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

Primary aldosteronism is a potentially curable cause of hypertension, especially when caused by an adrenal adenoma. Aldosteronomas because of their small size often elude techniques to locate them. This case illustrates the advantages, disadvantages and complications of noninvasive techniques used for their diagnosis. A patient with hypertension and hypokalemia underwent an adrenal venous effluent sampling for measurement of aldosterone concentrations. This procedure was complicated by an injury to the right adrenal gland. Subsequently, it was difficult to control the patient's hypertension and hypokalemia with medical therapy alone. A re-assessment years after his initial diagnosis included a CT scan, which now visualized a left adrenal tumor. The functional status of this tumor and lack of function of the previously injured right adrenal gland were demonstrated by NP-59 scintigraphy. This information modified the surgical intervention (adenectomy rather than total adrenalectomy) and the residual left sided adrenal tissue prevented adrenocortical insufficiency. A year later the patient remains euadrenal.
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PMID:Simultaneous scintigraphic depiction of aldosteronoma and adrenal infarction. 896 60

We measured Na(+)-H+ exchange as the amiloride-inhibited fraction of H+ efflux from red blood cells into a sodium-containing medium (pHo 7.95 to 8.05) at pHi values of 6.05 to 6.15, 6.35 to 6.45, 6.95 to 7.05, and 7.35 to 7.45 in 12 drug-free patients with primary aldosteronism before and after excision of histologically proven aldosterone-producing adrenal adenoma, 12 drug-free essential hypertensive patients, and 12 healthy control subjects. Red blood cell Na(+)-H+ exchange was increased in patients with primary aldosteronism similarly to the mean exchanger velocity in essential hypertensive patients compared with values in healthy subjects (334 +/- 25 and 310 +/- 29 versus 139 +/- 21 mumol H+/L cells per minute, respectively; P < .001 and .01). The kinetic parameters of Na(+)-H+ exchange returned to normal on day 2 after removal of the aldosterone-producing mass. Km for [Na+]o was not affected by aldosterone, whereas Km for [H+]i was decreased in patients with primary aldosteronism. The kinetic characteristics did not differ in essential hypertensive patients and control subjects. Protein kinase C inhibition in vitro by calphostin C (60 nmol/L) increased Km for [H+]i and caused up to a 65% suppression of Na(+)-H+ exchange (pHi 6.05 to 6.15). while diminishing Km for [Na+]o in red blood cells of patients with primary aldosteronism. The calmodulin antagonist W-13 (60 mmol/L) decreased exchanger velocity and increased Km for both H+ and Na+. We conclude that aldosterone stimulates red blood cell Na(+)-H+ exchange by a nongenomic mechanism that augments the exchanger affinity to Na+ and H+. In primary aldosteronism, protein kinase C and calmodulin seem to have synergistic stimulatory effects on red blood cell Na(+)-H+ exchange, and both increase the affinity of the exchanger to H+, while their effect on Na+ binding is opposite.
Hypertension 1997 Feb
PMID:Increased Na(+)-H+ exchange in red blood cells of patients with primary aldosteronism. 904 Apr 43

Primary hyperaldosteronism (adrenal adenoma and idiopathic hyperplasia) is a disorder with hypertension, hypokalemia, elevated serum aldosterone and suppressed plasma renin activity. Hyperplasia is managed medically whereas adenomas are treated surgically. Selective adrenal venous catheterization and aldosterone measurement is a useful tool in making the distinction in 95% of cases. We report a case of bilateral idiopathic hyperplasia of the adrenal glands adequately treated with medications for 6 years followed by worsening. Selective catheterization was consistent with a right sided adenoma. Surgical removal of the right adrenal gland alleviated her symptoms. Pathological examination showed focal nodular hyperplasia. We propose that in the course of the disease the focal hyperplastic nodule became autonomous and behaved like an adenoma. Monitoring of patients with adrenal hyperplasia for recurrence of symptoms is prudent as surgery is beneficial in patients who develop an autonomous nodule.
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PMID:Idiopathic hyperplasia of the adrenal gland behaving like an aldosterone producing adenoma. 907 69

A case of primary hyperaldosteronism and cardiomegaly due to a unilateral adrenal adenoma in a newborn is presented. Some peculiarities, most likely in relation to the onset of the disease during fetal life were evident: plasma cortisol was slightly increased before surgery, plasma renin activity was elevated 9 months after surgery and mineralcorticoid receptors remained suppressed 4 months after surgery. Unilateral adrenalectomy reversed both hypertension and cardiomegaly. We speculate that cardiomegaly was related to both hyperaldosteronism and hypertension and that individual factors are involved in the pathogenesis of cardiomegaly in hyperaldosteronism.
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PMID:Hypertensive cardiomegaly caused by an aldosterone-secreting adenoma in a newborn. 912 89

A 40-year-old male, with a past history of hypertension but receiving no medical treatment, was referred. He manifested malignant hypertension (190/130 mmHg; Keith-Wagener III), renal dysfunction (serum creatinine, 3.8 mg/dl), and elevated plasma aldosterone (450 pg/ml) and active renin concentration (ARC, 104 pg/ml). His blood pressure was controlled with multiple antihypertensive agents and ARC thus decreased (4.3 pg/ml), but aldosterone remained elevated. Abdominal magnetic resonance imaging (MRI) revealed a right adrenal adenoma, and aldosterone-producing adenoma was confirmed by adrenal venous sampling. Primary aldosteronism very rarely develops to malignant hypertension, and even in that case ARC is suppressed. Therefore this is a rare case of primary aldosteronism complicated with malignant hypertension and high ARC.
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PMID:Malignant hypertension in a patient with primary aldosteronism with elevated active renin concentration. 937 22

Excess 11-deoxycorticosterone (DOC) production, mostly due to an enzyme defect 11-beta-hydroxylase, is a rare cause of secondary hypertension. Even rarer are those forms due to an adrenal adenoma or to a bilateral hyperplasia. In this paper we report the case of 23-year-old woman with excess DOC production, presenting with arterial hypertension and oedema, whom we first observed in 1961. Complete clinical remission, persisting more than 30 years later, was obtained by monolateral adrenalectomy. The literature reports of DOC-induced hypertension due to adrenal adenoma or hyperplasia are reviewed and the possible pathogenetic mechanisms are discussed.
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PMID:Hypertension and oedema caused by cortexone hyperproduction and cured by monolateral adrenalectomy. Case report. 947 73

A less-than-normal decline in nocturnal blood pressure (BP) has been associated with excessive hypertensive complications. This is concerning because secondary hypertension is often associated with this so-called nondipper BP profile. A nondipping pattern is more frequently found in the presence of pheochromocytoma, Cushing's syndrome, and sleep apnea syndrome, but the prevalence is unclear in patients with primary hyperaldosteronism. We therefore studied ambulatory BP profiles in 16 hypertensive patients with primary hyperaldosteronism and an equal number of essential hypertensive subjects. The awake-sleep BP difference of the hyperaldosteronism patients was similar to that of essential hypertensives (15/14 +/- 3/2 versus 14/9 +/- 3/2 mm Hg, P=NS). The prevalence of dippers and nondippers (according to two distinct criteria) in the two groups was similar. Repeat ambulatory BP monitoring in 12 subjects with primary hyperaldosteronism after specific intervention (3 after surgical removal of an adrenal adenoma and 9 after commencement and titration of spironolactone therapy) showed highly significant reductions in office BP (22/10 +/- 6/4 mm Hg, P<.05) and awake and sleep BP. However, the extent of nocturnal BP decline was unchanged between the two studies (17/16 +/- 3/3 versus 16/12 +/- 2/2 mm Hg, P=NS). There was no correlation between the awake-sleep difference and serum or urinary aldosterone levels or the aldosterone-to-renin ratio. In this study, we did not detect any differences in the awake-sleep differences between a group of hypertensives with primary hyperaldosteronism and a control group of essential hypertensives.
Hypertension 1998 Mar
PMID:Circadian blood pressure variation in hypertensive patients with primary hyperaldosteronism. 949 70

We describe a case of Cushing's syndrome complicating pregnancy presented with acute heart failure, hypertension and glucose intolerance. A left adrenal adenoma was removed at 24 weeks of gestation. The pregnancy was ended with an emergency lower-segment Caesarean section at 31 weeks of gestation because of severe pre-eclampsia and HELLP syndrome. The case is reported not only because of its rarity but also to induce the discussion of surgical treatment during pregnancy.
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PMID:Cushing's syndrome in pregnancy secondary to adrenal adenoma. A case report and literature review. 956 49

A 58 year-old man with end-stage renal disease who had received a cadaveric renal transplant presented with persistent hypertension and hypokalemia. Allograft renal artery stenosis, rejection, and cyclosporine effects were excluded. Hypokalemia persisted despite potassium supplementation and antihypertensive medications with hyperkalemic effects. The biochemical findings of primary hyperaldosteronism with a normal adrenal anatomy imaged by magnetic resonance imaging (MRI) necessitated adrenal vein sampling to lateralize a left adrenal adenoma. His hypokalemia was cured by the removal of the adenoma, and his blood pressure (BP) control was easily achieved with a less complex regimen of antihypertensives. We suggest that the concomitant existence of resistant hypokalemia and posttransplantation hypertension, especially in the cyclosporine era, should stimulate a search for hyperaldosteronism; once transplant renal artery stenosis has been excluded, the patient should be investigated for primary hyperaldosteronism. When imaging studies fail to show adrenal pathology, adrenal vein sampling will likely do so.
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PMID:Primary hyperaldosteronism causing posttransplantation hypertension: localization by adrenal vein sampling. 959 Jan 97

Reduced adrenocortical (aldosterone and cortisol) and adrenomedullary (adrenaline) secretory mass after unilateral adrenalectomy for aldosterone-producing adenoma has been associated with long-term hypotension (more than 2 years) in some studies. In these patients, cortisol and aldosterone levels are low, whereas plasma renin activity is high. Other studies suggest that normotension and normal plasma renin activity and serum aldosterone and cortisol levels are achieved in 60% to 87% of the patients without evidence of decreased adrenal mass, whereas the remaining patients may continue to have hypertension. We report a unique case in which unilateral adrenalectomy for adrenal adenoma was followed by severe hyperkalemia, marked volume depletion and undetectable plasma renin activity, and serum aldosterone, suggesting marked, chronic suppression of the renin-aldosterone axis. One year later, a gradual return to normokalemia, normotension, and normal plasma renin activity and aldosterone levels was achieved, indicating resolution of the suppression of the renin-aldosterone axis. Patients undergoing unilateral adrenalectomy for aldosteronoma should be followed up closely after unilateral adrenalectomy of adrenal adenoma to avoid life-threatening hyperkalemia and severe intravascular volume depletion.
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PMID:Reversible suppression of the renin-aldosterone axis after unilateral adrenalectomy for adrenal adenoma. 966 38


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