Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate whether changes in the plasma concentration of aldosterone (PA) following the administration of captopril, an inhibitor of angiotensin-converting enzyme, will establish the diagnosis of primary aldosteronism we have used this test in 9 healthy subjects and in 22 patients with various forms of hypertension, including 5 patients with primary aldosteronism due to idiopathic adrenal hyperplasia (n = 4) or aldosterone-producing adenoma (n = 1). The response of PA to captopril (25 mg orally) was investigated on an outpatient basis, following a rest period of 120 minutes in the supine position. In healthy subjects PA decreased from a mean basal value of 11.5 +/- 5.9 ng/dl to less than 6.4 ng/dl (4.9 +/- 1.4 ng/dl [p less than 0.01]). Similarly, captopril induced a fall in PA concentration to less than 6.4 ng/dl in patients with essential hypertension, with renal artery stenosis or with an afunctional kidney. Post-captopril concentrations of plasma aldosterone were about twice the normal level in 3 of 4 patients with idiopathic adrenal hyperplasia and about four-fold raised above normal in the patient with an aldosterone-producing adenoma. In spite of a false-negative result in one patient with idiopathic adrenal hyperplasia, the administration of captopril appears to be of use in recognizing patients with primary aldosteronism on an outpatient basis.
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PMID:[Detection of primary aldosteronism using the captopril test]. 331 69

Twenty-eight patients with resistant hypertension were found to have primary aldosteronism; 25 had solitary adenoma and 3 had adrenal hyperplasia. All were severely hypertensive despite receiving three or more antihypertensive agents, including conventional doses of diuretics, sympatholytics, and vasodilators. Hypervolemia (24 patients) or normovolemia (2 patients) despite severe diastolic hypertension was the hallmark in 26 patients. Adequate salt and water depletion alone with spironolactone (200 mg/day) and hydrochlorothiazide (50-100 ng/day) reduced arterial pressure in all. Twenty-two patients had surgical removal of a solitary adenoma. Over 1 to 2 years of follow-up, 13 were normotensive without medication, and six required hydrochlorothiazide and three hydrochlorothiazide plus a beta-blocker to normalize blood pressure. Blood pressure response to surgery had no relation to either duration or severity of hypertension. Six patients (three with hyperplasia, three with adenoma) have continued diuretic therapy and are normokalemic and normotensive. These results indicate that primary aldosteronism can be associated with sever and drug-resistant hypertension, that maintained hypervolemia is the reason for resistance to therapy, that sustained volume depletion is the most important therapeutic goal for these patients, and that cure can be achieved despite prolonged and severe hypertension.
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PMID:Clinical implications of primary aldosteronism with resistant hypertension. 334 59

The long-term results of surgical and specific drug therapy were compared in a group of 57 patients with primary aldosteronism (PA) (46 with aldosterone-producing adenoma (APA), 11 with idiopathic hyperaldosteronism (IHA) and bilateral adrenal hyperplasia). Unilateral adrenalectomy completely normalized blood pressure (BP) in 77.1% of surgically treated APA, evidently improving hypertension in remaining 22.9%. No recurrence of the adenoma in the remaining adrenal was seen in any of the surgical APA cases. In 19 of the non-surgical patients (11 with APA, 8 with IHA) monotherapy with spironolactone reduced blood pressure in 73%, though total BP normalization was an exception. The treatment normalized hypokalemia, low total exchangeable potassium, tendency to hypernatremia, and high total exchangeable sodium. Surgical as well as conservative therapy increased to normal or above-normal levels plasma renin activity suppressed prior to treatment. Pre-operatively high urine and plasma aldosterone levels normalized in all adrenalectomized patients, but remained above the normal range during spironolactone therapy in spite of a small decline in its absolute values. The disturbances of maximum renal concentrating capacity due to impaired nephron responsiveness to sufficiently high endogenous vasopressin concentrations were completely eliminated after kaliopenic nephropathy had been repaired. The other renal functions remained within normal values. Echocardiographically diagnosed left ventricular hypertrophy was seen less often than in the other types of arterial hypertension, tending to regress after APA management. Our longitudinal study (2-16 years) showed primary aldosteronism as a well curable, albeit rare, cause of hypertension. As regards BP and laboratory tests normalization, better results were achieved in surgical APA cases than in patients treated with spironolactone. Older age, longer history of hypertension and more frequent incidence of obesity, nephrosclerosis and pyelonephritis may be responsible for hypertension persisting after surgical treatment.
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PMID:Long-term results of surgical and conservative treatment of patients with primary aldosteronism. 345 May 33

131I-19-iodocholesterol adrenal scans were obtained in seven patients with Cushing's syndrome. Characteristic imaging patterns were seen in three patients with bilateral adrenal hyperplasia with symmetrical uptake of the isotope. Two patients with adrenocortical adenoma and one patient with a well-differentiated adrenocortical carcinoma showed intense activity in one adrenal gland and absent activity in the contralateral gland. In one patient with adrenal nodular hyperplasia asymmetrical uptake was found with increased activity in the right adrenal gland where a larger adenomatous nodule was found at histologic examination. Adrenal imaging with radioactive cholesterol is a useful noninvasive technique for the diagnosis and treatment of Cushing's syndrome.
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PMID:Scanning of the adrenals in Cushing's syndrome. 360 68

Of 15 patients with primary aldosteronism, 7 had idiopathic adrenal hyperplasia (IHA) and 8 had aldosterone-producing adenoma (APA). In order to determine any renal problems involved in the treatment, the renal clearance of these patients was analyzed and the results compared with those obtained from 12 patients with essential hypertension. With water diuresis or under antidiuresis status, levels of urine volume, Cosm and CH2O in patients with APA were greater (p less than 0.05-p less than 0.001) than those of patients with essential hypertension, while the fractional tubular sodium delivery of the former patients was lower than that of the latter patients (p less than 0.001 or less than 0.05). A similar tendency was observed in clearance studies in patients with IHA, although to a lesser extent. Adrenal surgery for patients with APA normalized these values, but administration of trilostane (3 beta-hydrosteroid dehydrogenase inhibitor) to patients with IHA failed to improve these values. These results indicate that impaired urinary concentrating ability as well as reduced urinary diluting capability is a common feature of primary aldosteronism. Such impaired renal function was improved only in patients with APA after adrenal surgery.
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PMID:Evidence for a defect in urinary concentrating ability in primary aldosteronism and its reversal by adrenal surgery. 367 60

In 14 hypertensive patients aldosterone/cortisol ratio was always lower in a peripheral vein or low IVC than in either adrenal vein. In four patients with a right-sided aldosterone-producing adenoma (APA), the aldosterone/cortisol ratio in peripheral vein was always higher than in the left adrenal vein. If only the left adrenal vein is cannulated, right-sided APA can still be diagnosed with certainty. In three patients with glucocorticoid-suppressible hyperaldosteronism, urinary excretion of both 18-oxocortisol and 18-hydroxycortisol was elevated. In four patients with APA excretion of 18-oxocortisol was elevated. In two of three patients with bilateral adrenal hyperplasia (BH), excretion of both steroids was normal. 75Se-selenomethylcholesterol scanning correctly lateralized five APA, but falsely lateralized a patient with BH. Results with CT scans were often misleading.
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PMID:Distinguishing aldosterone-producing adenoma from other forms of hyperaldosteronism and lateralizing the tumour pre-operatively. 373 37

The effect of unilateral adrenalectomy in primary aldosteronism was analyzed in 38 patients with unilateral adenoma, 12 cases with idiopathic bilateral hyperplasia and 1 patient suffering from an aldosterone-producing carcinoma. Responses to surgery differed markedly. In all 38 adenoma cases plasma aldosterone dropped to normal levels and remained within normal range during a mean follow-up period of 75 +/- 12 months. 23 (61%) of these patients became normotensive without medication and thus could be classified as definitely cured. 34% (13 patients) improved (normotensive under medical treatment) and only 2 cases (5%) remained hypertensive despite sufficient medical treatment. In the hyperplasia group, however, the effect of adrenalectomy was disappointing. None of these subjects showed a long-lasting normalization of aldosterone secretion. A temporary remission for no more than 3-4 months was achieved in only 3 patients. In a fourth case with macronodular hyperplasia, primary aldosteronism relapsed after a 6-year period of normal blood pressure and aldosterone values. Therefore, 6 years after adrenalectomy no hyperplasia patient was definitely cured in contrast to 61% of the adenoma cases. The problems in the management of hypertension in adrenal hyperplasia are furthermore documented by a poorer blood pressure control despite antihypertensive medication and a high rate of vascular complications. During the follow-up, 3 of 12 hyperplasia patients experienced a cerebrovascular event and 1 a myocardial infarction.
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PMID:Adrenalectomy in primary aldosteronism: a long-term follow-up study. 390 26

In 72 patients with primary aldosteronism who were classified on the basis of adrenal pathology after adrenalectomy, analysis of routine clinical and laboratory data, of supine and upright plasma aldosterone, and of plasma renin activity were of limited value in differentiating patients with aldosterone-producing adenoma(s) (APA, n = 59) from those with idiopathic adrenal hyperplasia (IAH, n = 13). Normokalemic aldosteronism occurred in 6 patients (3 APA, 3 IAH). A correct classification of the adrenal lesion(s) was obtained in 80% of the patients by computed tomography and only in 69% by adrenal scintiscan. In addition, adrenal scintiscan was hampered by a relatively high rate of incorrect results independent of whether dexamethasone was used or not. Small adenomas (less than 1 cm) and more often adrenal hyperplasia may escape visualization by computed tomography.
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PMID:Primary aldosteronism: diagnosis and noninvasive lateralization procedures. 390 32

Cushing's syndrome continues to tax the most discerning clinician. I review pituitary-dependent adrenal hyperplasia (Cushing's disease), including recent experiences with Cushing's disease at Duke University, Durham, NC, and relate these observations to the current ideas as to pathophysiology, etiology, and management of Cushing's disease. Transsphenoidal microsurgery (TPS) performed by an experienced neurosurgeon offers selective removal of corticotropin (ACTH)-secreting adenoma, immediately cures the hypercortisolism, preserves pituitary function, and is associated with minimal morbidity. Postoperative hypoadrenalism appears to be the best marker of surgical cure. Transsphenoidal surgery has revolutionized our thoughts as to etiology and treatment of Cushing's disease, yet failures with TPS and uncertainty of recurrences leave room for radiotherapy, adrenalectomy, and adjunctive drug therapy in the management of this entity.
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PMID:Cushing's disease. A review. 392 62

Serum 18-hydroxycorticosterone, aldosterone, and potassium were measured under basal conditions in 34 patients with documented primary aldosteronism, 10 patients with essential hypertension, and 9 normal subjects. The results revealed that 22 of 23 patients with aldosterone-producing adenomas had 18-hydroxycorticosterone levels greater than 100 ng/dl, and all 9 patients with idiopathic adrenal hyperplasia had plasma levels less than 100 ng/dl. Two patients with unusual macromicronodular hyperplasia of the adrenal glands had levels greater than 100 ng/dl. We found a significant relationship between serum potassium and the ratio of 18-hydroxycorticosterone to aldosterone in patients with idiopathic adrenal hyperplasia, but not in those with an aldosterone-producing adenoma. We conclude that measurement of serum 18-hydroxycorticosterone is a useful predictor of the etiology of primary aldosteronism.
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PMID:The prediction of anatomical morphology of primary aldosteronism using serum 18-hydroxycorticosterone levels. 396 94


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