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

Described here is a 27-year-old female, who had centripetal obesity, broad reddish-purple striae on the lower abdomen and hypertension. Serum cortisol levels, the results of a dexamethasone suppression test and an adrenal scintigram with 131I-19-iodocholesterol were all compatible with Cushing's syndrome due to an adrenal adenoma that secretes cortisol autonomously. This was confirmed by gross and microscopic examination of the removed adrenal tumor. In addition, the patient had markedly diminished T4 and T3 concentrations in serum. Basal TSH levels were not elevated and did not rise significantly after TRH injection. Serum T4 and T3 concentrations were elevated to the normal range when the hyperadrenocorticism was corrected. The results indicate that the patient had "'corticogenic hypothyroidism."
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PMID:Cushing's syndrome associated with corticogenic hypothyroidism: a case study. 730 57

A modification of the Cortipac procedure (Radiochemical Centre, Amersham) for the estimation of urinary free cortisol was found to be of value in the diagnosis of Cushing's syndrome and in the differentiation of simple obesity from that due to Cushing's syndrome. The effect of renal failure and late pregnancy on the urinary free cortisol was also studied. The results were expressed both in terms of the urinary free cortisol and as a urinary free cortisol:creatinine ratio.
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PMID:Applications of a modified Cortipac procedure for the estimation of urinary free cortisol in various clinical situations. 735 63

Age-related somatic variability studied by 15 anthropometric parameters was assessed in 278 subjects (138 boys and 140 girls) aged between 5 and 20 years. Of these, 30% had simple obesity, 10.0% obesity associated with hypothyroidism, 10.0% obesity with diabetes, 25% obesity with adrenocortical reaction, 23.5% functional adiposo-genital syndrome and 1.5% Cushing's syndrome. The peculiarities related to the somatic development as a whole, the degree of bone development, and adiposity are interpreted in the main clinical forms of obesity, on the basis of the morphogram.
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PMID:Somatotyping in the obese children and adolescents. 743 66

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

Cushing syndrome in pregnancy is rare. This is explained by the syndrome's association with amenorrhoea, oligomenorrhoea, infertility and abortions. Cushing syndrome commonly presents with hypertension, weight gain, diabetes, striae or truncal obesity, all of which can be consistent with pregnancy in women without Cushing syndrome. We describe a case of Cushing syndrome in pregnancy secondary to an adrenal cortical tumour which was discovered after an abnormal glucose tolerance test. The woman developed classical features of Cushing syndrome including gestational diabetes and hypertension and was managed successfully to term after a unilateral adrenalectomy at 23 weeks. The case is reported not only because of its rarity but also because the diagnosis was made after a routine screening test for gestational diabetes. Early diagnosis and treatment of adrenal adenoma causing Cushing syndrome in pregnancy reduces maternal and fetal morbidity and mortality.
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PMID:Cushing syndrome in pregnancy secondary to an adrenal cortical adenoma. 767 97

Two hundred fifty women with hirsutism were studied, with a mean age of 25.5 years (ranging from 13 to 38 years). The evolution of hirsutism varied from 3 months to 13 years, being minimal in 82 patients (33%), mild to 101 (40%), moderate in 56 (23%) and severe in the remaining 11 women (4%). Polycystic ovary syndrome (PCOS) was diagnosed in 134 patients (53%), overweight or obesity in 45 (18%), late-onset adrenal hyperplasia in five (2%), ovarian tumor in two (0.8%), drug-induced hirsutism and Cushing's syndrome in one patient each (0.4%), and idiopathic hirsutism in 62 cases (25%). Among 67 patients with moderate or severe hirsutism, testosterone was elevated in 21 (31%). In 117 out of 206 (57%) cases polycystic ovaries were observed by ultrasound. Fifty-four patients were treated with a combination of 2 mg cyproterone acetate and 0.035 mg ethinyl estradiol, observing improvement of hirsutism in 32 patients (59%). It is concluded that PCOS is the most frequent cause of hirsutism, but an important proportion of cases without evident etiology remain classified as idiopathic hirsutism.
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PMID:Etiological review of hirsutism in 250 patients. 780 80

5-10% of all women have an androgen excess syndrome. Androgen excess signs and symptoms include hirsutism, acne, central obesity, male-pattern baldness, upper torso widening, increased waist-to-hip ratio, clitoral hypertrophy, and deepening of the voice. Physicians must be able to recognize these signs and symptoms. Presence of these signs and symptoms calls for a screening history and physical examination. Differential diagnoses of androgen excess in women include endogenous and exogenous causes. Endogenous-related diagnoses are those of ovarian origin (primary tumors, metastatic tumors, polycystic ovary syndrome, ovarian stromal hyperthecosis, androgen excess in pregnancy, and abnormal gonadal or sexual development) and those of adrenal origin (Cushing's syndrome/disease, late-onset congenital adrenal hyperplasia, and tumors). Exogenous causes of androgen excess include Danazol, Phenytoin, Diazoxide, Hexachlorobenzene, Hexachlorophene, Minoxidil, Cyclosporin, testosterone and other androgens, anabolic steroids, synthetic progestins (the pill), and Metapyrone. When physicians treat patients for one symptom of androgen excess, they should watch for other signs and symptoms. Serious health risks associated with androgen excess include cardiovascular disease, intravascular thrombosis, and insulin resistance. Physicians must be aware that timely clinical recognition of androgen excess, knowledge of androgen-related biochemical abnormalities underlying the risks linked to androgen excess, and risk modification behavior reduces associated morbidity and mortality. Risk reduction strategies are correction of dyslipidemias, low-dose aspirin for primary prevention of myocardial infarction, maintenance of ideal weight, smoking cessation, exercise, use of combined oral contraceptives (OCs) with a low-androgenic progestin, and postmenopausal estrogen replacement. OCs also slow progression of long-term sequelae (e.g., cardiovascular disease).
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PMID:Effects of sex steroids on women's health: implications for practitioners. 782 34

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

Endogenous Cushing's syndrome, obesity and chronic glucocorticod treatment are characterized by blunted GH secretion. The administration of GHRH is capable of stimulating a small but significant PRL increase in normal subjects. The current study was designed to determine plasma PRL levels in response to GHRH, studied in three different situations characterized by a blunted GH secretion. Obese patients (n = 6) with a weight over 30% of ideal body weight, patients with active Cushing's syndrome, and normal volunteers treated with dexamethasone 22 mg per os over two days before the pituitary challenge were studied. As a control group 18 normal subjects of similar age and sex were studied. GH and PRL was determined at intervals after GHRH (1 microgram/kg). GHRH-induced GH secretion was markedly reduced in patients with obesity, patients with endogenous Cushing's syndrome and volunteers treated with dexamethasone. In contrast, GHRH-induced PRL secretion was not affected in these three clinical situations. In summary, in three situations characterized for an impairment of the somatotroph cell, due to a primary intrinsic defect or to a functional hypothalamic alteration, there is a persistent GHRH-induced PRL secretion, suggesting that prolactin could be released by mammosomatotrophs that function normally in spite of hyposomatotropism.
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PMID:Persistent GHRH-induced PRL secretion in Cushing's syndrome, obesity and exogenous hypercortisolism. 788 70


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