Showing papers on "Spironolactone published in 1970"
172 citations
TL;DR: The inability to find an acute coronary occlusion in a patient who died with manifestations of acute cardiac infarction must not be necessarily ascribed to an oversight on the part of the pathologist.
Abstract: The fact that the adrenal cortex responds with increased secretion upon exposure to any type of stressor directed attention to its possible participation in the pathogenesis of diseases other than those caused by a simple deficiency or excess of corticoid production (Addison's disease, Cushing's disease, adrenocortical tumors). It became evident that the pathogenicity of corticoids depends largely upon conditioning factors which can modify their effects and thereby cause them to induce cardiovascular disease. Thus, an excess of mineralocorticoids can produce hypertension and hypokalemia, with or without hydrops, depending upon controllable conditioning factors. Both these reactions can be suppressed by antimineralocorticoids such as spironolactone. Combined pretreatment with gluco- and mineralocorticoids elicits a special predisposition for the development of cardiac necroses during stress or after excessive lipid ingestion. The induction of these necroses is enhanced by sodium (as is that of mineralocorticoid hypertension) and inhibited by potassium, magnesium or potassium-sparing agents such as amiloride, triamterene or spironolactone. Unlike the common myocardial infarcts, as described in textbooks, those elicited in animals after pretreatment with corticoids and sodium salts are unaccompanied by vascular occlusion. Hence, the inability to find an acute coronary occlusion in a patient who died with manifestations of acute cardiac infarction must not be necessarily ascribed to an oversight on the part of the pathologist. It remains to be seen to what extent the prophylactic measures effective in our experimental disease models will also be useful in clinical medicine.
147 citations
TL;DR: A spironolactone (Aldactone*) was administered for three weeks to a group of ten patients with primary aldosteronism and 80 other hypertensive patients who were categorized on the basis of their plasma renin activity (PRA) results into three other groups (Groups II—IV), those with a hyporesponsive PRA, a normal P RA, or an elevated PRA.
134 citations
TL;DR: A simple clinical method using the urinary Na/K ratio as a guide to spironolactone dosage is outlined, finding that it is a safe and effective means of inducing sustained uncomplicated diuresis in all these patients.
Abstract: Increased aldosterone levels with consequent or diuretic-potentiated electrolyte abnormalities are an important consideration when patients with cirrhosis and ascites undergo diuresis. A simple clinical method using the urinary Na/K ratio as a guide to spironolactone dosage is outlined. Patients with a ratio greater than 1 responded well to 100 mg. of spironolactone a day; those when it was one or less responded well to 200 to 1,000 mg. a day.Administration of spironolactone alone (11 patients) or as the main diuretic (three patients) was a safe and effective means of inducing sustained uncomplicated diuresis in all these patients.
65 citations
TL;DR: It is suggested that diabetic patients may have an abnormality of electrolyte homeostasis which predisposes them to hyperkalemia during administration of potassium-retaining diuretics during short-term administration of amiloride.
Abstract: We have observed two cases of hyperkalemia during short-term administration of the potassium-retaining diuretic, amiloride, to four diabetic patients. The response of serum potassium to intravenous glucose was also significantly modified by amiloride supporting a close association between carbohydrate and potassium metabolism. The hyperkalemia was not clearly associated with impaired renal function or excessive potassium retention and developed over a short time period at doses which are usually safe. There is evidence suggesting that both amiloride and triamterene share this toxic effect. Spironolactone should be considered suspect as a contributory agent since it has been co-administered in several fatal cases including one in this series. Attention is drawn to reciprocal decreases in serum sodium which occurred simultaneously with the development of hyperkalemia in our patients. The electrocardiogram was unreliable in assessing the clinical significance of the hyperkalemia. We suggest that diabetic patients may have an abnormality of electrolyte homeostasis which predisposes them to hyperkalemia during administration of potassium-retaining diuretics.
37 citations
TL;DR: Administration of spironolactone in standard dosage to nine women with mild renal disease resulted in amenorrhea in six and marked menstrual irregularity in a seventh, and cessation of therapy resulted in normal menstrual periods within two months in every patient.
Abstract: Administration of spironolactone in standard dosage to nine women with mild renal disease resulted in amenorrhea in six and marked menstrual irregularity in a seventh. Discontinuation of therapy resulted in normal menstrual periods within two months in every patient. The drug action causing this side effect may be responsible for previously reported gynecomastia, but this action is unknown. The high incidence of amenorrhea in this group may be due to increased drug susceptibility or decreased drug elimination in patients with kidney disease.
33 citations
TL;DR: In an early stage after removal of an aldosteroneproducing tumor plasma renin activity was markedly increased and exaggeratedly responded to restriction of sodium with a rise of serum potassium and augmented natriuresis between the 2nd and 5th postoperative weeks.
Abstract: The effects of preoperative treatment with spironolactone at high doses (300–400 mg/day) for more than 2 months on plasma renin activity and on its response to sodium restriction were studied in 4 patients with primary aldosteronism. The results were compared with those obtained in 2 patients with primary aldosteronism receiving no preoperative spironolactone therapy. All patients treated with spironolactone showed a significant elevation of plasma renin activity, which was further increased with a 4-day period of sodium restriction. In an early stage after removal of an aldosteroneproducing tumor plasma renin activity was markedly increased. In all patients receiving preoperative spironolactone therapy plasma renin activity exaggeratedly responded to restriction of sodium with a rise of serum potassium and augmented natriuresis between the 2nd and 5th postoperative weeks. On the other hand, in 2 patients without preoperative spironolactone therapy plasma renin activity remained at a subnormal le...
23 citations
TL;DR: Findings are consistent with the view that spironolactone influences its own biotransformation and the steroid is also a substrate of the hepatic drug-metabolizing enzymes which are induced by spironlactone itself.
15 citations
6 citations
TL;DR: The assay of urinary 17-ketosteroids and17-ketogenic steroids appears to be unaffected by the presence of spironolactone and can be used for the investigation of adrenal disease in patients taking the drug.
Abstract: A misleading, gross elevation of plasma cortisol levels was found in patients treated with spironolactone when a popular fluorometric technique for cortisol assay was employed. It was demonstrated that spironolactone interferes with the assay because its fluorescence emission spectrum is identical to that of cortisol. The assay of urinary 17-ketosteroids and 17-ketogenic steroids appears to be unaffected by the presence of spironolactone and can be used for the investigation of adrenal disease in patients taking the drug.
5 citations
01 Feb 1970
TL;DR: The administration of the two drugs together or in close succession appears to be hazardous, probably due to synergistic effects.
Abstract: The effect of adding amiloride or spironolactone to an antihypertensive regimen which consisted of hydroehlorothiazide and guanethidine was studied. Amiloride and spironolactone produced very similar effects including significant urinary sodium loss, decrease in serum bicarbonate, potassium retention and increase in serum potassium. In two groups of hypokalemic patients, neither spironolactone nor amiloride caused further lowering of blood pressure. Temporary moderate hyperkalaemia occurred in one patient when amiloride was substituted for spironolactone. The administration of the two drugs together or in close succession appears to be hazardous, probably due to synergistic effects.