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

In previous studies short-term cortisol increased cold pressor responses and the rise in forearm vascular resistance accompanying intra-arterial norepinephrine without an increase in overall resting sympathetic nervous activity. The present study examined whether these alterations in pressor response are glucocorticoid or mineralocorticoid effects, or both. Normal male subjects (n = 12) received either fludrocortisone, 0.3 mg daily (n = 6), or dexamethasone, 3 mg daily (n = 6), for 7 days. Hemodynamic studies were performed before and on day 7 of treatment. Fludrocortisone increased body weight from 69.3 +/- 1.8 to 71.1 +/- 2 kg (p less than 0.001), cardiac output from 5.0 to 6.0 l/min (+/- 0.1, p less than 0.01), mean arterial pressure from 82 +/- 1 to 91 +/- 1 mm Hg (p less than 0.001), cold pressor responsiveness from 13.0 to 39.0 mm Hg/ml per 100 ml per minute (R units) (+/- 4.3, p less than 0.01), and forearm vascular response to intra-arterial norepinephrine (F = 59.4, p less than 0.01) and angiotensin II (F = 30.8, p less than 0.01) infusions. Total peripheral resistance fell from 22.0 to 20.1 mm Hg/l per minute (+/- 0.3, p less than 0.05). Dexamethasone did not increase cardiac output, 5.1 to 5.2 l/min (+/- 0.1), or body weight but did increase mean arterial pressure from 82 +/- 3 to 91 +/- 3 mm Hg (p less than 0.001), cold pressor responsiveness from 8.6 to 17.1 R units (+/- 2.8, p less than 0.05), and forearm vascular response to intra-arterial norepinephrine (F = 33.0, p less than 0.01) and angiotensin II (F = 54.9, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1992 Jun
PMID:Pressor responsiveness in corticosteroid-induced hypertension in humans. 159 52

In recent years the treatment of bacterial meningitis has been modified on the basis of a better understanding of its physiopathological mechanisms. It has been shown, for example, that the inflammatory reaction is the primary cause of brain damage in bacterial meningitis. Inflammation and consequent brain damage are greatest in the first hours of antibiotic treatment when rapid and massive bacteriolysis takes place. In effect, the bacterial components activate metabolic pathways and cellular elements leading to the release of inflammation mediators: cytokines (TNF, IL-I) neutrophil degranulation products, complement components and clotting factors. Initially these substances make the blood-fluid and blood-brain barriers permeable. The result is cerebral oedema, excessive fluid pressure, congestion of the cerebral blood vessels and finally endocranial hypertension, reduced cerebral flow, cerebral hypoxia and brain damage. This sequence of events can be stopped by a multifactorial therapy that is not only aetiological (antibiotic) but also treats the inflammation, oedema (Dexamethasone, Mannitol) and symptoms. In this study 129 patients with non-tubercular bacterial meningitis were treated as described. All patients were administered Ceftriaxone (100 mg/kg per diem) Dexamethasone (0.2-0.3 mg/kg/per diem), Mannitol, fluid restriction and--where necessary--intensive symptomatic therapy (against shock, convulsions, fever). Both the antibiotic and the corticosteroid were also administered intrathecally at the time of the first lumbar puncture at intake. Of these 129 patients, 7 died very soon after admission as they had arrived in a moribund condition. Duration of therapy was 3-6 days in 90% of these cases. There were no recurrences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rational basis of modern therapy of bacterial meningitis. Review of the literature and our clinical experience of 122 pediatric cases. 180 76

Dexamethasone has recently been introduced for the treatment of bronchopulmonary dysplasia (BPD). Whereas the short-term effect of dexamethasone has been documented in previous publications, studies on the long-term effect do not appear to exist in the literature. The aim of this retrospective study was to investigate the influence of dexamethasone on respiratory parameters, the long-term efficacy, and the side-effects. Dexamethasone was given to premature babies with BPD who could not be weaned from the respirator. Twelve infants were included in this study. The gestational ages ranged from 26 to 30 weeks and the birth weights ranged from 640 to 1410 g. Dexamethasone treatment was initiated at the age of 14 to 44 days. After 6 days of dexamethasone therapy, ventilation rates and FiO2 values improved significantly. All infants were successfully weaned from mechanical ventilation and extubated at 2 to 40 days after the start of dexamethasone therapy. The follow-up for the estimation of the long-term efficacy ranged from 3 to 18 months. Ten out of twelve patients had been weaned permanently from the ventilator; one 12-months-old infant is still respirator-dependent. One patient died at 8 months from BPD. In 5 out of 12 infants we observed a leukocytosis with neither clinical signs nor microbiological signs of an infection. Septicaemia developed in one case and one patient suffered from pneumonia. Arterial hypertension was observed in one infant during dexamethasone therapy. The results suggest that dexamethasone facilitates the weaning of preterm infants with BPD from the ventilator. This treatment may prevent some infants from long-term ventilation.
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PMID:[Dexamethasone therapy in bronchopulmonary dysplasia]. 249 83

The mechanism of glucocorticoid-induced hypertension is not known. Although glucocorticoids can exert an inhibitory effect on prostaglandin synthesis in vitro, their in vivo influence on this system is controversial. The goal of the present study was to determine whether dexamethasone-induced hypertension in Wistar rats is due to inhibition of the synthesis of the vasodilator prostaglandin I2 (PGI2) in vivo. Dexamethasone caused a profound reduction (7 +/- 1 versus 21 +/- 5 ng per 24 h) in the urinary excretion of PGI-M (PGI-M), a major metabolite of PGI2, and a sustained rise in systolic arterial pressure which was maximal after 5 days (144 +/- 9 versus 103 +/- 3 mmHg). A study of the metabolism of [3H]-labeled 6-oxo-PGF1 alpha and PGI2 revealed that dexamethasone exerted a dual action on the prostaglandin system in vivo: an inhibition of PGI2 biosynthesis and an alteration of its metabolism, both effects contributing to the observed reduction in urinary levels of PGI-M. Exogenous arachidonic acid induced a fourfold increase in urinary PGI-M in normal rats (from 14 +/- 3 to 61 +/- 6 ng per 24 h). Despite a large decrease upon addition of dexamethasone, urinary PGI-M remained in the high-normal range in arachidonic acid-treated rats (21 +/- 8 ng per 24 h). Arachidonic acid exerted antihypertensive effects which were marginal initially but significant in the later phase of dexamethasone-induced hypertension (124 +/- 8 versus 139 +/- 8 mmHg in arachidonic acid-treated versus control rats after 7 days of dexamethasone).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostaglandin I2 and glucocorticoid-induced rise in arterial pressure in the rat. 250 53

We present a report on two sisters who have 17 alpha-hydroxylase deficiency with hyperaldosteronism. They have hypertension and hypergonadotropic hypogonadism. The steroid profiles suggest that they have 17 alpha-hydroxylase deficiency. In contrast to the classical biochemical findings in 17 alpha-hydroxylase deficiency, both of these patients have hyperaldosteronism. Thus this report describes a new variant of 17 alpha-hydroxylase deficiency with hyperaldosteronism. Dexamethasone suppressed the mineralocorticoid excess, including aldosterone, and improved their hypertension. In the untreated state, ACTH, instead of the renin-angiotensin system, regulated plasma aldosterone levels, but during dexamethasone treatment the renin-angiotensin system regulated these levels.
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PMID:A new variant of 17 alpha-hydroxylase deficiency with hyperaldosteronism in two Japanese sisters. 255 Feb 10

Dexamethasone-suppressible hyperaldosteronism (DSH) is a rare familial variety of primary aldosteronism in which the biochemical features of mineralocorticoid excess are corrected by treatment with glucocorticoids. We report a large new kindred with this syndrome, the second such family described in the British Isles and the first in Ireland. The family has a dramatic history of premature cardiovascular death. We have documented DSH in four members and found evidence of aldosterone excess in two others. The kindred is unique in that we have documented DSH in distant relatives (fourth cousins). All patients described are well controlled on potassium-sparing diuretics. Our report underlines the importance of a detailed family history in the assessment of hypertension due to primary aldosteronism.
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PMID:Dexamethasone-suppressible hyperaldosteronism: a large new kindred. 255 13

A 45 year old female with Cushing's syndrome due to non-ACTH dependent bilateral adrenal macronodular hyperplasia (AMH) is reported. The diagnosis of Cushing's syndrome was based on the typical clinical features and on the demonstration of high urinary levels of free cortisol (microF) (630 micrograms/24 h) and 17 hydroxysteroids (17-OHS) which failed to suppress during the Liddle test (17-OHS, (mg/g creat), Basal: 68.5, post Dexamethasone 2 mg: 59.6 and post Dexamethasone 8 mg: 69.9). The adrenal CT scan showed bilateral multinodular enlargement while the pituitary CT scan was normal. Due to the presence of severe hypertension (240/150) and depression, the patient was treated with ketoconazole (800 mg/d) during 8 months achieving eucortisolism (microF 14-39 micrograms/24 h); however, plasma ACTH was not detectable at the end of this period. A bilateral adrenalectomy was performed, and both adrenals showed multiple nodules (0.3-4.5 cm in diameter) and weighed 136 and 31 g respectively. The lack of suppression of the 17-OHS with 8 mg of Dexamethasone, the persistence of an adequate inhibition of cortisol biosynthesis with ketoconazole, and the absence of plasma ACTH suggest that the patient had a non-ACTH dependent AMH. The possible pathogenic factors involved in this case are discussed.
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PMID:[Cushing syndrome caused by macronodular adrenal hyperplasia, independent of ACTH: report of a case]. 256 12

We studied the effects of dexamethasone on the vascular responsiveness of the isolated perfused mesenteric vascular bed of the rats. Dexamethasone was infused at a low dose (2 micrograms/day) to avoid steroid-induced catabolic effects. The mesenteric arteries were perfused with increasing concentrations of noradrenaline, vasopressin and potassium chloride. Vascular responses to vasopressin and potassium chloride were similar in both dexamethasone-treated and control arteries. However, the dexamethasone treatment increased the sensitivity, but not the maximal pressor response, to noradrenaline. These results show that dexamethasone selectively increases the vascular sensitivity to noradrenaline in rats before the development of systemic hypertension.
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PMID:Dexamethasone therapy selectively increases the sensitivity to noradrenaline of the rat mesenteric circulation. 263 93

In humans, the syndrome of cortisol resistance is characterized by the absence of signs and symptoms of Cushing's syndrome, elevated total and unbound plasma cortisol concentrations, and increases in urinary free cortisol excretion and plasma adrenocorticotropic hormone. In one family, a severely affected member had hypertension and hypokalemic alkalosis associated with increased plasma concentrations of corticosterone and deoxycorticosterone. These patients are resistant to suppression of the pituitary-adrenal axis by dexamethasone. Dexamethasone therapy, however, effectively corrected hypertension and hypokalemic alkalosis in the severely affected patient, without causing signs of glucocorticoid excess. The glucocorticoid receptor from these patients has a low affinity for glucocorticoids and is unstable during thermal activation. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Transformation of B-lymphocytes with Epstein-Barr virus leads to induction of glucocorticoid receptors. Receptor induction, however, is lower in patient cells than those obtained from normal controls. This decreased induction parallels decreased expression of glucocorticoid receptor mRNA. Thus, in this form of glucocorticoid resistance the glucocorticoid receptor is abnormal and leads to diminished target organ responsiveness. Many New World primates exhibit glucocorticoid "resistance," without apparent pathology. These species have markedly elevated plasma cortisol, both total and unbound concentrations, increased urinary free cortisol excretion, and marked increases in plasma adrenocorticotropic hormone and beta-endorphin. The glucocorticoid receptors of these primates have decreased affinity for glucocorticoids, are thermolabile, and are not induced by Epstein-Barr virus transformation as indicated by specific binding and mRNA expression. Both the molecular weight of the glucocorticoid receptor and the size of the corresponding mRNA are similar to those of normal controls. Despite the high plasma cortisol concentrations in these primates, there is no sodium retention and aldosterone levels are actually increased. The kidney aldosterone receptor cross-reacts poorly with cortisol, explaining the absence of sodium retention. New World primates also have progesterone, estrogen, aldosterone, and vitamin D insensitivity, suggesting a common factor linking steroid hormone receptors.
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PMID:Glucocorticoid resistance in humans and nonhuman primates. 264 36

Endocrine hypertension secondary to disorders of the adrenal glands is uncommon, but by no means rare. The importance of correct biochemical diagnosis and subsequent localization of the responsible lesion(s) lie in the fact that many of these syndromes occur in younger patients, may exhibit familial patterns of inheritance and are frequently amenable to surgical cure. The radiopharmaceuticals (131)1-6 beta-iodomethyl-19-norcholesterol (NP-59), a marker of adrenocortical cholesterol uptake, and (131)1- and (123)1-metaiodobenzylguanidine (MIBG), a norepinephrine (NE) analog and marker of energy-dependent NE storage vesicle accumulation, can be shown to accurately localize adrenal cortex and sympathoadrenal dysfunction, respectively. In Cushing's syndrome (CS) not only does the pattern of NP-59 uptake depict the adrenal dysfunction and its pathophysiologic basis, but the level of NP-59 accumulation reflects the degree of adrenocortical hyperfunction. Adrenocorticotrophin-independent CS is uniformly and accurately localized, especially in bilateral cortical nodular hyperplasia where even high resolution computed tomography (CT) may fail to depict the often subtle, asymmetric anatomic abnormalities. Dexamethasone suppression NP-59 adrenal scintigraphy has been shown to be highly sensitive and specific, and exceeds the efficacy of CT in the differentiation of adenoma and bilateral hyperplasia in primary aldosteronism. MIBG is useful as a sympathoadrenal imaging agent whose clinical utility has been demonstrated in the localization of pheochromocytoma, especially as a modality to screen the body for multiple and extraadrenal, recurrent, or metastatic lesions. Moreover, the extent of metastatic involvement from neuroblastoma can also be accurately depicted using MIBG. In this review we will examine the role of adrenal scintigraphy in the characterization of hypersecretory disorders of the adrenal cortex, medulla, and related conditions that produce hypertension as part of their symptom(s) complex. This approach, which is complementary to other anatomical modalities of imaging, can be used to advantage in the localization of functioning cortical and medulla adrenal diseases and other neoplasms of adrenergic origin.
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PMID:Scintigraphic studies in adrenal hypertension. 265 11


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