Twenty-four year spironolactone therapy in an aged patient with aldosterone-producing adenoma

1992 ◽  
Vol 126 (2) ◽  
pp. 186-190 ◽  
Author(s):  
R Takeda ◽  
T Yamazaki ◽  
Y Ito ◽  
H Koshida ◽  
T Morise ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
Plasma Renin ◽  
Term Treatment ◽  
Aged Patient ◽  
Steroid Biosynthesis ◽  
Long Term Treatment ◽  
Hypokalemic Alkalosis ◽  
Aldosterone Producing Adenoma ◽  
Subsequent Withdrawal

A case of primary aldosteronism treated with spironolactone therapy has been followed up for 24 years. This is probably the longest case of spironolactone therapy for primary aldosteronism that has ever been reported. Long-term treatment with spironolactone controlled the hypertension and prevented hypokalemic alkalosis in this patient, without any deleterious effects on steroid biosynthesis. Based on data obtained during dose reduction and subsequent withdrawal of spironolactone, it is suggested that the suppressed plasma renin activity associated with adenoma-induced aldosteronism develops prior to hypokalemia and hypertension.

scholarly journals Successful Long-term Treatment with Once-daily Injection of Low-dose Octreotide in an Aged Patient with Insulinoma

2005 ◽  
Vol 52 (5) ◽  
pp. 629-634 ◽  
Author(s):  
Takuyuki KATABAMI ◽  
Hiroyuki KATO ◽  
Naoko SHIRAI ◽  
Satoru NAITO ◽  
Nobuhiko SAITO
Keyword(s):  
Low Dose ◽  
Term Treatment ◽  
Daily Injection ◽  
Aged Patient ◽  
Once Daily ◽  
Long Term Treatment

Long-term treatment of idiopathic hyperaldosteronim using trilostane

1986 ◽  
Vol 113 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Kaoru Nomura ◽  
Hiroshi Demura ◽  
Nobuo Horiba ◽  
Kazuo Shizume
Keyword(s):  
Antihypertensive Drugs ◽  
Competitive Inhibitor ◽  
Inhibitory Effect ◽  
Term Treatment ◽  
Continuous Treatment ◽  
Steroid Biosynthesis ◽  
Long Term Treatment ◽  
Idiopathic Hyperaldosteronism ◽  
Pre Treatment

Abstract. Three patients with idiopathic hyperaldosteronism were continuously treated with trilostane, a competitive inhibitor of adrenal 3β-hydroxysteroid dehydrogenase (3β-HSDH) (3 to 4⅔ years). Trilostane, in conjunction with antihypertensive drugs, effectively decreased plasma aldosterone levels and improved hyperaldosteronism symptoms without undesirable side effects. Trilostane continued to be effective even when treatment was continuous. Rapid ACTH testing (iv bolus of 0.25 mg α1–24 ACTH) was done on the day without trilostane after long-term treatment, and plasma levels of aldosterone and cortisol were compared to those obtained during a pre-treatment period. Results suggest that the inhibitory effect of trilostane on steroid biosynthesis rapidly disappears following discontinuance of trilostane administration even after long-term treatment, and that continuous treatment causes no significant or irreversible change in steroid biosynthesis. These results suggest that trilostane is a safe, feasible therapeutic agent for long-term treatment of idiopathic hyperaldosteronism.

Increase of Total Body Potassium and Decrease of Exchangeable Sodium after Long-Term Treatment with a β-Receptor-Blocking Agent (Prindolol) in Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 551s-554s
Author(s):  
H. M. Brecht ◽  
E. Werner ◽  
W. Schoeppe
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Term Treatment ◽  
Renin Activity ◽  
Exchangeable Sodium ◽  
Total Body Potassium ◽  
Long Term Treatment ◽  
Total Body

1. The effect of long-term treatment with prindolol on blood pressure, total body potassium (Kt), exchangeable sodium (Nae) and plasma renin activity was investigated in twelve patients with essential hypertension. 2. Systolic and diastolic pressures were significantly reduced from 164/112 to 127/90 mmHg under basal conditions. 3. Before treatment Na. in patients with essential hypertension was significantly higher than in normotensive individuals. After an average of 16 weeks on prindolol Nae in patients with essential hypertension was significantly decreased, despite an average increase in body weight of 2 kg in the patients. 4. In contrast to the decrease in Nae, Kt was found to be significantly increased after long-term treatment with prindolol. Kt values of patients before and after prindolol, however, did not differ significantly from the corresponding sex- and age-dependent normal values. 5. Plasma renin activity was slightly diminished under basal and orthostatic conditions; the stimulatory effect of orthostasis was not abolished but reduced by prindolol. 6. It is suggested that the changes in sodium balance contribute to the anti-hypertensive effect of prindolol in patients with essential hypertension.

scholarly journals Response to Effectiveness of Adrenalectomy and Aldosterone Antagonists for Long-Term Treatment of Primary Aldosteronism

Hypertension ◽  
2013 ◽  
Vol 62 (4) ◽  
Author(s):  
Gian Paolo Rossi ◽  
Maurizio Cesari ◽  
Cesare Cuspidi ◽  
Giuseppe Maiolino ◽  
Maria Verena Cicala ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
Term Treatment ◽  
Aldosterone Antagonists ◽  
Long Term Treatment

Long-Term Treatment of Hypertension in Man by an Orally Active Angiotensin-Converting Enzyme Inhibitor

1978 ◽  
Vol 55 (s4) ◽  
pp. 293s-295s ◽  
Author(s):  
H. R. Brunner ◽  
H. Gavras ◽  
G. A. Turini ◽  
B. Waeber ◽  
P. Chappuis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Term Treatment ◽  
Hypertensive Patients ◽  
Long Term Treatment ◽  
Treatment Of Hypertension ◽  
Term Administration ◽  
Orally Active

1. Captopril or SQ 14 225, administered orally twice a day, reduced the blood pressure of hypertensive patients whatever their clinical diagnosis and even when their plasma renin activity was ‘normal’ or low. 2. Long-term administration of captopril, either alone or together with diuretics, provides a powerful new tool with which to treat ambulatory hypertensive patients. 3. The renin system may play an important role in maintaining blood pressure in a majority of hypertensive patients.

scholarly journals Long-term re-evaluation of primary aldosteronism after medical treatment reveals high proportion of normal mineralocorticoid secretion

2013 ◽  
Vol 168 (4) ◽  
pp. 525-532 ◽  
Author(s):  
Barbara Lucatello ◽  
Andrea Benso ◽  
Isabella Tabaro ◽  
Elena Capello ◽  
Mirko Parasiliti Caprino ◽  
...  
Keyword(s):  
Medical Treatment ◽  
Primary Aldosteronism ◽  
Cross Sectional Study ◽  
Term Treatment ◽  
Duration Of Treatment ◽  
Cross Sectional ◽  
Long Term Treatment ◽  
Suppression Test ◽  
Mineralocorticoid Antagonists

ObjectiveIn most cases of primary aldosteronism (PA), an adrenal aldosterone-secreting tumor cannot be reasonably proven, so these patients undergo medical treatment. Controversial data exist about the evolution of PA after medical therapy: long-term treatment with mineralocorticoid antagonists has been reported to normalize aldosterone levels but other authors failed to find remission of mineralocorticoid hypersecretion. Thus, we planned to retest aldosterone secretion in patients with medically treated PA diagnosed at least 3 years before.DesignRetrospective, cross-sectional study.MethodsThe same workup for PA as at diagnosis (basal aldosterone to renin activity ratio (ARR) and aldosterone suppression test) was performed after stopping interfering drugs and low-salt diet, in 34 subjects with PA diagnosed between 3 and 15 years earlier, by case finding from subgroups of hypertensive patients at high risk for PA. Criteria for persistence of PA were the same as at diagnosis (ARR (pg/ml per ng per ml per h) >400, aldosterone >150 pg/ml basally, and >100 pg/ml after saline infusion) or less restrictive.ResultsPA was not confirmed in 26 (76%) of the patients and also not in 20 (59%) using the least restrictive criteria suggested by international guidelines. Unconfirmed PA was positively associated with female sex, higher potassium levels, longer duration of hypertension, and follow-up, but not with adrenal mass, aldosterone levels at diagnosis, and treatment with mineralocorticoid antagonists.ConclusionsThis study suggests that mineralocorticoid hyperfunction in patients with PA after medical treatment may decline spontaneously. Higher potassium concentration and duration of treatment seem to increase the probability of this event.

Renin-angiotensin mechanisms in oral contraceptive hypertension in conscious rats

1985 ◽  
Vol 248 (5) ◽  
pp. H695-H699 ◽  
Author(s):  
W. L. Fowler ◽  
J. A. Johnson ◽  
K. D. Kurz ◽  
C. G. Payne
Keyword(s):  
Oral Contraceptive ◽  
Arterial Pressure ◽  
Jugular Vein ◽  
Plasma Renin ◽  
Term Treatment ◽  
Ang Ii ◽  
Renin Substrate ◽  
Arterial Blood ◽  
Long Term Treatment

Rats were placed on powdered chow containing either no additives (controls), mestranol (a synthetic estrogen), norethynodrel (a synthetic progestin), or both mestranol and norethynodrel. After 6 mo on these diets, catheters were placed in the carotid artery and jugular vein of each rat. An arterial blood sample was obtained for plasma renin activity (PRA), plasma renin concentration (PRC), and plasma renin substrate concentration (PRS). Mean arterial pressure was measured in each rat. The angiotensin II (ANG II) antagonist, [Sar1-Ile8]ANG II, was infused intravenously for 30 min while blood pressure was recorded. Rats treated with mestranol and/or norethynodrel had PRA and PRC values that were not different from the control rats; however, mestranol-treated rats and rats treated with mestranol plus norethynodrel had PRS values that were substantially (P less than 0.01) higher than the controls. Arterial pressures in rats treated with mestranol and with mestranol plus norethynodrel were significantly (P less than 0.01) elevated when compared with the controls and with the rats treated with norethynodrel alone. Infusion of the ANG II antagonist failed to alter arterial pressure in any of the groups of rats. These results indicated that, in the steroid combination found in the oral contraceptive Enovid, it is the estrogenic component that results in hypertension in this rat model. Also this study found no evidence that ANG II plays a role in maintaining the elevated arterial pressure following long-term treatment with mestranol in rats.

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