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

From March 1978 to May 1987, 22 cases of primary adrenal tumors were examined by ultrasonography. The patients ranged in age from 21 to 79 years with an average of 42.6 year, including 11 cases of pheochromocytoma, 6 cases of primary aldosteronism, 4 cases of Cushing's syndrome and 1 case of ganglioneuroma. Visualization of tumors was successful in 19 of the 22 patients (86.4%). The detecting rate of right adrenal tumors was 100% (12/12), while the rate of the left was 80% (8/10). The sizes of detected adrenal tumors were larger than 10 mm on the right and larger than 20 mm on the left. Obesity and bowel gas degraded the image of left adrenal tumors, resulting in a lower detective rate of the tumors. The suprarenal area and small lesions were best demonstrated by a lateral intercostal approach using longitudinal scanning plane and by a right subcostal approach using transverse scanning plane. In pheochromocytoma, cystic lesions (echo free space) existed, and the fact that no cystic lesion in other adrenal tumors was helpful for diagnosis of pheochromocytoma. It is concluded that ultrasonography is a very useful method for diagnosis of adrenal tumors as an initial imaging procedure, because it is totally non-invasive, rapid and less expensive than all of the other techniques.
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PMID:[Detectability and characteristics of the primary adrenal tumor by ultrasonography--comparison with CAT scan and adrenal scintigraphy]. 269 53

To establish a rapid test for Cushing's syndrome we measured serum cortisol during and following iv dexamethasone infusion (5 micrograms.kg-1.h-1 for 5 h from 10.00 h) in simple obesity (N = 19) and in Cushing's syndrome (N = 12). We had first established that 5 micrograms.kg-1.h-1 was the lowest dose which consistently lowered serum cortisol in simple obesity. In obesity, serum cortisols ranged from undetectable (less than 30) to 48 nmol/l at 17.00, less than 30 to 37 at 19.00 and less than 30 to 38 at 08.00 h the following day. Serum cortisol at these three times did not show any overlap between simple obesity and Cushing's syndrome. Having established these findings we proceeded to study a group of patients with polycystic ovarian disease. These patients behaved differently. Their values at 17.00 and 19.00 h did not overlap those of Cushing's syndrome. However, at 08.00 h, 5 of the 7 had values within the range seen in Cushing's syndrome with a mean of 290 +/- 99 nmol/l. In conclusion, 17.00 and 19.00 h serum cortisol levels distinguish between Cushing's syndrome and both simple obesity and polycystic ovarian disease. However, in the latter, cortisol suppression is less prolonged than in simple obesity. This finding may be important for our understanding of the pathogenesis of the disease.
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PMID:A weight-related intravenous dexamethasone suppression test distinguishes obese controls from patients with Cushing's syndrome. 272 13

An increase in the number of diagnostic parameters (in addition to the determination of the urine level of 17-OCS, a study was also made of the level of 17-KS, blood concentrations of ACTH, prolactin, cortisol, and glucose before and after dexamethasone administration at a dose of 0.5 mg every 6 h for 2 days) and strict rules to be observed by examinees prepared for test performance made in possible to raise the differential-diagnostic role of Liddle's minor dexamethasone test. This conclusion was based on the examination of 34 persons without obesity, 25 patients with exogenous constitutional obesity, 75 patients with juvenile pubertal dyspituitarism, 107 patients with hypothalamic obesity, 8 patients with Cushing's syndrome determined by adrenal corticosteroma, one patient with ACTH-ectopic syndrome, and patients with Itsenko-Cushing disease (128 untreated patients, 99 patients with recurrence, 98 patients in remission). The comparison of clinico-instrumental results with the results of the test has shown its informative value for objective assessment of the gravity of disease. Stages of body responses to small doses of dexamethasone (the stage of lost responses, the stage of incomplete loss and the stage of recovered responses) were identified contributing to objective assessment of the gravity, course, presence, recurrence and remission of Itsenko-Cushing disease.
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PMID:[Use of the "extended" minor dexamethasone test in Itsenko-Cushing disease]. 285 54

A patient with Cushing's syndrome due to ectopic ACTH secretion was treated successfully with the new glucocorticoid antagonist RU 486 [17 beta-hydroxy-11 beta-(4-dimethylamino phenyl) 17 alpha-(1-propynyl)estra-4,9-dien-3-one]. This compound is a 19-nor steroid with substitutions at positions C11 and C17 which antagonizes cortisol action competitively at the receptor level. Oral RU 486 was given in increasing doses of 5, 10, 15, and 20 mg/kg . day for a 9-week period. Treatment efficacy was monitored by assessment of clinical status and by measuring several glucocorticoid-sensitive variables, including fasting blood sugar, blood sugar 120 min after oral glucose administration, and plasma concentrations of TSH, corticosteroid-binding globulin, LH, testosterone-estradiol-binding globulin, and total and free testosterone. With therapy, the somatic features of Cushing's syndrome (buffalo hump, central obesity, and moon facies) ameliorated, mean arterial blood pressure normalized, suicidal depression resolved, and libido returned. All biochemical glucocorticoid-sensitive parameters normalized. No side-effects of drug toxicity were observed. We conclude that RU 486 may provide a safe, well tolerated, and effective medical treatment for hypercortisolism.
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PMID:Successful treatment of Cushing's syndrome with the glucocorticoid antagonist RU 486. 299 27

The analysis of 24-h excretion profiles of urinary steroids in 18 patients suffering from Cushing's syndrome or adrenocortical tumors revealed typical patterns when compared to 37 healthy control persons, 24 patients with obesity, and 6 patients with hirsutism. The validation of eight criteria--increased excretion of free cortisol, 6 beta-hydroxycortisol, 20 alpha-dihydrocortisol, 11 beta-hydroxyandrosterone, and 3 beta-hydroxy-5-en steroids, decreased ratio of tetrahydrocortisone (THE) to tetrahydrocortisol (THF), and increased ratios of THF to allotetrahydrocortisol (a-THF) and metabolites of androgens (AM) to metabolites of cortisol (CM)--afforded reliable detection of disorders in steroid biosynthesis. The analysis of urinary steroid profiles can therefore be recommended as a screening procedure in patients with clinical symptoms of disorders in steroid production and/or metabolism.
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PMID:[Urinary steroid profile in Cushing syndrome and in tumors of the adrenal cortex]. 304 Nov

Femoral and abdominal adipose tissue cellularity and metabolism as well as muscle morphology and metabolism were examined in women with Cushing's syndrome and compared with those in nonobese women and obese women with the android and gynoid types of fat distribution. Cushing's syndrome was characterized by abdominal obesity and enlarged abdominal fat cells, with adipose tissue lipoprotein lipase activity elevated 2-3 times that in normal women and low lipolytic capacity. Muscle tissue in women with Cushing's syndrome had a relatively low proportion of type I (30%) and a high proportion of type IIB (32%) muscle fibers, similar to those in android obesity (45% and 25%, respectively) and in contrast to fiber composition in gynoid obesity (55% and 12%, respectively). Glycogen synthase activity in the lateral vastus muscle was very low. We suggest that the enlargement of abdominal fat depots in women with Cushing's syndrome is at least partially due to elevated adipocyte lipoprotein lipase activity and low lipolytic activity. Furthermore, the abnormal muscle fiber composition might be caused by the corticosteroid excess. Such muscle is known to be relatively insulin insensitive and might thus contribute to the marked insulin resistance that occurs during chronic corticosteroid excess.
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PMID:Muscle and adipose tissue morphology and metabolism in Cushing's syndrome. 314 10

In this study, we investigated the usefulness of the determination of evening urinary free corticoids/creatinine in samples collected from 20.00 to 24.00 h as a screening test in Cushing's syndrome. In controls (N = 61) the ratio values ranged from 1.1 to 9.4 mumol/mol, whereas in patients with Cushing's syndrome (N = 20), they ranged from 27.5 to 855.5 mumol/mol. However, in 28% of patients with major obesity (greater than 50% overweight) and no hypercortisolism, the ratio values were between 9.4 to 27.8 mumol/mol. A short (10 days) hypocaloric diet induced a decrease in the values in 75% of these patients; the normal range was reached in 50% of them. In addition, the evening urinary free corticoids/creatinine was slightly abnormal in 8 out of 10 patients with incidentally discovered 'silent' adrenal adenomas, whereas it was normal in all 6 with other adrenal masses. In conclusion, evening urinary free corticoids/creatinine is easy to obtain and it reaches a higher sensitivity (100%) and specificity (97%) than the 24 h urinary free corticoids. In the case of borderline values, the presence of overweight should be taken into account.
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PMID:Evening urinary free corticoids: a screening test in Cushing's syndrome and incidentally discovered adrenal tumours. 318 14

Cushing's syndrome in childhood is generally recognized by classical features such as truncal obesity, striae, easy bruising, moon facies, hypertension and growth retardation. Exceptionally, Cushing's syndrome has been reported to present as growth failure alone. We diagnosed transient hypercortisolism in 6 children who had poor growth as their only presenting abnormality. The 6 children all had integrated concentrations of cortisols (IC-F) (14.1 +/- 1.7 micrograms/dl; mean +/- 1 SD) which exceeded the IC-F in healthy children and adults (5.7 +/- 1.5 micrograms/dl; P less than 0.001). The IC-F of these 6 index cases overlapped the range of IC-F in patients with pathologically proven Cushing's syndrome (20.2 +/- 4.7 micrograms/dl). Four of the 6 patients were treated with human growth hormone for 8 months and showed a marked improvement in their growth rates. Four patients have entered puberty and are growing at normal rates. Three of the 6 children had normal repeat IC-Fs, subsequently, at a time they had normal growth rates. In 1-1/2 to 3 years of follow-up, none of the patients developed any other stigmata of Cushing's syndrome. We conclude that transient hypercortisolism, documented by the IC-F, may cause growth failure without other symptoms of Cushing's syndrome. Growth hormone therapy may improve the growth rate of these children at the time of their poor growth.
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PMID:Growth impairment due to transient hypercortisolism. 346 64

According to textbooks, Cushing's syndrome (CS) is associated with a loss of the circadian rhythmicity in circulating cortisol. Documented cases of a persisting rhythm in CS are regarded as an exception. Herein, we show that a circadian rhythmicity in plasma cortisol, albeit of much reduced amplitude and with altered timing, remains a group characteristic of patients with CS, characterized further by a circadian rhythm in circulating aldosterone. In Lubochna, Czechoslovakia, 28 patients with CS, 120 patients with obesity imitating CS, 70 subjects with simple obesity, and 19 nonobese controls were sampled at 0800, 1600, 2000, 0000, and again at 0800 on the following day. In Rome, five women and three men with CS and 27 women and 30 men in clinical health gave blood for aldosterone determinations at 0600, 0800, 1200, 1800, 2000, and 0000. Results were first analyzed by single cosinor and then summarized by population-mean cosinor. A group rhythm was demonstrated for all categories of subjects by the methods employed, although, compared to health and even to simple obesity or Cushing-imitating obesity, the amplitude of the rhythm in CS was much reduced. Subgrouping according to etiology and individualized assessment in practice are mandatory. The scope of this group rhythm assessment, however, is merely to document that as a general rule the circadian rhythms in circulating cortisol and aldosterone persist in CS documented by surgery or at autopsy.
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PMID:Altered circadian plasma cortisol and aldosterone group rhythms in Cushing's syndrome versus obesity and health. 362 33

The case of a 60-year-old woman with pheochromocytoma and concomitant adrenocortical adenoma in the same gland is presented. She complained of episodic headache, palpitation, nausea, vomiting and sweating. Physical examination revealed that the patient has generalized obesity, wet skin and paroxysmal hypertension, but no signs of Cushing's syndrome. Elevated levels of urinary noradrenaline, adrenaline and total metanephrine were sequentially observed. In addition, urinary 17-OHCS was also slightly elevated, but plasma cortisol was normal and suppressed after oral administration of 0.5 mg of dexamethasone. Abdominal echography and CT scanning demonstrated a left adrenal tumor, which took up both 131I-meta-iodobenzylguanidine and 75Se-scintadoren in the same region. A left adrenalectomy was performed and the tumor was found to consist of two parts, pheochromocytoma (2.5 X 2.5 X 2.5 cm) and cortical adenoma (2.5 X 3 X 5 cm). A total of 23 reported cases showing evidence of hyperfunction of the adrenal cortex and the medulla were noted. So far as we know, this patient was the second case of pheochromocytoma with adrenocortical adenoma in Japan.
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PMID:Pheochromocytoma associated with adrenocortical adenoma: case report and literature review. 372 Jun 79


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