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Query: UMLS:C0028754 (obesity)
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Adrenocortical tumors can be divided into two groups based on their histopathological characteristics, i.e., benign (adenoma) and malignant (carcinoma), and also classified as functioning (or hormonal) and non-functioning (or non-hormonal) tumors, depending on the presence or absence of recognizable clinical syndromes due to excessive steroids. The syndrome of functioning adrenocortical tumors includes Cushing's syndrome, primary aldosteronism and the adrenorge genital syndrome, of which a minority presents most of the specific clinical features: Cushing's syndrome; red face, typical moon face, truncal obesity, and purplisch red striae, primary aldosteronism; muscle weakness, noctural polyuria, hypertension and hypokalemia, adrenogenital syndrome; virilization or feminization, but many of them present complete clinical picture. The diagnosis of these syndromes needs to measure urinary 17-OHCS and 17-KS and plasma concentrations of cortisol, aldosterone, dehydroepiandrosterone (DHEA) and the other steroids. Dexamenthasone suppression test, various stimulation tests and the measurement of plasma ACTH are also useful for diagnosis. Usually, adrenocortical tumors can be detected preoperatively by physical examination or radiographic studies. Some are massive enough to be palpable through the abdominal wall. Some are large enough to cause displacement of the kidney, as seen intravenous urography. Most are visible by adrenal scintigraphy using 131I-iodocholesterol, computerized tomography, or adrenal arteriography. The standard treatment for adrenocortical tumors are surgical resection. Unresectable adrenocortical carcinomas may be treated with an adrenocorticolytic drug, o'p'-DDD. Metyrapone and aminoglutethimide can be also employed to inhibit the production of steroids.
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PMID:[Diagnosis and treatment of adrenocortical tumors]. 631

Epidemiologic studies suggest that obesity is a major factor in hypertension in industrialized societies. Possible mechanisms for this association include elevated cardiac output, increased body sodium due to hyperinsulinemia or abnormal aldosterone/renin relationships, and neuroendocrine abnormalities due to increased noradrenergic activity or opiate suppression. Although cardiac output and plasma volume of obese hypertensive patients are not different from what is found in non-obese persons when expressed in relation to body surface area, these results are from cross-sectional studies and do not relate to the effects of weight gain on arterial pressure. The role of hyperinsulinemia and that of other endocrine or neuroendocrine abnormalities have not been studied extensively enough for the association to be proved.
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PMID:Mechanisms of hypertension associated with obesity. 634 97

Applied anatomy and physiology of the kidney are briefly reviewed. This includes an account of renal blood flow, glomerular filtration rate, juxtaglomerular apparatus, renal autoregulation and intra-renal blood flow distribution, tubular transport mechanisms, solute handling in proximal tubule, function of loop of Henle and distal tubule system. This section concludes with a summary of changes in tubule fluid along the length of the nephron. Acute effects of anaesthesia are reviewed in detail. Indirect effects include those on circulatory and sympathetic nervous systems, autoregulation, endocrine systems such as those involving anti-diuretic hormone, adrenaline and noradrenaline, renin-angiotensin and aldosterone. Direct effects of anaesthesia on renal function have now been confirmed both in vitro and in vivo. Delayed direct nephrotoxicity of anaesthetics relates predominantly to methoxyflurane (MOF) and its metabolism to inorganic fluoride. Other factors are MOF dose, genetics, age, enzyme induction, obesity, other nephrotoxic drugs. Clinical implications are presented. Enflurane nephrotoxicity is rare but aetiologic factors are similar to the foregoing. Isoflurane and halothane are not nephrotoxic. A consideration of the influence of anaesthetic management on the incidence and severity of postoperative acute renal failure concludes the review.
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PMID:Anaesthesia and the kidney. 635 48

There is a close epidemiological association between obesity and elevated blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Mechanisms included in the development of hypertension in obesity are hyperinsulinemia, insulin induced sodium retention and increased sympathetic tone. Overnutrition with over intake of sodium and lack of physical exercise contribute to the metabolic syndrome of obesity. Thus, weight reduction by decreased energy uptake and increased physical exercise is recommended in the treatment of hypertension in obese patients. The resulting fall in insulin levels may lead to decreased sodium absorption in the kidney. Although treatment of obesity by weight loss decreases blood pressure substantially, a minority of patients do not respond to the weight loss. Blood pressure generally decreases before normal weight is achieved. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk of cardiovascular disease in the hypertensive patient is not only determined by the blood pressure, an overall treatment which aims at reduction of other risk factors such as glucose intolerance and hyperlipoproteinemia is advocated. Thus, in any obese hypertensive patient normalization of excess body weight and increased physical activity appears to be the first and most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: epidemiology, mechanisms, treatment. 636 45

Male and female, massively obese and nonobese, spontaneously hypertensive rat (SHR) which are hypersensitive to stress were kept under quiescent conditions; they were autopsied at 15 months of age. The blood pressure of the Obese/SHR plateaued at 166 mmHg versus 198 mmHg for the nonobese/SHR. The once massive thymi vanished in the Obese/SHR accompanied by greatly enlarged adrenal glands, pituitary basophilia, greatly elevated levels of adrenocorticotrophin, corticosterone, deoxycorticosterone, aldosterone, fatty liver, hyperlipidemia, and hyperglycemia. The Obese/SHR were hyperadrenocorticoid compared with their nonobese siblings and manifested a Cushingoid spectrum of degenerative changes (e.g., thin skin, hypertension, diabetes, kidney stones, and accelerated aging). The provision of a nonstressful environment is believed to have dampened the usual chronic hyperadrenocorticism and prolonged the lifespan of the Obese/SHR.
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PMID:Cushingoid pathophysiology of old, massively obese, spontaneously hypertensive rats (SHR). 682 32

The possible role of obesity in the development of hypertension was investigated in two study groups. In a population study of 961 subjects, 739 were found to be normotensive and 222 hypertensive. The prevalence of hypertension was 18.7 percent in the nonobese, and 33.2 percent in the obese subjects. Systolic and diastolic blood pressures increased progressively with the increase of relative body weight in both normotensive and hypertensive subjects. In addition, an endocrinologic study was made of 97 patients with essential hypertension; in 82, plasma renin activity (PRA) was inversely correlated with the increase of relative body weight but not with urinary Na excretion. Despite this decrease of PRA, the level of serum aldosterone was not influenced by relative body weight. Thus, the aldosterone/PRA ratio ratio increased progressively with the increase of relative body weight. Thiazide therapy normalized this inappropriately high ratio, and reduced body weight and blood pressure. Restriction of dietary calories and salt intake had a similar effect. With a high-salt intake in an obese subject, the aldosterone/PRA ratio is unduly increased. Apparently aldosterone contributes to the additional retention of sodium and water and thereby promotes hypertension in the presence of an expanded fluid volume.
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PMID:Changes in endocrine activities relative to obesity in patients with essential hypertension. 700 95

Several blood-pressure-regulating factors including exchangeable sodium, blood volume, plasma renin, aldosterone, norepinephrine (NE), and epinephrine (E) levels, urinary catecholamine excretion rates, and cardiovascular responsiveness to infused NE and angiotensin II (AII) were compared among age-matched subgroups of normal subjects (15 with normal weight, 15 with overweight) and patients with essential hypertension (15 with either normal weight, overweight, or obesity). Exchangeable sodium, blood volume, plasma and urinary sodium and potassium, plasma renin, aldosterone and epinephrine levels, and NE or E excretion rates did not differ significantly among the five subgroups. Minimal differences included a slightly higher heart rate in overweight patients than in overweight normal subjects (p less than 0.01) and a tendency for a higher plasma NE in overweight than in normal weight patients. Plasma NE obtained immediately before NE infusion as well as the plasma clearance of NE did not differ among the five subgroups except, however, for a somewhat low NE clearance in obese patients. The NE pressor dose tended to be lower in normal-weight hypertensive than in normal-weight normotensive subjects. No alteration was apparent in overweight or obese hypertensive patients. Pressor responses to AII were similar in the different subgroups. These findings suggest that overweight does not confer a unique aberration in the body sodium-volume state, circulating renin, aldosterone or catecholamines, or cardiovascular responses to NE or AII which result in hypertension.
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PMID:Pressor factors and cardiovascular pressor responsiveness in lean and overweight normal or hypertensive subjects. 704 22

There is a close epidemiological association between obesity and blood pressure for all age groups, although not every obese individual becomes hypertensive. In populations without age-related increases in body weight, an elevation of blood pressure with age is not seen. Treatment of obesity by weight loss decreases blood pressure substantially; however, in a minority of patients blood pressure does not fall with weight loss. Blood pressure generally decreases before normal weight is achieved. Blood pressure after weight loss remains reduced as long as there is no marked regain of body weight. Salt intake reduction does not appear to explain why weight reduction lowers blood pressure. Reduced levels of plasma renin activity, serum aldosterone levels, catecholamine levels, and serum insulin levels may be involved in the blood pressure lowering associated with weight loss. Since the risk to the hypertensive patient is not only determined by the blood pressure, an overall treatment that aims at reduction of all risk factors is advocated. Some risk factors, e.g., glucose intolerance, may be normalized only when desirable weight is achieved. Thus, in any obese hypertensive patient with other risk factors, normalization of excess body weight appears to be the first the most important step of any rational therapeutic strategy.
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PMID:Obesity and hypertension: cardiovascular response of weight reduction. 704 31

Individual features of the endocrine system were studied in 26 healthy men, divided into 2 groups, according to the characteristics of EEG, electrocutaneous thresholds and the time response (TR) upon sound signals of 40 to 120 decibels. The subjects of the 1st group were characterized by the high energy of EEG delta- and theta-rhythms, low energy of alpha-rhythm, low thresholds and TR40 : TR120 ratio. The patients of the 2nd group had the opposite parameters. In both groups the blood plasma and urine catecholamine content, ACTH, TTH, 11-hydroxycorticosteroids, cortisol, aldosterone, thyroxine, triiodothyronine, testosterone and plasmatic insulin were determined by means of spectrofluorometry and radioimmunoassay. The elevation of the cortisol level after ACTH injection and of the TTH concentration following thyroliberin administration were investigated. Two polar variants of the endocrine system organization were revealed. The patients of the 1st group had an elevated activity of the sympathico-adrenal, hypophyseal-adrenal system and insular apparatus, comparatively lowered activity of the hypophyseal-thyroid system and gonads. The subjects of the 2nd group demonstrated an opposite character of the endocrine system. It is suggested that the individual peculiarities of the human endocrine system promote the development of obesity, Icenko-Cushing's disease, hypertension, thyrotoxicosis, acromegaly and bronchial asthma.
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PMID:[Individual characteristics of the organization of the human endocrine system]. 712 44

Obesity and hypertension are closely correlated. Weight loss obtained with hypocaloric diet and without reduced sodium intake affected a considerable fall in systolic and diastolic pressures in overweight hypertensive patients. This pressure-weight reduction was maintained for at least 12-18 months. The mechanism(s) for the pressure reduction may be explained by a decreased sympathetic activity associated with a reduced participation of the renin-angiotensin-aldosterone system, natriuresis, contracted plasma volume, and a reversal of the high cardiac output state.
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PMID:Effects of weight reduction on arterial pressure. 717 70


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