Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case of posterior fossa medulloblastoma in which the initial symptom was severe hypertension that evolved into a hypertensive crisis. Initial diagnostic evaluation was suggestive of both pheochromocytoma and Cushing's syndrome: elevated plasma norepinephrine and urine VMA, normal ACTH level with elevated plasma and urine cortisol, and lack of suppressibility with dexamethasone. CAT scan and cerebral angiogram subsequently revealed the presence of an intracranial mass. After surgical removal of the tumor, blood pressure pattern and endocrine abnormalities reverted to normal.
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PMID:Cerebellar tumor causing hypertensive crisis and simulating pheochromocytoma and Cushing's syndrome. 278 84

A 48-year-old man was admitted for treatment of Cushing's syndrome due to right adrenal adenoma, associated with chronic renal failure (CRF) with a blood urea nitrogen level of 64.2 and serum creatinine level of 3.9 mg/dl. After removal of the adrenal adenoma, the CRF deteriorated with progressive symptoms of anorexia, vomiting and hypertension, and the patient was placed on hemodialysis. Prior to adrenalectomy, the 17 OHCS and 17 KGS in the urine were not so high. However, the urinary 17 KS was high with an elevated 11-oxy fraction. In comparison with 2 patients suffering from adrenal Cushing's syndrome with normal renal function, there were no large accumulated quantities of glucuronic conjugated and unconjugated metabolites in the plasma of the CRF Cushing's syndrome, with confirmation ascribable to the radioimmunoassayable cross-reactivity of the cortisol antiserum used in the radioimmunoassay kit. In the Cushing's syndrome with CRF, almost all the cortisol, which was hypersecreted from the adenoma, was presumed to be converted to the 11-oxy fraction of 17 KS, possibly by activation of hepatic enzymes.
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PMID:Cortisol and its metabolites in the plasma and urine in Cushing's syndrome with chronic renal failure (CRF), compared to Cushing's syndrome without CRF. 279 94

We report a 45-year-old female with left adrenocortical carcinoma resulting in Cushing syndrome. She visited the 3rd Department of Internal Medicine, Kanazawa University Hospital with complaints of moon face, amenorrhea and hypertension. A diagnosis of left adrenal tumor with Cushing syndrome was made and she was transferred to our clinic. Left thoracoabdominal adrenalectomy was performed. The histologic report was compatible with adrenocortical carcinoma with no invasion into adjunctive tissues. She is now on endocrinologic study and is being administered 1,1-dichloro-2-[o-chlorophenyl]-2[p-chlorophenyl] ethane. There is no evidence of local recurrence or remote metastasis.
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PMID:[Adrenocortical carcinoma with Cushing syndrome: report of a case]. 280 88

The mechanism of glucocorticoid-induced hypertension is not clarified. Recent data suggest an alteration of active electrolyte transport systems by glucocorticoids. We therefore studied the activities of the Na-K pump by measuring the Na-K-ATPase activity in erythrocyte ghosts and the ouabain-sensitive uptake of rubidium in erythrocytes of patients with Cushing's syndrome and of patients with exogenous glucocorticoid excess after treatment with fluocortolone or ACTH. Na-K-ATPase activity was significantly increased in patients with Cushing's syndrome and in patients treated with ACTH compared to the controls. Similarly, total uptake of 86Rb and the ouabain-sensitive uptake in erythrocytes were found to be above the control range both in patients with Cushing's syndrome and in patients treated with fluocortolone. There was no difference in furosemide-sensitive uptake of 86Rb. The results demonstrate an increased maximal activity of the Na-K pump in patients with glucocorticoid excess.
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PMID:Na-K pump activity in erythrocytes of patients with endogenous and exogenous glucocorticoid excess. 299 69

Primary cortisol resistance in man is a familial disease characterized by increased plasma cortisol concentrations, high urinary free cortisol excretion, a normal circadian pattern of cortisol secretion, resistance to adrenal suppression by dexamethasone and absence of the clinical stigmata of Cushing's syndrome or signs of adrenal insufficiency. In its severe form, hypertension and hypokalemic alkalosis are present, owing to increased secretion of the sodium-retaining corticoids, corticosterone and deoxycorticosterone. In subjects with a less severe resistance to cortisol, there are no clinical abnormalities and the disease is revealed only by detailed examination of several parameters of cortisol metabolism or by glucocorticoid receptor studies. In whole-cell glucocorticoid receptor assays (peripheral mononuclear leukocytes, fibroblasts, or B-lymphocytes transformed with the Epstein-Barr Virus) low receptor affinity for dexamethasone could be demonstrated conclusively only in the severely affected subject. When affected cells are transformed with the Epstein-Barr virus, receptor induction is less than that of normal cells. The decreased affinity of the receptor for its ligand is reflected in an increased rate of loss of specific bound ligand during thermal activation. The molecular weight of the receptor, determined by SDS-PAGE, is similar to that from normal cells (approximately 92,000). Only in the severely affected patient was the proportion of activated receptor remaining in the cytosol of thermally activated intact cells reduced. At saturating concentrations of dexamethasone, nuclear binding appears normal in cells from both the severe and the asymptomatic forms of this condition, providing an explanation for the apparently complete compensation of the target tissue resistance to glucocorticoids by the high plasma cortisol levels. The clinical manifestations of the disorder (hypertension, hypokalemia) can be corrected with high doses of dexamethasone (3mg/day).
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PMID:Cortisol resistance in man. 301 86

The case is described of a 61-year-old male who presented with hypertension and Cushing's syndrome which resolved on excision of a unilateral adrenal mass. Histology of the tumour revealed a benign phaeochromocytoma which immunostained for corticotrophin-releasing factor (CRF-41) but not for ACTH. Preoperative plasma concentrations of immunoreactive CRF-41 were increased, and gradients for both CRF-41 and ACTH were demonstrated across the tumour. Post-operatively, CRF-41 was undetectable in plasma. The tumour contained high concentrations of immunoreactive CRF-41 which co-eluted with synthetic human CRF-41 on reversed-phase high-performance liquid chromatography. Tumour CRF-41 stimulated the release of ACTH in a dose-dependent manner from isolated rat anterior pituitary cells. We conclude that this tumour secreted CRF-41 and ACTH and had the capacity to produce ACTH-dependent Cushing's syndrome directly by secreting ACTH and indirectly by secreting CRF-41 to stimulate ACTH secretion from the anterior pituitary.
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PMID:A phaeochromocytoma presenting with Cushing's syndrome associated with increased concentrations of circulating corticotrophin-releasing factor. 303 46

The adrenal glucocorticoid secretions undoubtedly perform necessary physiologic functions in maintaining normal blood pressure when secreted at their ordinary rate or in response to short term stress. Sustained glucocorticoid excess, in Cushing's syndrome or during prolonged therapy with synthetic steroids, leads to arterial hypertension and arteriosclerotic cardiovascular disease through a plentiful variety of pathogenetic mechanisms. Naturally occurring Cushing's syndrome should be readily detected, treated, and reversed unless due to metastatic malignancy. The benefits of glucocorticoid treatment as immunosuppressive and anti-inflammatory therapy are genuine, but the price includes cardiovascular disease. It is likely that the past role of glucocorticoid therapy will be supplanted by new strategies that minimize steroid dose, employ nonsteroid regimens, and perhaps lead to the development of specific steroids that possess only beneficial actions without potential for cardiovascular toxicity.
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PMID:Glucocorticoid excess syndromes causing hypertension. 306 45

A young male patient demonstrated unusual features of Cushing's syndrome, atrial myxomas and freckled skin pigmentation. At 4.5 years of age he presented with intermittent swelling of his face and abdomen associated with weight gain and mild hypertension. A left atrial myxoma, suspected from routine physical examination, was surgically removed at 6.1 years of age. The initial mild symptoms clinically thought to be due to Cushing's syndrome, persisted intermittently without any consistent biochemical abnormality. At 10 years of age height velocity decreased and at 12 years early osteoporosis was observed radiologically. Repeated dexamethasone tests revealed a paradoxical increase in cortisol and corticotrophin from normal basal levels. Further investigation showed a cyclical pattern of hypercortisolism. The removal of a pituitary microadenoma failed to correct the features of Cushing's syndrome or prevent intermittent hypercortisolism. At 15.3 years a second left atrial myxoma was removed. This was followed by bilateral adrenalectomy. Histologically the features were consistent with primary pigmented nodular adrenocortical disease. This is the first patient described with cyclical Cushing's syndrome as part of this unusual complex of disorders.
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PMID:Cyclical Cushing's syndrome presenting as short stature in a boy with recurrent atrial myxomas and freckled skin pigmentation. 316 6

Pregnancy in patients with Cushing's syndrome is rare. It is associated with a high fetal loss, increased frequency of preterm labour and excessive maternal morbidity. We describe a patient who became pregnant while investigations for hypertension were being done. Cushing's disease was diagnosed and the patient had transsphenoidal pituitary surgery at 22 weeks gestation. To our knowledge this is the first time this operation has been done during pregnancy for this condition. Cushing's disease was controlled, but because of worsening hypertension, she had a caesarean section at 30 weeks gestation. Subsequently her blood pressure fell and her hydrocortisone replacement therapy is being withdrawn. Her daughter is now thriving after initial problems with pneumothoraces.
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PMID:Successful management of Cushing's disease during pregnancy by transsphenoidal adenectomy. 332 96

The circadian blood pressure rhythm was compared in patients with Cushing's syndrome, essential hypertension, and primary aldosteronism. In patients with essential hypertension or primary aldosteronism, a clear nocturnal fall in systolic and diastolic blood pressure and heart rate was observed. This fall was seen in untreated subjects as well as in patients receiving combined treatment with a calcium antagonist, diuretic, converting enzyme inhibitor, alpha-blocker and beta-blocker, or sympatholytic drug. In these groups, there was a positive correlation between heart rate and systolic or diastolic blood pressure. On the other hand, in patients with Cushing's syndrome, there was no nocturnal fall in blood pressure but in some patients a rise was observed. In all patients there was a nocturnal fall in heart rate. Thus, there was no significant correlation between heart rate and blood pressure in these patients. Exogenous glucocorticoid eliminated the normal nocturnal fall of blood pressure in patients with chronic glomerulonephritis or systemic lupus erythematosus. These results suggest that the changed circadian blood pressure pattern in patients with Cushing's syndrome is not due to antihypertensive treatment or to the mineralocorticoid excess accompanying this disease, but it is attributable to excess glucocorticoid or the associated disturbance in the adrenocorticotropic hormone-glucocorticoid system (or both). This conclusion also implies that the normal circadian rhythm of blood pressure may be regulated at least in part by the adrenocorticotropic hormone-glucocorticoid system.
Hypertension 1988 Jul
PMID:Altered circadian blood pressure rhythm in patients with Cushing's syndrome. 339 72


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