Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A genetic variant of the spontaneously hypertensive rat (SHR) has been produced which becomes markedly obese as well as hypertensive, i.e. Obese/SHR weigh 800 g as against 300 g for non-obese cohorts. Serum enzymes (CPK, SGOT, SGPT and LDH) are frequently abnormally elevated, concomitantly with a high incidence of myocardial necrosis. Obese/SHR are hyperlipidaemic with severe fatty infiltration of the liver; they are hyperglycaemic with enormous islets of Langerhans and extensive beta-cell degranulation; despite elevated blood urea nitrogen (BUN) levels, they manifest little or no renal damage. Measurement of corticosterone, deoxycorticosterone (DOC) and aldosterone in Obese/SHR demonstrate marked hyper-responsiveness to moderate stress. Circulating prolactin levels are lower in Obese and non-obese/SHR compared to SHR, but Obese/SHR manifest unusually high increases incirculating prolactin levels in response to stress. Obese/SHR are hyperinsulinaemic and have subnormal growth-hormone levels. Desite mild hypertension, hyperglycaemia and hyperlipidaemia, Obese/SHR show no evidence of atheromatous change but do develop early polyarteritis nodosa. It is believed that the genetically programmed hypertension and hyperglycaemia is mediated by increased DOC, aldosterone and corticosterone production respectively, and that the obesity, hypertension, and diabetes in Obese/SHR may be likened to human Cushing's disease.
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PMID:Pathophysiological differences between obese and non-obese spontaneously hypertensive rats. 742 76

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

Since in patients with Cushing's disease, unlike in normal subjects, tonic inhibitory opioid control of ACTH secretion does not operate, use of the opiate agonist loperamide (LOP) has recently been proposed in the diagnosis of hypercortisolemic states. We compared the sensitivity, specificity and diagnostic accuracy of the LOP test (16 mg orally) with corresponding results of the dexamethasone test (DXM, 1 mg orally overnight) in 23 normal subjects and in a total of 42 patients, affected by Cushing's disease (n = 8), incidentally discovered adrenal masses with impaired function of the hypothalamic-pituitary-adrenal (HPA) axis (n = 6), obesity (n = 21) and depression (n = 7). While in controls both DXM and LOP strongly suppressed plasma cortisol and ACTH, in Cushing's disease and in incidentalomas no patient showed a decrease in cortisol levels below 50 ng/ml or a reduction in plasma cortisol greater than 50% of basal values in response to LOP and DXM. In obese subjects both drugs significantly reduced plasma cortisol and ACTH without giving false positive results. In the depressed group only 3/7 patients showed a decrement in cortisol levels below 50 ng/ml after LOP in contrast to 6/7 after DXM. Thus, in patients with impairment of the HPA-axis, i.e. in Cushing's disease and in patients with adrenal incidentalomas and hormonal abnormalities, LOP and DXM test sensitivity was 100%. In controls and in obese patients specificity was 100% both with LOP and DXM, while in depressed patients it was 43% and 86% with LOP and DXM, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison between the suppressive effects of dexamethasone and loperamide on cortisol and ACTH secretion in some pathological conditions. 769 14

To evaluate whether the PRL, TSH and gonadotropin secretion is altered in conditions with elevated body mass index, 7 patients with central Cushing's disease before and after transsphenoidal surgery, 7 untreated patients with Cushing's syndrome caused by adrenal adenoma, 17 simplex obese (obese) women and 9 non-obese controls (all females, aged 18-45 years) were tested with TRH (200 micrograms i.v. bolus) and GnRH (100 micrograms i.v. bolus) and the hormone responses were measured. There were no differences in the basal pituitary hormone secretion among the groups. In obese subjects the PRL response was reduced as compared to untreated patients with corticotrop pituitary adenoma. No significant differences of TSH release could be observed among the groups, whereas serum total T4 levels were higher in obesity than in patients with hypercorticism either caused by pituitary or adrenal Cushing's syndrome. No differences were found in the LH response, but the stimulated FSH release was lower in obesity, in patients with central Cushing's disease after transsphenoidal surgery and in patients with primary Cushing's syndrome as compared to the normal controls.
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PMID:[Anterior pituitary responsiveness in central Cushing disease and in Cushing syndrome caused by adrenal cortex tumors, as well as in simple obesity]. 786 32

Glucose tolerance was assessed in 100 cases of adrenocortical hyperfunction (79-Cushing's disease and 21-Cushing's syndrome). Overt diabetes was found in 19 cases. Of the remaining 81 patients 37 had normal glucose tolerance, in 23 glucose tolerance was impaired and in 21 patients diabetes was diagnosed. Glucose tolerance expressed as 60 and 120 min glucose values did no correlate with hormonal parameters of adrenocortical hyperfunction nor with age of the patients and degree of obesity. The authors discuss the complex mechanism of the effect of glucocorticoid excess on glucose tolerance.
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PMID:[Glucose tolerance in adrenocortical hyperfunction. Analysis of 100 cases]. 797 80

Forty-eight patients suffering from diabetes mellitus, obesity, hyper- and hypothyrosis, Icenko-Cushing's disease were examined to elucidate the relationship between blood plasma carbon isotopic composition and the type of the endocrine disease. This value varied within the range of -19.7 to -24.7/1000, the mean value being 5/1000. Blood plasma carbon in the diabetics is enriched for 12C light isotope (delta 13C from -23.0 to -24.5/1000) as against a similar characteristic in obese patients (delta 13C from -20.5 to 21.99/1000). Patients with hypo- and hyperthyrosis and the Icenko-Cushing's disease have a wider range of delta 13C values that seems to be explained by the Icenko-Cushing's disease heterogeneity and the presence of biorhythms. Clear-cut isotopic differences in the blood sera of adults and children were revealed whatever the disease type, these differences indicating the changes in cellular metabolism energy in the ontogenesis. These data can be satisfactorily explained within the frames of the model of cellular division of carbon isotopes, suggested previously.
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PMID:[Isotopic composition of blood plasma carbon in patients with endocrine diseases]. 805 61

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

We describe a rare case of familial Cushing's disease occurring in a 7-year-old boy, and 19 years of follow up. Our patient first presented soon after his maternal aunt had been treated for Cushing's disease. The clinical presentation was made complicated by the development of an intercurrent eating disorder resembling anorexia nervosa. This resulted in marked weight loss, and even though serum and urinary cortisol levels were elevated, many of the clinical stigmata of Cushing's disease were absent. Eating disorders are relatively uncommon in boys, and in this case there was an organic cause for the abnormal behaviour. This case shows, furthermore, that even the obesity of Cushing's disease can be overcome by the combination of diet and exercise.
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PMID:Familial Cushing's disease with severe weight loss occurring in late childhood. 906 50

In the present study, we characterized the changes in plasma leptin levels in patients with pituitary Cushing's disease and in age- and sex-matched controls. Plasma levels of ACTH, cortisol, and leptin were measured before and after iv administration of ovine CRH in controls once and in patients twice (while they had active hypercortisolism and 10 days after successful surgery). Cushing's patients had elevated body mass indexes (34 +/- 1.9 vs. 22.9 +/- 0.8) and plasma leptin levels (35.6 +/- 3.4 vs. 9.2 +/- 1.9 ng/mL) compared to controls, which remained unchanged 10 days after successful transsphenoidal surgery and directly proportional to the body mass index. Plasma leptin levels were not affected by CRH infusion in either the controls or the patients despite clear-cut elevations in plasma ACTH and cortisol. These findings suggest that although acute changes in plasma cortisol do not affect plasma leptin, chronic hypercortisolism results in elevated leptin levels, probably by causing visceral obesity.
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PMID:Plasma leptin levels do not change in patients with Cushing's disease shortly after correction of hypercortisolism. 925 64

The degree of thyroid impairment and the effects on growth have not been investigated in children with Cushing's disease. We followed the thyroid function of 24 children and adolescents (12 males and 12 females) with CD (age, 12.9 +/- 3.2 years; mean +/- SD), who were successfully treated by transsphenoidal surgery. Patients were evaluated before, and 3, 6, and 12 months after TSS. Analysis of variance and linear correlation were performed between thyroid function tests and body weight and mass index and bone age. Preoperative free thyroxine levels (1.37 +/- 0.03 ng/dl) were significantly higher than those at 3 months (1.17 +/- 0.05 ng/dl, p < 0.05), but similar to those at 6 and 12 months postoperatively. Preoperative T3 (114.2 +/- 7.7 ng/dl) and TSH (1.36 +/- 0.2 IU/ml) were significantly lower than the postoperative values at 3 (158.9 +/- 6.8 and 2.3 +/- 0.3, respectively), 6 (159.1 +/- 10.8 and 2.5 +/- 0.3, respectively), and 12 months (136 +/- 6.5 and 2.2 +/- 0.3, respectively) (all p < 0.05). One patient had frank hypothyroidism (fT4 < 1 ng/dl) before surgery. Five additional patients had secondary hypothyroidism in the immediate postsurgical period; two of them had normal thyroid function 2 and 3 years postoperatively. One patient has remained hypothyroid for more than 5 years since surgery. No significant correlation was found between thyroid function and body weight, BMI, or BA. We conclude that hypothyroidism was an infrequent complication of CD and TSS. Mild suppression of thyroid function occurs in most children and adolescents with CD before and in the first few months after TSS, but it fully resolves after 6 months and does not correlate with the growth delay and obesity of these patients.
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PMID:Thyroid function in children with Cushing's disease before and after transsphenoidal surgery. 942 98


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