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)

Cushing's syndrome, a characteristic pattern of obesity with hypertension due to the hyperfunction of the adrenal cortex, is relatively rare in infancy. Thirty-six infants have been reported in world literature, most of whom have had adrenal tumours. There are only eight reported cases of infants under the age of 1 year with adrenal hyperplasia responsible for Cushing's syndrome. This is a report of an 8 month old child with bilateral nodular adrenal hyperplasia.
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PMID:Cushingoid adrenal hyperplasia in infancy. 372 27

The STH level was studied in the blood of 105 patients with the hypothalamic pubertal syndrome (HPS). A tendency toward STH hyperproduction was revealed. A comparison of the STH level in the blood and the degree of obesity of the HPS patients showed a clear decrease of the growth hormone in Stage IV obesity. The STH level was almost the same in Stages I, II, III obesity. The STH secretion in the HPS patients correlated with age. The period of disease did not influence hypophysial somatotropic function in the HPS patients. No interrelationship between the content of hydrocortisone and STH in the blood was established. In most of the patients with the HPS, the growth hormone secretion in response to hypoglycemia was undisturbed. Preliminary results obtained with parlodel tests showed an opposite reaction in the HPS patients as compared to healthy ones. Our results confirmed once more that the HPS should not be interpreted as a variant of Icenko-Cushing's syndrome or constitutional obesity in which STH production was lowered.
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PMID:[Somatotropic function of the hypophysis in the hypothalamic puberty syndrome]. 388 63

Insulin resistance is well established in Cushing's syndrome, but its mechanisms are not completely understood. We performed the euglycemic insulin clamp technique on four patients with Cushing's syndrome, five obese patients and five normal volunteers, in order to determine the role of impairments in insulin responsiveness and insulin clearance in hypercorticism and obesity. Insulin was infused at 0.3, 1, 3 and 10 mU/kg/min, and steady-state glucose-infusion rates required to maintain euglycemia were determined. Glucose disposal at maximal insulin levels was 11.9 +/- 0.4 mg/kg/min in normals, with a 29% decrease in obese and a 42% decrease in Cushing's syndrome patients. Half maximally effective insulin concentrations were increased in both abnormal groups compared to normals. Maximal insulin clearance rates were 1460 +/- 200 ml/min/m2 in normals, not significantly changed in obese and 40% decreased in Cushing's syndrome patients. These results indicate that the insulin resistance in Cushing's syndrome is distinct from that occurring in obesity and is characterized by both decreased insulin responsiveness and decreased insulin clearance. These impairments could be caused by a common defect which may be at or distal to the glucose transport level.
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PMID:Insulin resistance in Cushing's syndrome. 390 56

The clinical response of 57 adult patients with Cushing's syndrome due to bilateral adrenocortical hyperplasia or adrenocortical adenoma is documented following resolution of hypercortisolaemia by various forms of treatment. Despite satisfactory biochemical remission of the disease the clinical result was far less satisfactory when assessed by persistence of obesity (55%), menstrual irregularity (41%), hypertension (29%) and insulin-dependent diabetes (22%). Myopathy, hirsuitism and psychological abnormalities persisted to a lesser extent. The mortality rate of the series over a 30 year follow-up period was 4 times that of a general population matched for sex, age and year of entry into the series. Cardiovascular disease was the cause of death in 85%. Irreparable cardiovascular disease is produced early in the course of hypercortisolaemia, emphasizing the vital importance of the earliest possible recognition and treatment of this disease.
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PMID:The clinical response to treatment in adult Cushing's syndrome following remission of hypercortisolaemia. 398 55

The right suprarenal mass was found in a 21-year-old housewife. Her major clinical features were amenorrhea, polydipsia and buffalo hump obesity. Endocrinological and roentgenological studies suggested the presence of Cushing's syndrome due to adrenocortical carcinoma in addition to ipsilateral renal stone. The huge adrenal tumor and renal calculus were successfully removed. The histological diagnosis was adrenocortical carcinoma. Seventeen days after the operation, cis-platinum was administered to prevent the recurrence of tumor development. No recurrence has been observed for approximately 2 years after the surgery. Long follow-up must be pursued to clarify the real efficacy of cis-platinum treatment.
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PMID:[Cis-platinum used for the prevention of the recurrence of adrenal cortical carcinoma: report of a case]. 405 Jun 25

We have reviewed 58 patients on whom adrenal scintigraphy has been performed using 75Se selenonorcholestenol. For 15 patients whose adrenal function was biochemically normal, the upper limit of normal of the 7 day adrenal uptake test was 0.45%, considerably higher than the generally accepted value of 0.3%. There is evidence from this group of patients that stress and obesity might account for uptakes in the range 0.3-0.45%. The sensitivity of the uptake test is poor, with 7 out of 23 patients with Cushing's syndrome having uptakes within the normal range. Scintigraphy of such patients may still be useful in differentiating between unilateral and bilateral adrenal involvement.
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PMID:Adrenal scintigraphy with 75Se selenonorcholestenol: a review. 406 75

Plasma concentrations of glucagon, insulin, glucose, and individual plasma amino acids were measured in normal nonobese and obese subjects before and after 3 days of dexamethasone treatment (2 mg/day) and in patients with Cushing's syndrome. The subjects were studied in the basal postabsorptive state and following the infusion of alanine (0.15 g/kg) or ingestion of a protein meal. In nonobese subjects dexamethasone treatment resulted in a 55% increment in basal glucagon levels and in a 60-100% increase in the maximal glucagon response to alanine infusion or protein ingestion. In obese subjects, basal glucagon rose by 110% following dexamethasone, while the response to alanine increased fourfold. In patients with Cushing's syndrome basal glucagon levels were 100% higher and the glucagon response to alanine infusion was 170% greater than in normal controls.Dexamethasone treatment in normal subjects resulted in a 40% rise in plasma alanine concentration which was directly proportional to the rise in basal glucagon. The remaining 14 amino acids were unchanged. In the patients with Cushing's syndrome alanine levels were 40% higher than in normal controls and were directly proportional to basal glucagon concentrations. No other plasma amino acids were significantly altered in the group with Cushing's syndrome. It is concluded that (a) glucocorticoids increase plasma glucagon concentration in the basal state and in response to protein ingestion or aminogenic stimulation; (b) this effect of glucocorticoids occurs in the face of obesity and persists in chronic hypercorticism; (c) hyperalaninemia is a characteristic of acute and chronic glucocorticoid excess, and may in turn contribute to steroid-induced hyperglucagonemia; and (d) increased alpha cell secretion may be a contributory factor in the gluconeogenic and diabetogenic effects of glucocorticoids.
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PMID:Influence of glucocorticoids on glucagon secretion and plasma amino acid concentrations in man. 474 10

A patient with Cushing's syndrome whose clinical manifestations began at approximately 9 years of age was followed for a period of four years. Initial laboratory studies revealed urinary 170HCS and 17 KS levels which were elevated for her age, with a normal diurnal variation of plasma cortisol and normal suppression of urinary 170HCS by 1.5 mg. of dexamethasone daily. It was not until four years after the onset of the disease that laboratory studies unequivocally supported the diagnosis of Cushing's syndrome resulting in definitive therapy. Clinical features consisted primarily of cessation of growth, obesity, and hirsutism, with no evidence of protein depletion. It is suggested that the clinical and laboratory features of Cushing's syndrome in childhood may present differences from those found in the adult. Failure to recognize these differences may result in delay in therapy with subsequent persisting stigmata of the disorder.
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PMID:Cushing's syndrome in childhood. 505 86

The etiology of several specific types of hypertension are described in order of increasing difficulty of diagnosis: glycyrrhizine poisoning, oral contraceptives, coarctation of the aorta, pheochromocytoma, Conn syndrone, Cushing syndrome, parenchymal nephropathy, unilateral renal atrophy, and renovascular hypertension. Glycerryyzine and oral contraceptive etiologies can be diagnosed by questioning the patient and improved by eliminating their intake. Coarctation of the aorta is easily identified by clinical signs, but surgical repair is probably mor e risky than drug treatment. A pheochromocytoma is signaled clinically and by catecholamine excretion. Conn syndrome has characteristic clinical signs, particularly hypokalemia during intake of diuretics. Cushing syndrome is recognized by corticosteroid excretion as well as peculiear obesity, acne, erythrosis, and diabetes. Bilateral nephropathy is common (25% of hypertensions) and rather difficult to dia gnose and treat. Unilateral renal atrophy can be demonstated by renal arteriography and cystography, but predicting the outcome of nephrectomy is problematic. Renovascular hypertension due to occlusion of the renal artery requires the most sophisticated tests and care for an effective treatment. A table and an outline of diagnostic tests to differentiate these disorders are included.
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PMID:[Etiologic survey of arterial hypertension. Its justifications and practical modalities]. 549 42

Adrenocortical tumors can be divided into two groups based on their histopathological characteristics, i.e., benign (adenoma) and malignant (carcinoma), and also classified as functioning (or hormonal) and non-functioning (or non-hormonal) tumors, depending on the presence or absence of recognizable clinical syndromes due to excessive steroids. The syndrome of functioning adrenocortical tumors includes Cushing's syndrome, primary aldosteronism and the adrenorge genital syndrome, of which a minority presents most of the specific clinical features: Cushing's syndrome; red face, typical moon face, truncal obesity, and purplisch red striae, primary aldosteronism; muscle weakness, noctural polyuria, hypertension and hypokalemia, adrenogenital syndrome; virilization or feminization, but many of them present complete clinical picture. The diagnosis of these syndromes needs to measure urinary 17-OHCS and 17-KS and plasma concentrations of cortisol, aldosterone, dehydroepiandrosterone (DHEA) and the other steroids. Dexamenthasone suppression test, various stimulation tests and the measurement of plasma ACTH are also useful for diagnosis. Usually, adrenocortical tumors can be detected preoperatively by physical examination or radiographic studies. Some are massive enough to be palpable through the abdominal wall. Some are large enough to cause displacement of the kidney, as seen intravenous urography. Most are visible by adrenal scintigraphy using 131I-iodocholesterol, computerized tomography, or adrenal arteriography. The standard treatment for adrenocortical tumors are surgical resection. Unresectable adrenocortical carcinomas may be treated with an adrenocorticolytic drug, o'p'-DDD. Metyrapone and aminoglutethimide can be also employed to inhibit the production of steroids.
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PMID:[Diagnosis and treatment of adrenocortical tumors]. 631


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