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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

In assessing the pituitary-adrenal axis of uraemic Nigerians, we investigated the circadian rhythm of plasma cortisol secretion, the response to the overnight dexamethasone (1 mg) suppression test and the pattern of excretion of urinary free cortisol (UFC) in 10 uraemic subjects and nine non-uraemic controls. Basal (0800 h) plasma cortisol levels were similar in both uraemic (mean +/- s.e.m.; 224 +/- 36 nmol/l) and non-uraemic (218 +/- 47 nmol/l) subjects. The non-uraemic subjects demonstrated the normal late night (2300 h) reduction in cortisol levels but this was absent in uraemic subjects in whom the basal and late night values were similar. Post-dexamethasone (0800 h) values were suppressed by 80% in non-uraemic subjects (P less than 0.01) from 218 +/- 47 nmol/l (at 2300 h) to 44 +/- 16 nmol/l (at 0800 h), whereas there was lack of suppression (P greater than 0.05) in values from uraemic subjects (224 +/- 36 nmol/l at 2300 h and 210 +/- 39 nmol/l at 0800 h). Irrespective of the degree of renal impairment in uraemic subjects, the 24 h UFC excretion was significantly greater (P less than 0.05) (1126 +/- 403 nmol/24 h) compared with non-uraemic subjects (342 +/- 94 nmol/24 h). These results confirm previous observations in Caucasians and reaffirm the existence of a pseudo-Cushingoid state in uraemia which may contribute to the associated hypertension and electrolyte abnormalities.
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PMID:Uraemia and adrenocortical function in Nigerian subjects. 210 19

Inappropriate ACTH secretion with bilateral diffuse or macronodular adrenal hyperplasia is the most common cause of Cushing's syndrome. This report describes a patient with Cushing's syndrome and feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia. A 47-yr-old black man presented with Cushingoid features, diabetes mellitus, hypertension, impotence, and gynecomastia. Urinary cortisol and 17-hydroxycorticosteroid excretion were 94 nmol/mmol creatinine (normal, less than 32) and 5.8 mumol/mmol creatinine (normal, 0.6-3.6), respectively. Both decreased by less than 30% after administration of dexamethasone (8 and 16 mg/day), and urinary 17-hydroxycorticosteroid excretion did not increase after metyrapone (750 mg, orally, every 4 h for six doses). Plasma ACTH was undetectable (less than 1 pmol/L) and was not stimulated by administration of metyrapone or ovine CRH. Serum testosterone was 5.2 nmol/L (normal, 7-30), FSH was 5 U/L (normal, 3-18), LH was 2.8 U/L (normal, 1.5-9.2), and estrone was 767 pmol/L (normal, 55-240). Both adrenal glands were enlarged, with a total weight of 86 g (normal, 8-10), and contained multiple nodules (diameter, greater than 0.5 cm) composed of two active cell types, one of which was also observed between the nodules. Cushing's syndrome with feminization due to ACTH-independent bilateral macronodular adrenal hyperplasia is an unusual process of unknown etiology that should be included with the other known causes of Cushing's syndrome.
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PMID:Adrenocorticotropin-independent bilateral macronodular adrenal hyperplasia: an unusual cause of Cushing's syndrome. 253 45

Because of the advance of techniques and age-matched apparatus for blood pressure measurement, and because of the availability of age-related normal values in childhood, the knowledge of the number of children having elevated blood pressures has recently improved. In a group of healthy children, the first important task is to determine how many incidences of "essential hypertension" there are among them, which may appear in childhood and persist into adulthood. This should urge us to undertake periodical examinations of healthy children. On the other hand, the treatment of "secondary hypertension" has similarly been improved. Since 1979 in particular, captopril, an orally active angiotensin I-converting enzyme inhibitor, has successfully been administered to treat children with malignant hypertension and who respond poorly to conventional antihypertensive therapies. We report 3 cases that received captopril for refractory hypertension: a 2-year-old boy with renal and renovascular anomalies, a 7-year-old boy with moyamoya disease after surgical operation, and a 17-year-old youth with Cushingoid syndrome due to chronic administration of steroids against mixed connective tissue disease. After the introduction of captopril, good pressure control was obtained in all 3 cases, although reasonable effects of measurement values of the renin-angiotensin-aldosterone system (decrease in angiotensin I & II, increase in I/II ratio, etc.) were found only in the first case.
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PMID:Refractory hypertension in childhood--efficacy of captopril therapy. 332 1

Although some psychiatric patients may have a disorder of hypothalamic-pituitary-adrenal (HPA) function equal in character and severity to that noted in milder cases of Cushing's disease, it is generally accepted that such patients do not show Cushingoid stigmata. This conclusion, however, appears to be based more on clinical observation than on the results of formal scientific investigation. Since some depressed patients appear to overlap with Cushing's disease patients in incidence of such signs and symptoms as amenorrhea, hypertension, sleep disturbance, and insulin resistance, we were interested in examining whether a group of psychiatric patients showing evidence of marked nonsuppression might not also show physiological changes consonant with the effect of glucocorticoid excess. Nonsuppressors selected on this basis differed slightly from a matched suppressor control group on percentage of polyneutrophils and lymphocytes in blood. A discriminant function constructed from blood sample measurements of 12 factors and systolic/diastolic blood pressure successfully predicted suppressor or nonsuppressor status in the original and in an independent group of psychiatric patients. A comparison group of Cushing's disease patients was also successfully reclassified on the basis of the discriminant function. These data are interpreted as evidence for a subtle physiological effect of HPA dysregulation and suggest that behavioral symptom complexes may be similarly shaped by changes in this neuroendocrine system. The long-term functional significance of such changes is at present speculative.
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PMID:Evidence for physiological effects of hypercortisolemia in psychiatric patients. 385 48

Male and female, young (2 months old) and mature (10 months old), obese and nonobese, spontaneously hypertensive rats (SHR) were treated with dexamethasone, 5 micrograms/rat and 10 micrograms/rat, respectively, subcutaneously (SC) 2 times daily for 5 months. Steroid treatment stilled the voracious appetite of the obese SHR, and the massively obese, mature animals were reduced to almost normal size. The young, steroid-treated, obese SHR did not develop their genetically programmed corpulency. The untreated, young and mature, obese SHR ate voraciously, became massively obese, and developed their characteristic Cushing's disease-like spectrum of degenerative changes, eg, hypertension, hyperlipidemia, hyperglycemia, muscle wasting, kidney stones, thin skin, and accelerated aging. The blood pressure of the steroid-treated animals was lowered concomitant with reduced levels of circulating ACTH, beta endorphin, insulin, triglycerides, and cholesterol. Dexamethasone caused hyperlipidemia, hyperglycemia, and increased BUN levels in young obese and nonobese SHR only. The mature obese SHR had giant-sized thymus glands that were further enlarged with steroid treatment; dexamethasone was thymolytic in young, obese and nonobese SHR. Dexamethasone caused severe reduction of pituitary and adrenal gland size, simulating the condition of hypophysectomy. These findings demonstrate that dexamethasone suppression of the pituitary-adrenal axis palliates and prevents the spontaneous development of Cushingoid degenerative changes in these genetically obese and hypertensive rats.
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PMID:Dexamethasone suppression of cushingoid degenerative changes in obese spontaneously hypertensive rats (SHR). 631 58

Male, 5 months old, massively obese, spontaneously hypertensive rats (Obese/SHR) were given 10 mg alloxan/100 g b.w., s.c., to induce diabetes. Control Obese and non-obese/SHR were given saline. Insulin therapy was withheld. All of the animals were killed at 6 months of age. Alloxan caused a slight but statistically significant increase in blood pressure, pituitary and adrenal glandular hyperplasia, hyperlipidemia, hyperglycemia, and increased BUN levels. The giant sized islets of Langerhans in Obese/SHR showed only partial degranulation of the insulin-producing beta cells concomitant with residual but apparently adequate blood insulin levels, whereas the islets of non-obese/SHR exhibited virtually total beta cell degranulation and only trace amounts of blood insulin. The alloxanized, non-obese rats were severely emaciated; the alloxanized Obese/SHR maintained their obesity. Alloxan-treated, Obese and non-obese/SHR manifested gross and microscopic degenerative changes suggesting acceleration of the normal aging process. The genetically-programmed pathogenesis of diabetes, obesity, hypertension, and Cushingoid pathophysiology of Obese/SHR may be due to hyperadrenocorticism.
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PMID:Resistance of obese and non-obese, spontaneously hypertensive rats to alloxan-induced diabetes. 635 Jul 80

Male and female, massively obese and nonobese, spontaneously hypertensive rat (SHR) which are hypersensitive to stress were kept under quiescent conditions; they were autopsied at 15 months of age. The blood pressure of the Obese/SHR plateaued at 166 mmHg versus 198 mmHg for the nonobese/SHR. The once massive thymi vanished in the Obese/SHR accompanied by greatly enlarged adrenal glands, pituitary basophilia, greatly elevated levels of adrenocorticotrophin, corticosterone, deoxycorticosterone, aldosterone, fatty liver, hyperlipidemia, and hyperglycemia. The Obese/SHR were hyperadrenocorticoid compared with their nonobese siblings and manifested a Cushingoid spectrum of degenerative changes (e.g., thin skin, hypertension, diabetes, kidney stones, and accelerated aging). The provision of a nonstressful environment is believed to have dampened the usual chronic hyperadrenocorticism and prolonged the lifespan of the Obese/SHR.
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PMID:Cushingoid pathophysiology of old, massively obese, spontaneously hypertensive rats (SHR). 682 32

Naturally occurring kidney stones are rare in animals. The Japanese strains of spontaneously hypertensive rats (SHR) are normotensive at birth but develop high blood pressure, hyperglycaemia and hyperlipidaemia as they mature. The SHR strain is prone to develop kidney stones. A unique sub-strain of SHR has been developed in which some animals develop hypothalamic obesity concomitantly with their rising blood pressure, i.e. Obese/SHR. The Obese/SHR characteristically develop microscopic kidney stones which become detached at an early stage of formation, migrate to the bladder, and grow by concretion into huge, rounded calculi. The stone nidus starts as a subepithelial cyst-like focus containing oedema, colloidal acidic mucoprotein, and red and white blood cells suspended on a delicate network of fibrils. THe nidi grow by concretion of an admixture of calcium and acidic protein in a lamellar arrangement. The disparate morphogenesis and anatomic location of kidney stones in Obese is opposed to non-obese/SHR suggest that calculus formation may be governed by specific differences in genetic programming. The incidence of kidney stones parallels the severity and chronicity of the hypertension in SHR, non-obese and Obese/SHR, and the Cushingoid habitus in the Obese/SHR.
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PMID:Kidney and bladder calculi in spontaneously hypertensive rats. 729 30

A 57-year-old woman who presented with depression and hypertension for which she had received anti hypertensive therapy including diuretics was found to have Cushingoid features. All medication was stopped and subsequent investigation demonstrated markedly elevated urinary free cortisol (UFC) levels. An increase in UFC occurred in response to the low dose dexamethasone suppression test and a further increase was noted during the high dose test. Plasma cortisol levels did not change significantly. Detailed examination of the data revealed that over the 6-day testing period the plasma creatinine had fallen from 1.4 mg/dl to 0.7 mg/dl while the creatinine clearance had doubled--presumably due to withdrawal of the diuretic. When the UFC was expressed per 100 ml of plasma filtered, there was no difference between any of the daily excretions. We conclude that a concurrent increase in glomerular filtration rate is one mechanism by which a 'paradoxical' increase in UFC in response to dexamethasone suppression may occur.
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PMID:A rise in the glomerular filtration rate as the cause of a 'paradoxical' increase in urinary free cortisol during dexamethasone suppression in a patient with an adrenal adenoma: a case report. 730 83


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