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

Cushing's syndrome in childhood is generally recognized by classical features such as truncal obesity, striae, easy bruising, moon facies, hypertension and growth retardation. Exceptionally, Cushing's syndrome has been reported to present as growth failure alone. We diagnosed transient hypercortisolism in 6 children who had poor growth as their only presenting abnormality. The 6 children all had integrated concentrations of cortisols (IC-F) (14.1 +/- 1.7 micrograms/dl; mean +/- 1 SD) which exceeded the IC-F in healthy children and adults (5.7 +/- 1.5 micrograms/dl; P less than 0.001). The IC-F of these 6 index cases overlapped the range of IC-F in patients with pathologically proven Cushing's syndrome (20.2 +/- 4.7 micrograms/dl). Four of the 6 patients were treated with human growth hormone for 8 months and showed a marked improvement in their growth rates. Four patients have entered puberty and are growing at normal rates. Three of the 6 children had normal repeat IC-Fs, subsequently, at a time they had normal growth rates. In 1-1/2 to 3 years of follow-up, none of the patients developed any other stigmata of Cushing's syndrome. We conclude that transient hypercortisolism, documented by the IC-F, may cause growth failure without other symptoms of Cushing's syndrome. Growth hormone therapy may improve the growth rate of these children at the time of their poor growth.
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PMID:Growth impairment due to transient hypercortisolism. 346 64

The mechanisms causing high blood pressure in patients with Cushing's syndrome were investigated by measurements of humoral factors and pharmacological maneuvers. Twelve patients with adrenal adenomas were studied. The mean systolic and diastolic pressures of the patients were 171 +/- 28 and 109 +/- 15 mm Hg (+/- SEM), respectively, which were significantly higher than those of normal subjects. PRA, plasma renin concentration, plasma renin substrate, plasma cortisol, plasma aldosterone, urinary kallikrein, and urinary prostaglandin E2 were measured as the humoral factors. PC values were markedly elevated in patients with Cushing's syndrome. Among the components of the renin-angiotensin system, only plasma renin substrate was increased. Urinary kallikrein and prostaglandin E2 were decreased in patients with Cushing's syndrome. Oral administration of captopril lowered blood pressure, but infusion of an angiotensin II analog did not. Furthermore, the pressor responses to infusion of both norepinephrine and angiotensin II were increased. We conclude that blood pressure is elevated in patients with Cushing's syndrome because they have enhanced pressor responses to vasoactive substances, suppression of depressor systems, and some abnormalities of the renin-angiotensin system.
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PMID:Multiple factors contribute to the pathogenesis of hypertension in Cushing's syndrome. 351 Feb 23

Hypertension is a common finding in patients with Cushing's syndrome (CS), but the cause is unknown. One possibility is excess production of nonaldosterone mineralocorticoids, such as 19-nor-deoxycorticosterone (19-Nor-DOC). To evaluate this possibility we measured urinary 19-Nor-DOC glucuronide in normal subjects (n = 14) and patients with essential hypertension (n = 10), pituitary-dependent CS (n = 8), and adrenal tumors producing CS (n = 6). The subjects were admitted to a metabolic unit where 24-h urine samples were collected while they ate an isocaloric diet (128 meq Na+ 80 meq K+/day). 19-Nor-DOC glucuronide was purified by extraction and chromatography and measured by RIA. Urinary 19-Nor-DOC glucuronide excretion was significantly higher in patients with both pituitary CS and adrenal CS compared to that in normal subjects, while the values in the two CS groups were similar. The patients with essential hypertension also had elevated urinary 19-Nor-DOC glucuronide excretion, although the values were lower than those in either CS group. These results demonstrate that a nonaldosterone mineralocorticoid, 19-Nor-DOC, is produced in excess in patients with either pituitary or adrenal CS and, thus, suggest a possible role for 19-Nor-DOC in the pathogenesis of some hypertensive disorders.
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PMID:Elevated urinary 19-Nor-deoxycorticosterone glucuronide in Cushing's syndrome. 355 30

The case of a 60-year-old woman with pheochromocytoma and concomitant adrenocortical adenoma in the same gland is presented. She complained of episodic headache, palpitation, nausea, vomiting and sweating. Physical examination revealed that the patient has generalized obesity, wet skin and paroxysmal hypertension, but no signs of Cushing's syndrome. Elevated levels of urinary noradrenaline, adrenaline and total metanephrine were sequentially observed. In addition, urinary 17-OHCS was also slightly elevated, but plasma cortisol was normal and suppressed after oral administration of 0.5 mg of dexamethasone. Abdominal echography and CT scanning demonstrated a left adrenal tumor, which took up both 131I-meta-iodobenzylguanidine and 75Se-scintadoren in the same region. A left adrenalectomy was performed and the tumor was found to consist of two parts, pheochromocytoma (2.5 X 2.5 X 2.5 cm) and cortical adenoma (2.5 X 3 X 5 cm). A total of 23 reported cases showing evidence of hyperfunction of the adrenal cortex and the medulla were noted. So far as we know, this patient was the second case of pheochromocytoma with adrenocortical adenoma in Japan.
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PMID:Pheochromocytoma associated with adrenocortical adenoma: case report and literature review. 372 Jun 79

Among the many potential causes of secondary hypertension are renal parenchymal disease, occlusive renal arterial disease, adrenocortical abnormalities, and pheochromocytoma. Renovascular hypertension can result from either renal parenchymal or occlusive renal arterial disease. Laboratory testing can help in identification and differentiation. Parenchymal diseases usually modify the urine substantially without producing urographic abnormalities, while occlusive arterial lesions produce urographic abnormalities but the urine remains normal. The diagnosis of renal occlusive arterial disease is best defined by arteriography. The only definite criterion for the existence of hypertension of renal origin is cure by either nephrectomy or renal revascularization. Adrenocortical causes of hypertension include enzymatic deficiencies, Cushing's syndrome, and primary aldosteronism. In enzymatic deficiencies, the physical findings provide the most important clues to the type of enzyme deficiency involved. In Cushing's syndrome, accurate determination of the cause of the hypercortisolism is important in terms of choice and success of treatment. The diagnosis of primary aldosteronism rests primarily on the demonstration of nonsuppressible aldosterone excretion rate during salt loading; the presence of inappropriate kaliuresis and/or suppressed plasma renin activity provides corroborative evidence of primary aldosteronism, but the absence of either or both does not preclude the diagnosis. Pheochromocytoma, although rare, is a serious and potentially fatal cause of hypertension. Definitive diagnosis depends on laboratory test results, and the tumor is usually localized by computed tomography.
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PMID:Secondary hypertension. A streamlined approach to diagnosis. 372 9

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

A 2-year-old girl who presented with blindness, aphasia and inability to move the right arm and leg following a convulsive episode was found to have hypertension, precocious pseudopuberty, features of Cushing syndrome and an ovarian tumour. The hormonal profile suggested an adrenal cortical tumour, which turned out to be located in the ovary and the cause of the ovarian enlargement. Following removal of the mass, all the abnormal features regressed and the blood pressure returned to normal.
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PMID:Adrenal rest tumour of the ovary associated with isosexual precocious pseudopuberty and cushingoid features. 376 85

A 26-yr-old woman presented with hirsutism, male pattern scalp baldness ("geheimratsecken"), and menstrual irregularities. She had no hypertension or other signs and symptoms of Cushing's syndrome. Plasma cortisol levels were greatly elevated and did not suppress normally in response to dexamethasone. Cortisol binding to transcortin was normal. Plasma androstenedione and testosterone levels were also increased, but 17-hydroxyprogesterone and aldosterone levels were normal. Further studies revealed an increased cortisol production rate, increased 24-h urinary cortisol excretion, increased plasma ACTH levels, a normal diurnal rhythm of cortisol at an elevated level, and normal increments of plasma ACTH, cortisol, GH, and PRL in response to insulin-induced hypoglycemia. The father and two brothers also had increased plasma cortisol levels, which did not suppress normally in response to dexamethasone. Chronic therapy with dexamethasone (at first 1 and later 0.5 mg, three times daily) for more than 30 weeks resulted in decreased hirsutism, normalization of scalp hair and menstrual cyclicity, and normal plasma testosterone and androstenedione levels. No signs or symptoms of Cushing's syndrome developed, and the central regulation of secretion of ACTH, cortisol, GH, and PRL (insulin test, diurnal rhythm) remained qualitatively normal at a lower set-point. We conclude that this patient had autosomal dominantly inherited hereditary (partial) cortisol insensitivity, which had resulted in increased adrenocortical cortisol and androgen secretion. The latter had not resulted in clinical symptoms in the three afflicted male members of the family, but had in the propositus. The results also indicate the potential usefulness of the insulin test in distinguishing this disorder from Cushing's disease.
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PMID:Familial cortisol resistance: differential diagnostic and therapeutic aspects. 378 21

The association of the Ehlers-Danlos syndrome with many cardiovascular abnormalities is well known. To our knowledge, however, renovascular hypertension due to renal arterial aneurysms has not previously been reported in patients with this disease. We describe a patient with type IV Ehlers-Danlos syndrome who had multiple systemic and bilateral renal arterial aneurysms and hypertension. The hypertension could have been related to compression of renal tissue or arteries (or both) by the large aneurysms, associated stenoses, or small peripheral renal infarctions. A review of all patients in whom the Ehlers-Danlos syndrome had been diagnosed at our institution between 1967 and 1985 revealed that 4 of the 200 patients had hypertension. Three of these patients, and probably all four, had secondary causes of hypertension: Cushing's syndrome, renal insufficiency, or renovascular hypertension (in the present case). We conclude that hypertension is rare in patients with the Ehlers-Danlos syndrome and that, if present, it most likely is secondary hypertension. A thorough search for secondary causes of hypertension should be undertaken in these patients.
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PMID:Renovascular hypertension: a rare cardiovascular manifestation of the Ehlers-Danlos syndrome. 382 Nov 83

Plasma prolactin level and plasma renin activity were determined in normal subjects and patients with low and normal renin essential hypertension, renal hypertension, renovascular hypertension, primary aldosteronism, Cushing syndrome, pheochromocytoma and malignant hypertension. In both normal subjects and the normal renin essential hypertensives, plasma prolactin was significantly higher in females than in males. Plasma prolactin was also significantly higher in the normal renin essential hypertensives than in normal subjects of both sexes, while no significant difference was found between the low renin group and normal subjects of either sex. A significantly positive correlation was observed between plasma renin activity and the plasma prolactin level in male essential hypertensives, but not in females. Although no significant difference in plasma prolactin level could be detected between patients with secondary hypertension and normal subjects, this level was significantly higher in malignant hypertensives than in normotensives. From these results, it was shown that significant differences of plasma prolactin levels exist between normal renin essential hypertensives, and low renin essential hypertensives or normal subjects, and that these differences may partly depend on renin status which might be related to the central dopaminergic activity. In malignant hypertensives, the high level of plasma prolactin may be caused by diminished renal function, but the suppression of central dopaminergic activity cannot be excluded in the mechanism of plasma prolactin increment.
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PMID:Plasma prolactin levels in patients with essential hypertension, malignant hypertension and secondary hypertension. 388 34


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