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)

Measurement of plasma aldosterone concentrations (PAC) at 8 a.m. and after 4 h in the upright posture can further assist in identifying the adrenal pathologic lesion in patients with primary aldosteronism. Increases in PAC are associated with hyperplasia, and decreases with adenoma. Normal increases in response to upright posture are observed in patients with essential hypertension with normal or reduced renin concentration.
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PMID:Effect of posture on the plasma concentrations of aldosterone in hypertension and primary hyperaldosteronism. 22 May 44

1. Amiloride (40 mg/day) was given to nineteen patients with primary hyperaldosteronism. There were significant falls in systolic and diastolic blood pressure, in total exchangeable sodium and in serum sodium and bicarbonate, while total exchangeable potassium, total body potassium, serum potassium, chloride and urea, plasma renin, angiotensin II and aldosterone all increased significantly. Amiloride was effective in reducing the blood pressure in patients with and without adrenocortical adenoma. No carry-over effect was seen on withdrawing amiloride. Similar changes were associated with amiloride treatment in five patients with essential hypertension; hyperkalaemia was not observed. 2. Only negligible side effects were encountered in the entire series of 24 patients.
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PMID:Amiloride in the treatment of primary hyperaldosteronism and essential hypertension. 35 30

1. The determination of aldosterone-18-glucuronide (pH 1-labile aldosterone) was complemented by concomitant measurements of free urinary aldosterone and tetrahydroaldosterone in 307 patients, most of whom were hypertensive. In 38 cases (12.3%) the normal, aldosterone-18-glucuronide concentration was clinically misleading, but increased free aldosterone and/or tetrahydroaldosterone values suggested the presence of hyperaldosteronism, which in many of these cases was confirmed by elevated excretion of the possible major aldosterone precursor 18-hydroxycorticosterone (18-OH-B). 2. Of 224 patients with essential hypertension and normal or low plasma renin activity 18 had an elevated free aldosterone and/or tetrahydroaldosterone excretion without increased aldosterone-18-glucuronide. These cases may represent early or pre-symptomatic forms of primary hyperaldosteronism. In other cases, particularly when tetrahydroaldosterone was increased alone, abnormalities of aldosterone metabolism were suspected. 3. In two out of 15 patients with primary hyperaldosteronism, aldosterone-18-glucuronide values were frequently found to be normal, although elevations were noted in other variables. However, no relation to the morphological abnormality (adenoma versus hyperplasia) was seen.
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PMID:Dissociation in the excretion of different aldosterone metabolites and unmetabolized ('free') aldosterone in hypertension. 51 48

To determine the effect of aldosterone antagonist on renal prostaglandin E synthesis, the rate of urinary excretion of immunoreactive prostaglandin E was measured radioimmunologically before and during the oral administration of an aldosterone antagonist, spironolactone, in 5 patients with essential hypertension, 3 with primary aldosteronism and 2 with postoperative primary aldosteronism. Spironolactone was administered at an oral dose of 25 mg 4 times daily for about 1 week. In the control state, the rates of urinary prostaglandin E excretion ranged from 151 ng/day to 4,527 ng/day in essential hypertension. The rates were not augmented in primary aldosteronism but decreased after the removal of an aldosterone producing adenoma. No obvious relationship was observed between plasma aldosterone concentration and the rate of urinary prostaglandin E excretion. On the first day of spironolactone administration, the excretion rates of urinary prostaglandin E were markedly increased independently of basal plasma aldosterone level in all cases except one case of essential hypertension. Urinary prostaglandin E excretion was increased with the concominant increase of urinary Na/K ratio in essential hypertension and primary aldosteronism. After the second day, the augmented urinary prostaglandin E excretion was decreased and the changes of urinary prostaglandin E excretion varied from case to case. These results suggest that synthesis of renal prostaglandin E is not mainly regulated by aldosterone in essential hypertension and primary aldosteronism.
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PMID:Effect of spironolactone on urinary excretion of immunoreactive prostaglandin E in essential hypertension and primary aldosteronism. 66 29

Adrenal scintigraphy was performed on 23 patients with low renin essential hypertension (LREH). After baseline scintigraphy was shown not to be helpful, 13 of these 23 patients underwent dexamethasone suppression adrenal scintigraphy. Four adrenal imaging patterns were observed: unilateral imaging with adenoma; bilateral early or late imaging with hyperplasia; no uptake with normal adrenals. These imaging patterns were shown to be predictive of the individual patient's response to spironolactone administration of functional adrenal cortical abnormalities in LREH supplies direct evidence for the hypothesis that LREH has an adrenal mineralocorticoid etiology.
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PMID:Adrenal scintigraphy in low renin essential hypertension. 70 82

In a Zurich outpatient clinic in 1975 hypertension was found in 10.4% of 8228 patients (3657 females and 4571 males). Essential (primary) hypertension was found in 92.9% of all hypertensives. Among secondary forms of hypertension (7.1%) renal hypertension was the most common (5.8%) with 4.9% for hypertension of renal parenchymatous origin, .8% renovascular hypertension, and .1% hypertension associated with unilateral hydronephrosis. In 2 patients (.2%) the underlying disease was primary aldosteronism and in 5 (.6%) coarctation of the aorta. In 4 females (.5%) hypertension was caused by oral contraceptives. Patients with essential hypertension had higher body weight than those with normal blood pressure. These differences were statistically significant in young and middle-aged patients. The percentage of primary hypertension was significantly high. In only 18 (2.1%) of 854 hypertensives was a curable form of high blood pressure found (hypertension caused by renal artery stenosis, hydronephrosis, aldosterone-producing adenoma of the adrenal gland, and oral contraceptives). The very low percentage of curable forms of high blood pressure should be kept in mind when deciding on expensive procedures in a search for secondary forms of high blood pressure.
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PMID:[Primary and secondary hypertension in polyclinical patients]. 85 17

Serial measurements of urinary sodium excretion, sodium space, plasma volume, and plasma renin concentration were made during the development of hypertension in patients who were exposed to an excess of endogenous or exogenous mineralocorticoid activity. Five patients with primary aldosteronism due to adenoma were followed during spironolactone treatment, for 35-55 days after the drug had been stopped, and finally, after surgery. Blood pressure rose continuously after stopping spironolactone. Sodium balance, however, showed an initial phase of sodium gain, followed by a phase of gradual sodium loss. Sodium space and exchangeable sodium rose by 5.0 +/- 0.48 liters/1.73 m2 of body surface area (BSA) (P less than 0.005) and by 865 +/- 97 mEq/1.73 m2 BSA (P less than 0.005), respectively; the values were maximal after 10-15 days, declined afterward, but remained higher than during spironolactone treatment. Plasma and blood volumes rose by 624 +/- 90 ml/1.73 m2 BSA (P less than 0.005) and by 327 +/- 74 ml/1.73 m2 BSA (P less than 0.01), respectively; they were maximal after 20-25 days, and then returned to their initial values. Exchangeable sodium, during the phase of sodium loss, was inversely correlated with the rise in blood pressure (P less than 0.01). Renin fell during the phase of sodium gain, and remained low afterwards. Blood pressure and sodium space declined after surgery, but plasma volume showed no change. The postsurgery values of these parameters were not significantly different from those measured during spironolactone treatment. Two subjects with adrenocortical insufficiency, who were followed for 45-60 days during treatment with dexamethasone and 9alpha-fluorocortisol acetate, also showed a transient rise in sodium space and plasma volume. The results suggest a redistribution of body fluids during development of hypertension. They also suggest that the tendency of body fluid volumes to return to normal is pressure-dependent. The long-term effects of mineralocorticoid excess on the interrelations between pressure, volume, and renin bear some resemblance to the pattern observed in patients with established essential hypertension, i.e., pressure remains elevated despite a decrease of volume, and renin is "inappropriately" suppressed in relation to the sodium and volume status.
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PMID:Volume-pressure relationships during development of mineralocorticoid hypertension in man. 85 75

Amiloride (40 mg/day) was given to nineteen patients with primary hyperaldosteronism. There were significant falls in systolic and diastolic blood pressure, in total exchangeable sodium, and in serum sodium sodium and bicarbonate; while total exchangeable potassium, total body potassium, serum potassium, chloride and urea, and plasma renin, angiotensin II and aldosterone all increased significantly. Amiloride was effective in reducing blood pressure in patients with and without adrenocortical adenoma. No carry-over effect was seen on withdrawing amiloride. Similar changes were associated with amiloride treatment in five patients with essential hypertension; hyperkalaemia was not observed. Only negligible side-effects were encountered in the entire series of twenty-four patients.
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PMID:Amiloride in the treatment of primary hyperaldosteronism and essential hypertension. 89 Sep 99

We used 131I-19-iodocholesterol as an adrenal-imaging agent in 27 hypertensive patients who had biochemical evidence of abnormalities in the renin-angiotensin-aldosterone system. In 10 of 12 patients in whom the biochemical findings suggested the presence of an aldosterone-producing adenoma the adrenal uptake was asymmetric. The adenoma was subsequently confirmed in all eight patients in this group who underwent operation. In contrast, the adrenal uptake was asymmetric in only one of 13 patients with biochemical evidence of iodopathic hyperaldosteronism or low-renin essential hypertension. Two patients with adrenal carcinoma causing primary aldosteronism did not concentrate the isotope in their tumors. When metabolic studies suggest an aldosterone-producing adenoma, adrenal imaging with 131I-19-iodocholesterol may locate the tumor before operation.
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PMID:Location of aldosterone-producing adenomas with 131I-19-iodocholesterol. 124 8

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38


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