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

A case of male pseudohermaphroditism aged 48 years with systemic hypertension and hypokalaemic alkalosis is described. Results of metabolic studies point to a 17alpha-hydroxylase deficiency demonstrated by low cortisol (0-56 mg/24 h), high corticosterone (270 mg/24 h) and 11-deoxycorticosterone (5 mg/24 h) secretion rates. Adrenocorticotrophin and gonadotrophin levels were markedly raised but plasma androstenedione (3 ng/dl), testosterone (17 ng/dl), oestrone (3 ng/dl) and oestradiol(1-8 ng/dl) were all low. Plasma aldosterone levels and secretion rates in urine were low and were surprisingly unaffected by dexamethasone therapy although low renin levels rose with a marked return of the erect posture effect. Therapeutic levels of dexamethasone were, however, followed by incipient renal failure.
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PMID:Male pseudohermaphroditism with hypertension due to a 17alpha-hydroxylation deficiency. 17 42

1. A double-blind comparison of the effect of tienylic acid and hydrochlorothiazide on blood pressure was made in patients with moderate hypertension. 2. The antihypertensive effect of 500 mg tienylic acid was comparable to 100 mg hydrochlorothiazide; mean decrease in supine blood pressure after 6 weeks treatment was 20/12 mmHg with tienylic acid and 17/9 mmHg with hydrochlorothiazide. Onset of antihypertensive action was within 1 week and was associated with significant weight loss. 3. Tienylic acid caused a marked decrease in serum uric acid to a mean of 0.18 mmol/1 (n = 11, P less than 0.001), this persisted through the treatment period and returned to placebo values 1 week after treatment ceased. Some patients had uric acid crystaluria and some had post-treatment uric acid levels higher than on placebo. 4. Tineylic acid and hydrochlorothiazide caused mild hypokalemia and alkalosis with proportional decrease in plasma chloride. 5. Blood urea and serum creatinine rose with both drugs and there was an unimportant decline in plasma sodium. 6. Tienylic acid is an effective antihypertensive agent with powerful uricosuric action and appears relatively free of side effects. Further studies are necessary to determine optimal dosage regimes and long term safety.
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PMID:A double-blind comparison of the effects of hydrochlorothiazide and tienylic acid (a diuretic with uricosuric properties) in hypertension. 35 19

In two patients with severe hypertension and moderately severe renal insufficiency, metolazone and furosemide were used in combination with propranolol, methyldopa, and hydralazine to augment control of blood pressure. This combination of diuretics also was used in five patients with refractory congestive heart failure. The patients developed severe electrolyte disturbances with a general pattern of hyponatremia. disproportionate hypochloremia, alkalosis, and phyokalemia. These abnormalities were transient in the patients with severe hypertension and moderately severe renal insufficiency. Effective long-term control of blood pressure was obtained. In the patients with heart failure, edema persisted. Due to the severity of the electrolyte derangements, metolazone and furosemide were discontinued. Because of potential untoward effects, this combination of diuretics should be used with caution.
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PMID:Severe electrolyte disturbances associated with metolazone and furosemide. 63 11

A 2-year-old girl presenting with features of both Bartter's syndrome and renal tubular acidosis was investigated. Hypokalemia, increased plasma renin activity in the absence of hypertension, insensitivity to the pressor effects of angiotensin and a histological picture of juxtaglomerular hyperplasia were characteristic of Bartter's syndrome, but an unusual finding was the presence of metabolic acidosis instead of alkalosis. Functional studies revealed a proximal tubular defect in sodium and bicarbonate reabsorption and a distal defect in sodium reabsorption, urinary acidification and concentrating mechanism. Indomethacin administration was followed by an excellent clinical response and improvement of most functional abnormalities. The defect in distal sodium reabsorption was, however, not corrected by prostaglandin inhibition, and could represent the primary event leading to potassium wasting and secondary hypersecretion of prostaglandins.
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PMID:Bartter's syndrome presenting with features resembling renal tubular acidosis. Improvement of renal tubular defects by indomethacin. 65 58

This is a case report of a 43 years old phaenotypic female (karyotype 46 XY) with congenital adrenal hyperplasia and male pseudohermaphroditism presenting with severe hypertension and hypokalaemic alkalosis. Evaluation of the steroid biosynthesis of the adrenals as well as of the intraabdominal testes demonstrated a severe degree of 17-alpha-hydroxylase deficiency in this patient. This defect was associated by a complete lack of deoxycortisol and cortisol as well as of testicular testosterone synthesis, and by an overproduction of DOC and corticosterone. Sruvival of the patient in spite of severe cortisol deficiency was due to the glucocorticoid activity of corticosterone. This compound and DOC account also -- due to their mineralocorticoid properties -- for the hypertensive state of this male pseudohermaphrodite.
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PMID:Hypergonadotrophic male pseudohermaphroditism due to complete 17-alpha-hyroxylase deficiency. 91 71

The development of modern pharmacologic diuretic agents has revolutionized the therapy of arterial hypertension. The diuretics currently available are easily administered orally, are effective in the presence of alkalosis or acidosis, are non-toxic and have a low incidence of side effects which are readily circumvented or treated. Loop diuretics such as furosemide have the capacity to be effective in patients with diminished renal function or clinical situations that have a powerful stimulus to sodium retention. In clinical circumstances when renal potassium loss is to be prevented such as in patients receiving digitalis, the addition of a potassium-sparing diuretic to either a thiazide or furosemide will achieve the clinical goal of providing an effective diuresis while inhibiting potassium excretion. The mechanism of antihypertensive activity of the diuretic agents appears to be the reduction of extracellular fluid volumes and plasma volumes. Hence, the clinical dictum that to be effective as an antihypertensive agent, diuretics should be administered in diuretic doses. Besides being the cornerstone of initial antihypertensive therapy, diuretics also play an important role in antihypertensive therapy of patients with moderate to severe hypertension who are receiving potent antihypertensive drugs of the vasodilator or sympatholytic class of compounds. Indeed, one of the most important steps in the successful therapy of these patients receiving multiple drugs, is the re-assessment of the diuretic agent. The sodium retention and consequent fluid volume expansion associated with the administration of these potent antihypertensive agents may often cause these patients to develop apparent drug resistance since the thiazide diuretics are not potent enough to counteract the powerful stimulus to sodium retention caused by these antihypertensive agents. The re-evaluation of the diuretic agent at this point will usually necessitate the substitution of furosemide for thiazide or the doubling of the dose of the present loop diuretic. A working knowledge of the physiology of urine formation and the sites of action of currently available diuretic agents will enable the clinician to tailor the diuretic agent to the clinical circumstances of an individual patient and allow the clinician to rationally select a diuretic for the treatment of arterial hypertension.
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PMID:The rational use of diuretics in the treatment of arterial hypertension. 105 79

In a group of hypertensive patients it has been shown that moderate sodium chloride restriction has a hypotensive effect that is similar to that produced by thiazide diuretics. Blood pressure changed in relation to body weight in individual patients, and appeared to correlate with their sodium balance. The more a patient was depleted of sodium, the lower was the blood pressure. The serum potassium level fell with the use of thiazide diuretics, but in this group of patients there was little change in total body potassium content. The fall in serum potassium level appeared to relate to a shift into the cells due to the accompanying alkalosis. Potassium supplementation appeared to have had little effect and was unnecessary for most patients who were given diuretics for hypertension. Amiloride corrected the alkalosis and restored the serum potassium level to normal.
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PMID:Sodium restriction and thiazide diuretics in the treatment of hypertension. 115 72

The most common ectopic production of a pituitary hormone is the one of ACTH leading to Cushing's syndrome. Ectopic ACTH-hypersecretion is the cause of Cushing's syndrome in 10-15% of all cases. The ACTH-secreting tumours are often oat-cell carcinomas of the lung, less frequently pancreatic cancers, hypernephromas, or C-cell carcinomas of the thyroid. Some of these tumours may be benign or semi-benign as the rare carcinoid tumours and cause great problems in the differential diagnosis of ACTH-dependent hypercortisolism. Out of 173 of our patients with Cushing's syndrome observed in the last 12 years 21 were caused by ectopic ACTH-production. Of these 21 patients 13 have a small cell carcinoma of the lung. The ectopic ACTH-syndrome often has typical clinical features caused by the levels of ACTH and cortisol leading to hypocalcemic alkalosis with muscle weakness and wasting, carbohydrate intolerance, and hypertension with oedema. The survival time in many of these patients is not long enough to allow them to develop typical signs of Cushing's syndrome though they are often highly pigmented. These patients are easily diagnosed. However, patients with small tumours which do not cause very elevated ACTH-levels and who have the more typical clinical signs of full-blown Cushing's syndrome are difficult to recognize. For the differential diagnosis of ACTH-dependent Cushing's syndrome the corticotropin-releasing hormone (CRH) stimulation test and dexamethasone suppression test with high doses are helpful. In special cases the venous sampling procedure for ACTH-measurements is necessary, also CT or NMR is helpful. Ectopic CRH-production is a rare cause of ACTH-dependent Cushing's syndrome. Patients with ectopic CRH-production and consecutive ACTH-hypersecretion from the pituitary have not been studied extensively. There are especially no well documented results of the use of the CRH-stimulation test in vivo in this group of patients with Cushing's syndrome. On the other hand, in the documented cases, not only CRH-, but also ACTH-production was found in the tumours. So far, this rare cause of ACTH-dependent Cushing's syndrome has to be excluded or confirmed by the measurement of endogenous CRH-levels. But until now we have not been able to detect one single case of ectopic CRH-production using a sensitive homologous CRH-radioimmunoassay over a period of more than 8 years in which we have seen nearly 120 newly diagnosed patients with ACTH-dependent Cushing's syndrome. Only in the plasma and tumour tissue of two patients of other groups have we found high CRH-levels.
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PMID:Ectopic production of ACTH and corticotropin-releasing hormone (CRH). 132 73

The Authors report a case of left adrenal mass incidentally discovered by upper abdominal echogram in a 40 year old man. Physical examination showed no signs of hypercortisolism and plasma cortisol and ACTH levels were in the normal range as well as urinary free cortisol. After adrenalectomy, 4 and 8 month follow-up was performed, without clinical, hormonal and TC evolution. Thirteen months later the patient was referred to our department for widespread oedema, hypertension, hypokalemia and alkalosis. These symptoms were associated with dramatically elevated concentrations of plasmatic and free urinary cortisol. TC showed a large mass in the same adrenal region and diffuse hepatic metastases. In spite of mitotane and ketoconazole therapy the patient died few weeks later.
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PMID:[Unusual endocrine behavior in adrenal carcinoma. A case study]. 181 20

Clinical findings in a female patient aged 49 years suggested Conn's syndrome (hypokalemia, alkalosis, hypertension) developing in the course of renal failure. During treatment biochemically confirmed porphyria manifested itself, and the patient died several days later. On autopsy and in histological examinations malignant nephrosclerosis of vascular origin, nodular hyperplasia of the adrenal cortex and lesions of other organs were found. The largest content of porphyrins was shown in the adrenals, and then in the liver, pituitary gland, thyroid and pancreas. A study of other family members confirmed the genetic background of porphyria. Probably, this hereditary latent hepatic porphyria manifested itself after a breakdown of the feedback mechanisms between the kidneys and the endocrine glands, the adrenals in particular.
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PMID:Hereditary porphyria manifesting itself during renal failure in a 49-year-old woman. 184 98


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