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)

The authors studied 8 patients (4 males and 4 females) with Cushing's syndrome due to ectopic ACTH secretion. Chronological age ranged from 15 to 45 years and duration of the disease ranged from 3 to 48 months. All patients presented typical signs of Cushing's syndrome, blood hypertension, and four of them had hyperpigmentation of the skin. Five patients had fasting hyperglycemia and all patients but one had serum hypokalemia (serum K = 2.2 to 3.9mEq/l). The circadian rhythm of cortisol was absent in all patients and basal cortisol levels were elevated in all patients but one. Basal ACTH levels evaluated in 7 patients were elevated in 6 (29 to 1050 pg/ml-MRC). One patient presented normal depression of urinary 17-OH after two days of dexamethasone and normal increase of urinary 17-OH and serum 11-dexycortisol after methyrapone. Four patients had carcinoid tumor (3 thymic and 1 bronchial), two had pancreatic islets cell tumors, one had bilateral pheochromocytoma and medular carcinoma of the thyroid, and one had oat cell carcinoma of the lung and medular carcinoma of the thyroid. Thoracic X-rays identified the ectopic ACTH secretion tumor in four cases, all confirmed by CT scan. Abdominal CT showed a difuse enlargement of the adrenals in seven cases and bilateral nodules in one case (pheochromocytomas). Six patients died within 3 years of the diagnosis. The authors concluded that clinical and hormonal findings could mislead the findings of ACTH ectopic secretion and Cushing's disease, and suggest that thoracic X-rays and CT scans of the skull, thorax, and abdome should be done in all cases of Cushing's syndrome.
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PMID:[Cushing syndrome due to ectopic ACTH secretion]. 255 51

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

Measurements of blood plasma ACTH, hydrocortisone, STH, somatostatin, insulin, glucagon levels and plasma renin activity in 70 patients with borderline hypertension (BAH) and in 20 normal male subjects have revealed increased ACTH, hydrocortisone, and somatostatin levels, elevated plasma renin activity, and reduced STH and insulin levels in the patients. A possible role of the pressor hormone system activation in the pathogenesis of borderline arterial hypertension and in BAH transformation into essential hypertension is discussed.
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PMID:[Hormonal disorders in borderline arterial hypertension]. 257 58

New findings obtained from basic research works using novel techniques in protein analyses, molecular biology and applied chemistry have broadened the knowledge of pathophysiological and biochemical aspects in various endocrine disorders, which often led to establishment of new diagnostic and/or therapeutic approaches. Among many interesting recent topics in endocrinology, the following themes were chosen in this symposium entitled "basic and clinical aspects of certain endocrine and metabolic diseases": ACTH secretion in adrenocortical disorders by Dr. Ohgo, pregnancy and PRL secretion by Dr. Miyakawa, auto-antigens in autoimmune thyroid diseases by Dr. Kotani, new active D3 derivatives and their clinical application in bone disorders by Dr. Okamoto, pathophysiological roles of atrial natriuretic peptide (ANP) in hypertension by Dr. Kida, and recent trends in diagnosis and treatment of diabetes mellitus by Dr. Sugiyama. We believed that each lecture covered and clarified new developments and their clinical implications, which should satisfy and stimulate your interest.
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PMID:[New basic and clinical aspects of endocrine and metabolic diseases]. 258 51

A 40 year-old man was admitted to our hospital for detailed examination of hypokalemia (2.7 mEq/l). His blood pressure was normal. Metabolic alkalosis, ACTH dependent hyperaldosteronism (18 ng/dl) and over-response to synthetic ACTH were observed. Plasma renin activity, on the other hand, was within the normal range (1.7 ng/ml/hr). Serum potassium was normalized to 4.1 mEq/l and the responsiveness of the renin-angiotensin-aldosterone system was recovered after the administration of dexamethasone. These results led us to suggest that this case might be normotensive glucocorticoid-suppressible hyperaldosteronism. The etiology which was not associated with hypertension and low plasma renin activity has not been clarified but may be related to the shortness of duration of this disease. Our case was also afflicted with mild hypercortisolemia and excessive excretion of urinary 17-hydroxycorticosteroid and 17-ketosteroid which was suppressed by the administration of dexamethasone (2 mg/day). These findings may be related to hypersensitivity of the fascicular zone of the adrenal gland to ACTH.
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PMID:Normotensive glucocorticoid-suppressible hyperaldosteronism in adult. 263 10

Corticosteroid-dependent hypertension can be cured by surgical removal of steroid-producing adrenocortical adenomas or, in case of other etiopathologic factors, specific drug therapy may be introduced for preventing irreversible complications of the hypertension process. In most cases, corticosteroid-dependent hypertension fails to manifest itself with clearcut endocrine symptoms. Therefore, an endocrine evaluation is strongly recommended in all patients with hypertension who are susceptible to hypokalaemia and whose blood pressure is poorly controlled with conventional antihypertensive drugs. The increased blood pressure in corticosteroid-producing adrenocortical adenomas may be attributed not only to the main glucocorticoid, cortisol, and the main mineralocorticoid, aldosterone, but also to the actions of weak mineralocorticoids which may be occasionally predominant. Adrenocortical adenomas including incidentalomas produce in different quantities at least 6 corticosteroids which play direct or indirect roles in hypertension. These adenomas are lacking autonomous hormone secretion and they respond to different regulatory impacts (i.e. stress and, by analogy, CRF or ACTH administration) with markedly-increased hormone secretion. Consequently, hypertension and hypokalaemia develop, often in the absence of other endocrine symptoms. The weak mineralocorticoids may not entirely account for the hypertension, although they may be useful indicators or may serve as precursors for the generation of more potent hypertensinogen steroids and steroid metabolites. This is patently indicated by the disappearance of hypertension, hypokalemia and mineralocorticoid-excess induced suppression of the renin-angiotensin system after the surgical removal of adrenocortical adenomas which produce only weakly-hypertensinogen corticosteroids.
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PMID:[The hypertensive role of corticosteroids in the light of adenoma of the adrenal cortex]. 266 40

The adrenal glands produce glucocorticoids (approximately 25 mg cortisol/day), mineralocorticoids (approximately 100 micrograms aldosterone/day) and androgens (e.g. dehydroepiandrosterone = DHEA approximately 10 mg/day) in their cortex and catecholamines in their medulla. Excessive cortisol production leads to Cushing's syndrome. In approximately 2/3 of the cases this is due to ACTH oversecretion most often from a pituitary adenoma and can be cured by removal of this adenoma. Cushing's syndrome caused by an adrenal adenoma, carcinoma or bilateral nodular adrenal hyperplasia is treated by adrenal surgery. Nelson's syndrome consists of hyperpigmentation of the skin and an often aggressively growing pituitary adenoma which secretes excessive amounts of ACTH. Treatment is surgical. Conn's syndrome (primary hyperaldosteronism) is due to aldosterone hypersecretion most often from an adrenal adenoma (therapy: unilateral adrenalectomy), more seldom from bilaterally hyperplastic adrenals (therapy: spironolactone). Excessive adrenal androgen secretion is found in the adrenogenital syndrome in which defective cortisol biosynthesis leads to ACTH oversecretion and ACTH-stimulated overproduction of cortisol precursors, some of which are androgens. Treatment consists of glucocorticoids which suppress the ACTH oversecretion. Pheochromocytomas produce excessive amounts of catecholamines and cause hypertension which can be persistent as well as episodic. Therapy consists of adrenalectomy. Malignant tumors of the adrenals have a poor prognosis. Incidentally found adrenal masses ("incidentalomas") are observed at regular intervals if they are small and should be surgically removed if they have a tendency to grow or are large (greater than or equal to 5 cm phi).
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PMID:[Normal and pathologic endocrinology of the adrenal glands]. 268 Oct 84

One must consider the 17-DOS as a biosynthetic pathway with multiple regulatory factors. ACTH is its dominant regulator but in the absence of ACTH and in conditions where plasma renin activity is increased, this biosynthetic pathway maintains its sensitivity to exogenous ACTH. Suppression of the renin system delays the general recovery of aldosterone after the removal of an aldosterone producing adenoma but not of the 17-DOS: a pattern also showed after the removal of a DOC-producing adenoma. In addition to the possible role of the renin system there remain inexplicable situations in its regulation that cannot be explained by ACTH and renin. Our studies suggest that a non-renin, non-ACTH factor may influence the basal production of these steroids, and by its reduction, permits deviation of steroid substrate to cortisol production. This sequence may be operative in the "stress syndrome". Finally, one of the more interesting phenomenonologic patients who has been observed is a young male who has the biochemical findings and clinical signs of DOC excess with hypertension, hyperplasia, suppression of aldosterone and the RAS, and normal cortisol levels. All the 17-DOS are elevated and both adrenal veins have high concentrations. He represents excessive stimulation of this pathway by putative 17-deoxy regulator excess. The renin system is suppressed and ACTH levels are normal. Treatment with suppressive doses of glucocorticoid hormones diminishes the elevated 17-DOS and cortisol and ameliorates blood pressure. In summary, there seems to occur in clinical disorders and contrived experimental settings, suggestions that a non-renin, non-ACTH factor can regulate the 17-DOS, absence can explain some of the unusual conditions described (Fig. 1). The 17-DOS, while a vestigial pathway, may still cause disease, and provide clues to central organization of the adreno-cortical response to injury, stress, and disease.
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PMID:The regulation of the 17-deoxy steroids in man. 275 48

In previous studies, administration of adrenocorticotrophin (ACTH; 0.5 mg i.m. b.d. for 5 days) to normal subjects produced an adrenally dependent rise in blood pressure (BP) of some 20 mmHg, accompanied by an increase in cardiac output and an increase in plasma volume. The BP and metabolic effects of ACTH (increase in plasma glucose, fall in eosinophils, increase in body weight and urine sodium retention) were reproduced by infusion of the glucocorticoid (GC) cortisol at rates (6-8 mg/h) which reproduced the blood concentrations of the steroid achieved with ACTH administration. Oral administration (hydrocortisone 200 mg daily) produced similar changes qualitatively, although the cortisol concentrations and increase in pressure (12 mmHg) were less. Plasma volume was increased. To determine the role of urine sodium retention and plasma volume expansion in the hypertension, we gave synthetic steroids to six normal subjects for 5 days, at doses which were calculated to be similar for GC activity, but which had little or no mineralocorticoid (MC) activity. Prednisolone (40 mg/day), methylprednisolone (32 mg/day), triamcinolone (40 mg/day) and dexamethasone (8 mg/day) all produced equivalent GC effects (increase in plasma glucose, increase in total white cell count, fall in direct eosinophil count). There were no MC effects with any of the steroids. Body weight did not increase and urinary sodium excretion increased rather than decreased. Plasma volume (125I human serum albumin) and haematocrit were unchanged. BP rose with all four steroids: systolic BP rose by 13 mmHg with prednisolone, by 9 mmHg with methylprednisolone, by 10 mmHg with triamcinolone, and by 6 mmHg with dexamethasone. Diastolic BP increases were 8, 11, 8 and 7 mmHg, respectively. Thus, neither MC activity nor an increase in plasma volume is essential for steroids to induce an increase in blood pressure. Therefore, screening of synthetic GCs to minimize MC activity will not prevent hypertensive complications.
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PMID:The hypertensive effect of synthetic glucocorticoids in man: role of sodium and volume. 276 Apr 58

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


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