of renal microarteries (eventually with mild thickening of tubular basement membranes, but with negative immunofluorescent glomerular studies) were observed in 25 patients (22 males) in whom renal biopsy have been performed for proteinuria (P). Selection criteria were: pathological lesions by definition; absence of hypertension (HT) in clinical and at the time of biopsy; minimum follow up of 4 years after the first statement of the proteinuria (4 to 29 years; mean 14 years). Three groups have been isolated: 1. 3 patients have had an acute glomerulonephritis followed by disappearance of proteinuria. It reappears 1 to 5 years later. HT was discovered 2, 8 and 11 years after the proteinuria. Renal failure occurred 1 and 3 years after HT. 2. 14 patients had hereditary or acquired vascular risk factors (obesity, smoking, ethylism). In 7, HT occurred 3 to 15 years after P. In 2, renal failure occurred 4 to 8 years later. 3. 8 patients had no vascular risk factor; in 3 of them Ht developed 7, 13 and 20 years after the first statement. A positive immunofluorescence with IgM or C3 on renal arterioles had been found in only 3 of the 10 patients who in group 2 and 3 became hypertensive. A proteinuria may precede the occurrence of HT without being induced by glomerulonephritis. Group 2 and 3 suggest that these renal lesions of arterial sclerosis precede and may be a factor of HT. Indeed, this entity may be considered as a prehypertensive condition.
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PMID:[Primary microvascular lesions of the kidney or pre-hypertensive nephroangiosclerosis. 25 cases]. 309 92

Coexistent diabetes and hypertension affect an estimated 2.5 million persons in the United States. Hypertension occurs approximately twice as frequently in persons with diabetes as without and contributes to most of the chronic complications of diabetes, including coronary artery disease, stroke, lower extremity amputations, renal failure and, perhaps, to diabetic retinopathy and blindness. The proportions of complications in the diabetic population attributable to hypertension range from 35 to 75 percent. Hypertension in the diabetic population increases with age and is particularly associated with obesity and nephropathy. Limited data suggest the control of hypertension in the diabetic population may be better than in the general population, perhaps due to greater contact that persons with diabetes have with the health care system. Yet, in approximately half, hypertension is not controlled. Control strategies for hypertension in the diabetic population must take into account the higher frequency of hypertension, increased risks for adverse sequelae from the coexistent conditions, more complicated clinical management, and the greater contact with the health care system experienced by persons with diabetes. Community programs to improve hypertension control in the diabetic population may target a subset of the diabetic population and should tailor strategies to meet the needs of the target population. Hypertension control in the diabetic population must be addressed at multiple levels in the health care system, including improved detection, evaluation, and treatment of hypertension; improved adherence to antihypertensive therapy and long-term followup; provision of quality professional education and patient education and support; and systematic health care monitoring and program evaluation. Hypertension control should be emphasized in all comprehensive diabetes control programs.The treatment and control of hypertension may significantly reduce morbidity and mortality in the diabetic population.
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PMID:The control of hypertension in persons with diabetes: a public health approach. 311 83

Atherosclerosis and hypertension are, by far, the most common cardiovascular diseases affecting women, and both are influenced by diet. Atherosclerosis occurs more commonly in men than women; generally women are 10 to 15 years older than men when symptoms develop. The prevalence of hypertension is about equal in the two sexes, particularly in middle aged and older persons. These cardiovascular diseases are major causes of death and disability in this country. Atherosclerosis results in myocardial infarction, thrombotic strokes, and claudication. Hypertension, when severe, damages small blood vessels, causing kidney failure, hemorrhage, strokes, and heart failure; when the condition is mild to moderate, it produces atherosclerosis. Nutritional factors are of primary importance in both atherosclerosis and hypertension. Risk factors for atherosclerosis related to nutrition are hypercholesterolemia, hyperglycemia-diabetes, and for hypertension, obesity, high salt intake, and excessive use of alcohol. Of all these risk factors, obesity seems to be the most important because it is strongly linked to hypertension and diabetes. Dietary intake of saturated fat is a potent factor in determining the blood cholesterol level, and reducing intake often decreases the level, thus lessening the risk of atherosclerotic complications. Although high salt intake and excessive alcohol use produce hypertension in susceptible people, less is known about the frequency of this adverse effect than is known about obesity.
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PMID:Nutrition and cardiovascular diseases of women. 312 Feb 15


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