133I-cholesterol scanning of five patients with primary hyperaldosteronism due to adrenocortical adenoma, gave correct lateralization and localization in three, while in two cases lateralization was not definitively determined. In two patients with phaeochromocytoma unilateral localization was clear-cut in the scan. In two patients with hormone-producing adrenal carcinoma the adrenals were localized poorly or not at all on both sides, because of the size of the tumours and suppression of the healthy contralateral adrenal by the autonomous hormone production. In case of retroperitoneal tumour with destruction of the adrenal the scan demonstrated a hyperplastic but healthy adrenal on the other side. Because 133I-cholesterol scanning exposes the steroid-producing gonads to high radioactivity, the method should only be used for diagnosing which side a unilateral adrenal tumour is on. It should not be used to complement a diagnosis of bilateral adrenal disease achieved by other means.
The saralasin test was performed in 68 hypertensives. A clear-cut dependence of the test results on initial plasma-renin concentration and particular sodium balance was demonstrated. Because of this dependence the saralasin test should be performed only under constant conditions. A mild stimulation of the renin-angiotension system by salt restriction to a mean sodium excretion of 50 mmol daily and 80 mg furosemide by mouth 12 hours before the test seems best. In this way essential and renovascular hypertension could be distinguished with considerable reliability (P less than 0.001). Among patients with essential hypertension one could clearly separate those with high plasma-renin concentration from those with a normal or low one. Among patients with renovascular hypertension those with haemodynamically significant renal artery stenosis could with high probability be distinguished from those with non-effective stenosis. A positive saralasin test without testing the function of the normal contralateral kidney does not provide an indication for operation.
The regulation of aldosterone secretion by sodium restricted and enriched diet was assessed in 21 patients with primary aldosteronism for differentiation between unilateral aldosterone-producing adenoma and adrenocortical hyperplasia causing autonomous aldosterone hypersecretion. Compared to 10 patients with idiopathic adrenocortical hyperplasia, urinary aldosterone excretion after 4 days of sodium restricted diet was significantly higher in 11 patients with established adenoma (41.3 +/- 16.3 micrograms/24 h vs 19.8 +/- 8.5 micrograms/24 h; P less than 0.005). After six days of sodium loading these differences became even more obvious (35.3 +/- 14.0 micrograms/24 h vs 12.7 +/- 3.7 micrograms/24 h; P less than 0.0005). Sodium excretion did not influence aldosterone secretion in the adenoma group. In patients with hyperplasia both parameters showed a negative correlation (r = -0.522; P less than 0.001). Differentiation without overlap between both patient groups was achieved by comparison of the quotient of aldosterone excretion and serum potassium level during sodium enriched diet.
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