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

The incidence of polycystic ovarian disease (PCOD) varies from 0.6 to 92%, depending on the parameters analysed, PCOD has been reported to appear in association with Cushing's Syndrome, adrenal hyperplasia, hypothyroidism, adrenal and ovarian tumours and some genetic abnormalities. The controversy regarding the pathophysiological mechanism underlying the disease still persists. Critical evaluation of old data, assessment of new findings concerning the possible role of insulin, growth factors and their binding proteins, and extrapolation of neuroendocrinological experiments enabled the construction of a concise hypothesis of the pathophysiology of PCOD. According to this hypothesis, PCOD is a multifactorial disease. The sequence of events finally leading to clinical manifestation of the disease (hyperandrogenism, abnormal luteinizing hormone pulsatility pattern and ovulation disturbances) may originate in different organs or be triggered by different mechanisms. It may stem from the adrenals, the hypothalamus or higher central nervous system centres, or from the ovary itself; it may originate from excess of fat tissue usually combined with hyperinsulinism; or may be the result of a net increase in active growth factors. Each of the above disturbances probably appears early in life, much before the clinical signs of the disease are evident. Predisposing factors such as gestational diabetes of the mother, childhood obesity, borderline adrenal hyperplasia and late menarche have to be looked for as early as possible in order to prevent the late consequences of the disease, such as increased risk of infertility, endometrial and breast cancer and cardiovascular disease.
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PMID:Pathophysiology of polycystic ovarian disease: new insights. 180 58

To determine the sensitivity of the overnight 1-mg dexamethasone suppression test in diagnosing Cushing's syndrome, we evaluated the cortisol responses of 55 subjects (25 non-obese individuals with body mass index less than 25 kg/m2, 20 obese individuals with body mass index greater than 30 kg/m2, and 10 patients with surgically proven Cushing's syndrome) following ingestion of 1 mg dexamethasone at midnight. The basal 8 AM plasma cortisol levels among non-obese and obese individuals and patients with Cushing's syndrome were 310 +/- 85, 377 +/- 91, and 813 +/- 270 nmol/L, respectively. Following 1 mg of dexamethasone, Cushing's syndrome patients showed minimal suppression of cortisol to 609 +/- 180 nmol/L (P = 0.79). Non-obese and obese individuals suppressed to 18.7 +/- 6.0 nmol/L (P less than 0.001) and 22 +/- 7.1 nmol/L (P = 0.003), respectively. The results demonstrated similar cortisol responses to overnight dexamethasone suppression in obese and non-obese groups, and clearly distinguished these subjects from those with Cushing's syndrome. Obesity is not a confounding factor in the 1-mg dexamethasone suppression test.
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PMID:Overnight (1 mg) dexamethasone suppression testing reliably distinguishes non-cushingoid obesity from Cushing's syndrome. 181 20

A 55-year-old woman with bilateral multiple adenomas showed hypertension, muscle weakness, hypokalemia, moon-like face and truncal obesity. Increased serum and urinary levels of aldosterone were observed. Serum cortisol level did not show a normal circadian rhythm. Microscopic examination of the resected tumors showed two types of adenoma cells; one (golden yellow tumor) was a large clear cell with foamy cytoplasm which possibly secreted aldosterone and the other (dark brown tumor) was an acidophilic cell with lipofuscin which might have produced cortisol. This is a very rare case of primary aldosteronism with Cushing's syndrome due to multiple bilateral adrenal adenomas.
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PMID:Primary aldosteronism with cortisol overproduction from bilateral multiple adrenal adenomas. 186 73

A 42-year-old female was admitted to our hospital with a chief complaint of hypertension. Endocrinologically, the plasma cortisol level was increased, but its diurnal rhythm had disappeared and the plasma cortisol level was not suppressed by dexamethasone loading at 2 mg or 8 mg. The plasma ACTH level was low. Computerized tomographic scan, echography and adrenocortical scintigraphy showed an adrenocortical tumor on the right adrenal gland. Physical examination did not reveal typical Cushingoid symptoms such as moon face, central obesity and violaceous striae. Thus we diagnosed this case as non-Cushingoid Cushing's syndrome and performed right adrenalectomy. Histological examination showed adreno-cortical adenoma without malignancy.
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PMID:[A case of non-Cushingoid Cushing's syndrome]. 196 57

The manifestations of endocrine derangements in the musculoskeletal system in infancy and childhood are disturbances in growth and maturation and in adulthood are disturbances in maintenance and metabolism. Hypercortisolism during skeletal immaturity suppresses growth. In the adult, hypercortisolism leads to osteoporosis, osteonecrosis, and muscle wasting. Deficiency of growth hormone during skeletal development results in short stature. An excess of growth hormone in a skeletally immature individual results in gigantism, an excess in a skeletally mature individual results in acromegaly. Patients with gigantism have extreme height with normal body proportions. Musculoskeletal manifestations of acromegaly include soft-tissue thickening, vertebral body enlargement, characteristic hand and foot changes, and enthesal bony proliferation. Hyperthyroidism causes catabolism of protein and loss of connective tissue, which manifest as muscle wasting. Deficient levels of thyroid hormone cause defects in growth and development. Severe growth retardation from congenital hypothyroidism is rare because neonatal screening recognizes the disorder and leads to early treatment. The skeletal manifestation of hypergonadism in children is precocious growth and early skeletal maturation. Although the initial precocious growth spurt results in a tall child, early closure of the growth plates results in a short adult. Hypogonadism in the prepubertal child results in delayed adolescence and delayed skeletal maturation. Diabetes mellitus in childhood results in decreased growth, a phenomenon presumed to be secondary to nutritional abnormalities. Generalized osteoporosis and short stature are common. In the adult, generalized osteoporosis may accompany insulin-dependent diabetes mellitus if obesity is absent. Calcification of interdigital arteries of the foot is common in diabetics and uncommon in other conditions. Additional skeletal manifestations relate to complications of diabetes such as peripheral neuropathy and diabetic foot disease.
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PMID:Radiologic manifestations in the musculoskeletal system of miscellaneous endocrine disorders. 198 24

Cushing's syndrome has been recently compared to visceral-type obesity, since it is characterised by the accumulation of adipose tissue at a deep abdominal site, to the detriment of the subcutaneous adipose panniculus, and is associated with insulin-resistance and hyperlipemia. The aim of the present study was to evaluate the influence of glucocorticoid hormones on lipolytic activity (index of FFA mobilisation) and on lipoproteinlipase (LPL) activity (an index of the accumulation of triglycerides) in subcutaneous and perirenal adipose tissue in order to clarify the mechanisms involved in this type of accumulation in Cushing's syndrome. Five patients (4 F and 1 M) were included in the study, mean age 27.8 +/- 3.7 years and BMI 21.3 +/- 1.2 kg/m2; patients were hospitalised in the 2nd Surgical Clinic at the University of Padua and underwent surgery for secondary corticosurrenal hyperplasia with ACTH secreting hypophysial adenoma. Lipolytic activity in subcutaneous adipose tissue in these patients was significantly lower (p less than 0.05) than in control subjects, in particular after noradrenalin stimulation (p less than 0.01). No significant difference was observed when lipolytic activity in subcutaneous adipose tissue was compared to that one in perirenal tissue. LPL activity in subcutaneous adipose tissue did not reveal statistically significant differences compared to control subjects, although values were lower. A further decrease in LPL activity, which was not however significant, was observed in perirenal tissue in comparison to subcutaneous tissues in the same patients. The mean weight of adipocytes (ug) was slightly lower in subcutaneous adipose tissue compared to control subjects and even lower in perineal tissue in comparison to the subcutis in the same patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lipolytic and lipoprotein lipase activity of subcutaneous and visceral adipose tissue in Cushing's syndrome]. 210 37

Androgens arise from either adrenal or ovarian secretion or by peripheral conversion of secreted precursors. The adrenals and ovaries normally contribute about equally to testosterone and AD production. DHAS is the major adrenal 17-KS. Testosterone is the major circulating form of androgen. More than 96% of plasma testosterone is bound to SHBG; the free testosterone seems to be the bioavailable fraction. Hyperandrogenism must be considered in any girl with premature or excessive development of public hair or acne, menstrual irregularity (whether it be oligo-amenorrhea or dysfunctional uterine bleeding), or obesity. The most common cause of premature public hair development (pubarche) is premature adrenarche. The most common cause of hyperandrogenism presenting in a teenage girl is polycystic ovary syndrome. However, the differential diagnosis includes "exaggerated adrenarche," late-onset congenital adrenal hyperplasia, virilizing tumors, Cushing's syndrome, hyperprolactinemia, acromegaly, and abnormalities of androgen action or of metabolism. The plasma free testosterone is a more sensitive indicator of hyperandrogenism than is the total testosterone concentration. The pattern of response of plasma free testosterone, DHAS, and cortisol to dex-suppression testing is diagnostic of the source of androgen excess. Most hyperandrogenic adolescents will be found to have PCOS. The treatment is chosen according to particular symptoms, such as menstrual irregularity, hirsutism, or obesity.
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PMID:Hyperandrogenism in peripubertal girls. 225 43

Cushing's disease and Cushing's syndrome-like lesions were observed in four male rats. 2 revealed ACTH-positive pituitary tumours associated with bilateral adrenal cortical hyperplasia (case 1, 2). The other 2 rats had metastasizing adrenal cortical carcinomas with marked adrenal cortical atrophy of the opposite adrenal glands (case 3, 4). Pathological lesions observed varied between the animals and included "potbelly", severe obesity, fatty degeneration of the liver, atrophy of the pancreas and greater sublingual glands with fatty infiltration, testicular atrophy, ulcers of the forestomach and purulent inflammation in different organs.
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PMID:Cushing's syndrome- and disease-like lesions in rats. 226 69

The predictive value of the Cockcroft-Gault equation in patients with Cushing's syndrome was evaluated in 23 patients. Patients were subdivided based on total body weight into two groups, obese and nonobese. Estimated creatinine clearance (EClcr) values were obtained by the Cockcroft-Gault method using ideal body weight (IBW) and total body weight (TBW). These values were then compared with a 24-hour measured creatinine clearance (MClcr). EClcr values based on TBW consistently overestimated measured values in all patients (p less than 0.05). In obese patients with Cushing's syndrome IBW predictions were not statistically different. However, linear regression analysis revealed a poor correlation (r = 0.32). Daily creatinine production rates (Ucr) were calculated and contrasted with an appropriate historical control for obese and nonobese subjects. Nonobese patients revealed a marked reduction in total Ucr compared with normal-weight controls (p less than 0.05). Obese patients also showed a reduction in Ucr when compared with a normal obese control population (p less than 0.05). Difficulty in predicting creatinine clearance in patients with Cushing's syndrome appears to be related to alterations in Ucr. These data suggest that the pathophysiologic changes that accompany Cushing's syndrome are sufficient to alter Ucr and may limit the usefulness of existing methods to predict creatinine clearance and renal function in these patients.
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PMID:Estimation of creatinine clearance in patients with Cushing's syndrome. 260 51

It is important to diagnose hyperandrogenism in women. By disturbing ovulation, it is actually one of the most frequent causes of infertility. In this particular case, its diagnosis has specific implications: sometimes specific treatment is indicated, or the risk of fetal virilization should be prevented. There is always the possibility of a diagnosis of polycystic ovary, prompting precautionary measures to be taken that are likely to limit the risks linked to the multifollicular development that is so frequent with this disorder. In addition, hyperandrogenism exposes the patient to various gynecological and general complications: cancer of the endometrium, progressive increase in menstrual disturbances and infertility, obesity, metabolic disturbances and probably increase in cardiovascular risks. Certain types of hyperandrogenism give rise to diseases that expose the patient to specific risks: virilizing tumors, Cushing's syndrome, neonatal risks linked to congenital hyperplasia of the adrenal glands. Hyperandrogenism should be borne in mind not only when the clinical picture is that of virilization, but also when there is any disturbance in eugonadal ovulation, whether or not this is manifested as menstrual disturbances or as infertility, and especially whether or not it is accompanied by hirsutism.
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PMID:[When and why should hyperandrogenism be searched for in women?]. 267 67


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