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)

Particular aspects of plasma ACTH radioimmunoassay are examinated. The results obtained with this method in adrenocortical diseases (Addison's disease, Cushing's syndrome, congenital adrenal hyperplasia) are reported and clinical value in etiological diagnosis of Cushing's syndrome is outlined. Moreover the results obtained in other syndromes of endocrinologic interest (massive obesity, Turner's and Klinefelter's syndromes, Laurence-Moon-Biedl syndrome, true precocious puberty, primary hypothyroidism, hypopituitary dwarphism) are reported and discussed.
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PMID:[Technical notes and clinical use of radioimmunologic determination of plasma ACTH]. 17 22

A rare case of the Cushing syndrome, due to bilateral adrenal hyperplasia is described. Because of generalized obesity, normal height, normal bone age and family history of obesity, a boy 10 years of age had at first been misdiagnosed as simple obesity. A reduction in height velocity, advancement of bone age and development of precocious pseudopuberty led to a more detailed biochemical investigation and to the correct diagnosis. The clinical picture can be misleading in the differential diagnosis of Cushing's disease versus simple obesity. From a comparison of reports on pediatric Cushing's syndrome, it is obvious that in most pediatric cases fat distribution differs from that of adult Cushing's syndromes. Stunted growth is reported to be more frequent, but normal and excessive height in Cushing's syndrome is not uncommon. In adrenal hyperplasia a retardation of bone age is usually expected. Interpretation of endocrine functions must take into account that simple obesity leads to secondary endocrinopathies, which are similar to the findings in Cushing's syndromes. Plasma cortisol at midnight and 12 hourly excretion of free cortisol in urine as well as overnight Dexamethasone suppression of morning plasma cortisol are judged to be good screening parameters. Plasma ACTH assays can help in the initial diagnosis and are mandatory during the follow up for an early detection of Nelson's syndrome.
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PMID:Cushing's syndrome or obesity. Bilateral adrenal hyperplasia in a boy 10 years of age. 17 22

The diagnosis of florid Cushing's syndrome is usually made without difficulty but diagnostic problems may arise. Five such cases are described. Difficulties may occur when the features of the syndrome are incomplete. Three such cases were encountered. In each only one clinical feature was present; these respectively were hypertension, osteoporosis and obesity. The diagnosis was confirmed, however, biochemically and eventually histologically and there was a good response to surgery in each case. Another diagnostic problem, both clinically and biochemically is the obese, hirsute, hypertensive female. Two such cases are described, in whom Cushing's syndrome was diagnosed clinically and biochemically but in whom there was no response to adrenalectomy. Retrospectively the validity of the original diagnosis is questioned. It is concluded that Cushing's syndrome may present in a very incomplete form and should be considered in the differential diagnosis, even if only one feature is present. It is stressed that obesity, hirsutism, hypertension and depression are commonly found in association with normal adrenal function. Urinary free cortisol and cortisol response to insulin induced hypoglycaemia may be of value in distinguishing these cases from those with endocrine disease.
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PMID:Problems in the diagnosis of Cushing's syndrome. 19 80

Insulin resistance may occur to a variable degree in various disease conditions. Obesity is frequently accompanied by insulin resistance. The anti-insulin antibodies in patients treated with insulin are a classical cause, but in fact rare. Insulin resistance of variable degree may accompany certain metabolic disorders, e.g. diabetic ketosis and acidosis, and endocrine disorders, e.g. Cushing's syndrome, acromegaly. The measurement of insulin receptors brings a new dimension to the investigation of insulin resistance. Insulin receptors are reduced in number during obesity. The abnormality, partly responsible for insulin resistance, is reducible by reduction in calory intake. Circulating insulin anti-receptor antibodies appear to be responsible for insulin resistance which is particularly marked although exeptional, in nonobese diabetics with acanthosis nigrans and auto-immune symptoms.
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PMID:[New data in the domain of insulin resistance]. 19 31

Cushing's syndrome is characterized by protein wasting secondary to hypergluconeogenesis, which produces thin skin, poor muscle tone, osteoporosis and capillary fragility. These features distinguish patients with true Cushing's syndrome from those who have some of the clinical findings often associated with the syndrome, such as obesity, hypertension, striae and hirsutism. The dexamethasone suppression test helps identify patients with pseudo-Cushing's syndrome.
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PMID:'Not Cushing's syndrome'. 22 Aug 64

Ectopic ACTH syndrome is a clinicopathologic condition produced by certain tumors which release hormone that is indistinguishable from ACTH. It orginates the chemical and clinical anomalies characteristic of Cushing's syndrome by its action on the adrenal glands. The tumors may be present in any organ, though they are most frequently found in the lungs, thymus, pancreas or gastrointestinal tract. They may be benign or malignant, though usually the latter. Secretion of the hormone is completely autnomous; it is release in a way similar to that of the hypophysis. Not infrequently other hormones besides ACTH are also produced, such as MSH, serotonin, and CRF. Ectopic ACTH is of higher molecular weight than hypophyseal ACTH, which suggest it may be comprised of the latter bounded covalently to a peptide. The clinical course is rapid, so that not all of the symptoms of Cushing's syndrome develop. Moon face, osteoporosis, and obesity are typically lacking; melanodermia and hypokalemic alkalosis ofter appear. Laboratory data include an increase in ACTH and cholesterol concentrations, disappearance of the nictameral rhythm, and an increase in urinary excretion of 17-hydroxycorticoids and 17-ketosteroids. Stimulation and supression tests are abnormal. The prognosis is poor and the only possible treatment is a complete surgical removal of the tumor. Irradiation or chemotherapy could be applied as well as the correction of the adrenal hyperfunction by the administration of drugs or by total bilateral adrenalectomy.
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PMID:[Ectopic ACTH syndrome (author's transl)]. 22 77

The common obesity of middle age presents a set of features that strongly resembles the cardinal symptoms of Cushing's syndrome: obesity of the face (moon face), upper back (buffalo hump) and trunk (pot belly) accompanied by signs of protein-wasting. In non-obese individuals who remain at a constant weight throughout life, the proportion of adipose tissue increases with age at the expense of lean tissue loss. Thus, a mild version of Cushing's syndrome may be part of the normal aging process. A more intense version of this process may occur in overweight adults. Excess and chronic activity of two pituitary hormones may contribute to this adiposity. Both hormones are produced in the same pituitary cell by cleavage from a common large precursor known as pro-opiocortin. One hormone is adrenocorticotrophin (ACTH), which stimulates the release of the glucocorticoid hormones. These hormones promote the conversion of bodily proteins to glucose (gluconeogenesis). The other pituitary hormone is beta-endorphin, a stimulant of appetite that causes the release of insulin. This pancreatic hormone promotes the conversion of glucose and fatty acids to triglycerides (lipogenesis). Three different etiologies are suggested for the excessive and chronic action of these two pituitary hormones: tumors that increase the number of cells that synthesize pro-opiocortin; mutant strains that produce excessive amounts of ACTH and beta-endorphin such as the genetically obese mouse (ob/ob) and rat (fa/fa); and an age-determined shift in the type of cleavage enzymes present in the pro-opiocortin cell that favors ACTH and beta-endorphin production.
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PMID:The obesity of middle age: a common variety of Cushing's syndrome due to a chronic increase in adrenocorticotrophin (ACTH) and beta-endorphin activity. 22 74

In 17 normal subjects and 126 patients with various endocrine disorders, including 13 patients with Cushing's syndrome, plasma levels of fluorogenic corticosteroid were measured at 9 AM and midnight, and again at 9 AM the following morning, after the patient had received 1 mg of dexamethasone by mouth immediately after the midnight sampling. Basal morning levels of plasma corticosteroids were of little diagnostic value in differentiating between Cushing's syndrome and non-Cushing's states because of the wide overlap of values observed. At midnight the overlap almost completely disappeared. After overnight suppression, only one patient with a mild form of Cushing's disease had normal (false-negative) results in two of four instances. There were virtually no false-positive results, except for two patients with anorexia nervosa showing minor abnormalities of the test. The results were in general agreement with those of the classic Liddle test. However, one patient with Cushing's disease had repeatedly abnormal responses to overnight suppression and normal responses to the Liddle test. When the inhibitory tests gave equivocal results in the differential diagnosis between exogenous obesity and Cushing's disease due to adrenal hyperplasia, the response of plasma corticosteroids to hypoglycemia, normal in obesity and absent in Cushing's disease, proved to be an excellent ancillary test in differentiating between the two conditions.
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PMID:Clinical experience with a simple screening test for Cushing's syndrome combining the determination of plasma cortisol circadian rhythm with the overnight dexamethasone suppression test. 66 10

Mediastinal lipomatosis is a common benign cause of mediastinal widening. While it may be associated with exogenous obesity, steroid ingestion, or Cushing's syndrome, these factors often are not present. Evaluation of the mediastinum by CT should be the initial diagnostic study in the work-up of patients with abnormalities of the mediastinal contour; indeed, in many cases it can eliminate the need for other procedures.
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PMID:Mediastinal lipomatosis. CT confirmation of a normal variant. 67 33

Mediastinal abnormalities can present a challenging differential diagnosis. One of the many causes of superior mediastinal widening is excess deposition of fat or mediastinal lipomatosis. Mediastinal widening was evaluated by routine chest radiography, conventional tomography, and computed tomography in four patients with steroid induced Cushing's syndrome or simple obesity. Computed tomography was the only modality that definitively diagnosed mediastinal lipomatosis in each case.
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PMID:Computed tomography in the evaluation of mediastinal lipomatosis. 70 14


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