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

We are presenting a series of 23 patients with Cushing disease selected from a larger study in which the ectopic production of ACTH (paraneoplastic or tumoral), adrenal adenoma or carcinoma were discarded. Sixteen were female and seven male. Diagnosis was fundamentally realized by clinical manifestations derived from hypercortisolism (obesity, muscular atrophy, diabetes, osteoporosis or polyglubulia). The polytomography demonstrated a deformed sella in 19 patients. Endocrine exams showed an alteration in rhythm of Cortisol and elevated levels of urinary metabolites. Others exams, Liddle Test, Metopirona Test, or stimulation of exogenic ACTH did not always permit diagnosis of pituitary adenoma. Plasmatic dosage of ACTH is the best test although results did not always agree with clinical manifestations. In each case we performed clinical treatment in preparation for surgery and later selective removal of adenoma or total pituitary ablation by transphenoidal approach. Of 21 patients, we found an adenoma during surgery in 15; the other 6 on whom we performed a total hypophysectomy, the pathological study showed an adenoma in 5 and a hyperemic gland with thick capillaries in 1. Another type of treatment was used on 2 due to their age. Nine patients were given post-operative radiotherapy. We conclude that microsurgery by transphenoidal approach offers the best possibilities for patients with Cushing disease.
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PMID:[Surgical treatment in Cushing's disease (authors' translation)]. 731 90

A 52-year-old woman with rheumatoid arthritis experienced painless spontaneous hemorrhage, tearing, and necrosis of the skin on the lower laternal aspect of both legs. Thereapy with systemic prednisone had been used to suppress active synovitis for almost four years and was associated with moon facies, hirsutism, truncal obesity, thinning of the skin, extensive purpura on the extremities, and other manifestations of hypercortisolism. There was no evidence of rheumatoid vasculitis, trauma, or blood dyscrasia. The leg lesions may represent an exaggerated type of steroid-induced purpura resulting in localized areas of gangrenous skin.
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PMID:Spontaneous skin tearing during systemic corticosteroid treatment. 735 83

The authors have explored the suitability of the Mongolian gerbil as a model in aging research and reviewed data on major factors in gerbil morbidity and mortality. The gerbil is a semi-desert rodent, introduced relatively recently into biomedical research. It is moderately prolific, has a maximum survival of about 208 weeks and is easily maintained. Maternal neglect, fighting and epidemic diseases (Tyzzer's disease, salmonellosis, pneumonia) are potential causes of mortality in gerbil colonies. Obese or breeding gerbils may exhibit hyperadrenocorticism, diabetes, non-lipoid arteriosclerosis and secondary lesions in several organs. There is a high prevalence of spontaneous neoplasms in aged gerbils, especially tumors of the adrenal cortex, ovary and skin. The gerbil is a useful model of experimentally-induced stroke, but has proven unsuitable for studies of cholesterol-induced atherosclerosis. The normal and pathological anatomy of periodontal disease in the gerbil is similar in many respects to that of man.
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PMID:The Mongolian gerbil in aging research. 739 11

Hypercortisolism alters the distribution of body fat, causing truncal obesity, moon facies, buffalo hump, and other localized fatty deposits. In a patient with a mixed collagen vascular disease (overlap syndrome), who received high systemic doses of prednisone, prominent painless bitemporal masses developed in association with moon facies. Punch biopsy specimens of the lesion disclosed normal adipose tisue. This unappreciated feature of hypercortisolism is described, and other clinical manifestations of glucocorticoid excess involving fat tissue are reviewed briefly.
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PMID:Temporal fat pad sign during corticosteroid treatment. 743 47

Cushing's syndrome, an unusual group of disorders characterized by hypercortisolism, must be considered in the differential diagnosis of such common clinical problems as hirsutism, menstrual irregularity, hypertension, diabetes mellitus, and obesity. Its distinct forms--pituitary-dependent Cushing's syndrome (Cushing's disease), adrenal tumor and ectopic ACTH syndrome--must be identified correctly so that specific therapy can be administered. In the majority of cases, use of a relatively simple diagnostic sequence will provide accurate and rapid diagnosis. However, in our experience with more than 60 patients, diagnostic difficulties may arise from a variety of conditions (e.g., drug interference, alcohol ingestion, and depression). In addition, unusual circumstances, such as unexpected responses to dexamethasone, may complicate the diagnosis. Our approach to these problems is illustrated through a report of seven cases, and we emphasize that the proper management of Cushing's syndrome mandates a thorough marshalling of all the available data.
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PMID:Cushing's syndrome: problems in diagnosis. 745 63

A 46-year-old man with known arterial hypertension for 10 years had, over the last two years, developed increasing obesity, particularly of the trunk, with other symptoms typical of Cushing's syndrome. Hormone analysis demonstrated hypercortisolism and decreased plasma ACTH concentration. The dexamethasone inhibition test failed to show any significant suppression of serum cortisol. Plasma ACTH was not increased in the corticotrophin-releasing hormone and the metyrapone tests. In the short ACTH test there was an excessive cortisol increase. Abdominal computed tomography revealed both adrenals to be enlarged (6 x 4 cm) and coarsely nodular. Adrenolytic treatment with ketoconazole (400 mg daily) caused symptoms of adrenal insufficiency, but a reduced dosage of 200 mg daily lowered the cortisol level to between 5 and 11 micrograms/dl and normalized the blood pressure and clinical signs of Cushing's syndrome disappeared. Subsequent bilateral adrenalectomy confirmed the diagnosis of massive macronodular adrenal hyperplasia. Substitution treatment with twice daily 25 mg cortisone acetate and 0.05 mg fludrocortisone was started postoperatively.
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PMID:[Bilateral massive macronodular adrenal gland hyperplasia. A rare cause of Cushing's syndrome]. 830 53

Obesity is a multifactorial heterogenous condition. The location of excess fat on the body determines the risk of morbidity and mortality for significant disease. Visceral, or intraabdominal, fat is the fat depot most highly associated with illness and death from cardiocerebrovascular disease and diabetes. Visceral fat is also associated with a quartet of metabolic disturbances. Referred to as the metabolic syndrome, these abnormalities include hypertension, hyperlipidemia, hyperinsulinemia, and insulin resistance. The metabolic syndrome is also present in Cushing's syndrome, which is characterized by primary hypercortisolism as well as profound visceral adiposity and obesity. The interrelationship between hyperactivation or hypersensitivity of the stress axis and disease can be elucidated by an understanding of the effect of excess glucocorticoids upon energy storage and metabolism. The complex interactions of the stress axis upon the growth and reproductive axes, as well as upon the adipose tissue, suggest that chronic stress, whether psychological and/or physical, exerts an intense effect upon body composition, which, in turn, significantly affects the longevity and survival of the organism.
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PMID:Hypercortisolism and obesity. 859 40

Previous experience has shown that a non-invasive (indirect) technique using an oscillometric monitor in conjunction with a tail cuff makes routine clinical blood pressure measurement practicable in dogs. The relationship between indirect and direct readings has been evaluated in both anaesthetised and conscious dogs (Bodey and others 1994, 1996). In this study, more than 2000 pressure measurements were taken from 1903 dogs. It was found that systolic is the most variable pressure parameter and that it depends on age, breed, sex, temperament, disease state, exercise regime and, to a minor extent, diet. Diet was not a significant determinant of diastolic and mean arterial pressure. Age and breed were the major predictors for all parameters. Heart rate was primarily affected by the temperament of the animal, though other factors also play a part in prediction. The distribution of systolic, diastolic, mean arterial pressure and heart rate across the dog population approximates to a log normal distribution. On the basis of these results it is possible to describe normal ranges for canine blood pressure; definition of hypertension, though, demands attention to age and breed normal values. The existence of statistically defined hypertension in an individual or breed does not imply adverse effects justifying therapy. Among the secondary causes of hypertension, such as diabetes, obesity and hyperadrenocorticism, hepatic disease was a new addition also undocumented in humans. The hypothesis that dogs, though classic model animals for hypertension, are resistant to its development found support from the modest increase in mean pressure values observed among dogs with renal disease, notably those with substantial reduction of glomerular filtration rate. The existence of breeds such as deerhounds with average pressures in the borderline range for hypertension in humans (and many individuals, therefore, well above) suggests that dogs may also be resistant to some of the adverse effects of high blood pressure.
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PMID:Epidemiological study of blood pressure in domestic dogs. 868 54

Most patients with hypertension in the United States have essential (primary) hypertension (95%), the cause of which is unknown. The remaining 5% of adults with hypertension have the secondary form of hypertension, the cause and pathophysiologic process of which are known. Internists and other primary care physicians refer to this as treatable or curable hypertension, because the hypertension can be managed or even controlled with medications. Similarly, the condition is called surgical hypertension by surgeons in the belief that once the cause is determined and identified, surgical intervention will result in cure of hypertension. Secondary causes of hypertension include renal parenchymal disease, renovascular diseases, coarctation of the aorta, Cushing's syndrome, primary hyperaldosteronism, pheochromocytoma, hyperthyroidism, and hyperparathyroidism. Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. The evaluation of secondary hypertension is of interest and can bring together different facets of anatomy, physiology, pharmacology, and radiology in the medical and surgical treatment of these disorders. Despite enthusiasm that can be generated in the evaluation of these conditions, evaluation can be expensive and should not be conducted for all patients with hypertension. Features that aid in the diagnosis of secondary hypertension include the following: 1. Onset of hypertension before the age of 20 or after the age of 50 years. The presence of hypertension at a young age may suggest coarctation of the aorta, fibromuscular dysplasia, or an endocrine disorder. Hypertension found for the first time after the age of 50 years may suggest the presence of renovascular hypertension caused by atherosclerosis. 2. Markedly elevated blood pressure or hypertension with severe end-organ damage, as in grade III or IV retinopathy. These findings suggest the presence of renovascular hypertension or pheochromocytoma. 3. Specific body habitus and ancillary physical findings. For example, truncal obesity and purple striae occur with hypercortisolism, and exophthalmos is associated with hyperthyroidism. 4. Resistant or refractory hypertension (poor response to medical therapy usually necessitating use of more than three antihypertensive medications from three different classes). 5. Specific biochemical test that suggest the existence of certain disorders, such as hypercalcemia in hyperparathyroidism, hyperglycemia in Cushing's syndrome and pheochromocytoma, and unprovoked hypokalemia with renin-producing tumors, primary hyperaldosteronism, or renin-mediated renovascular hypertension. 6. Other characteristics that may suggest secondary hypertension such as abdominal diastolic bruits (renovascular hypertension), decreased femoral pulses (coarctation of the aorta), or bitemporal hemianopias (Cushing's disease). A combination of a good history and physical examination, astute observation, and accurate interpretation of available data usually are helpful in the diagnosis of a specific causation.
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PMID:Secondary hypertension: evaluation and treatment. 894 19

Serum leptin concentrations and the levels of ob mRNA in adipocytes in obese humans are elevated. Hyperphagia and obesity are characteristics of hypercortisolism. We have therefore asked whether or not leptin levels were elevated in very obese children, and whether or not dexamethasone would increase leptin levels in obese children. A single dose dexamethasone suppression test was performed in ten obese children (5 girls, 5 boys; age 6 to 16 yrs, mean 12 +/- 1, median 12 yrs) to rule out hypercortisolism. Body mass index (BMI) in the ten children was calculated to be 27-45 kg/m2. Venous blood was sampled before dexamethasone was given in the evening and at 9.00 a.m. the following morning. Endogenous cortisol production was suppressed in all patients. Leptin levels, as measured by a newly developed specific radioimmunoassay, were 31.6 +/- 12.9 microg/l, range 19.2-59.9 microg/l before dexamethasone and 39.9 +/- 16.5 microg/l, range 26.3-80.3 microg/l after dexamethasone in the obese children (ANOVA, p = 0.01). Simple regression analysis revealed that serum levels correlated significantly with body mass index (r = 0.82, p < 0.001). Non-obese children (BMI < 27 kg/m2) had leptin levels between 0.1 and 33.3 microg/l, median 2.2 microg/l (N = 713). Girls (5.5 +/- 4.6 microg/l) (N = 401) had significantly higher leptin levels than boys (1.7 +/- 2.1 microg/l (N = 312) (p < 0.0001). We conclude that 1) high serum leptin concentrations are present in obese children. 2) A single dose of dexamethasone significantly increases the high leptin serum levels in these children. We hypothesize that glucocorticosteroids up-regulate leptin levels in the human.
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PMID:High leptin concentrations in serum of very obese children are further stimulated by dexamethasone. 901 47


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