CONN'S SYNDROME CAUSED BY ADRENOCORTICAL HYPERPLASIA. PATHOGENESIS OF THE SIGNS AND SYMPTOMS
- 1 November 1956
- journal article
- research article
- Published by Oxford University Press (OUP) in Acta Endocrinologica
- Vol. 23 (3), 313-330
- https://doi.org/10.1530/acta.0.0230313
Abstract
A patient with primary aldosteronism due to adrenocortical hyperplasia was described. An attempt was made to explain the pathogenesis of the signs and symptoms, based on pre- and post-operative investigations and on a study of the literature. The polyuria was attributed to changes in the renal tubules resulting from K depletion. The polydipsia was due to the hypertonic cellular dehydration. The retarded growth and genital development are not the consequence of endocrine disturbances, but were caused by the K deficiency. The metabolic alkalosis was likewise a result of the K depletion. In addition to the metabolic alkalosis there was an intracellular acidosis. The neutral to alkaline urine results from the active K excretion, caused by the increased aldo-sterone production. Pre-operatively there was a histamine-refractory achylia, and post-operatively a fairly high HC1 excretion. When comparing the excretion of Na and K before and after the operation, the gastric juice also gave indications of an increased K and decreased Na excretion due to increased aldosterone production. Only during the first few post-operative days did the patient show muscular weakness, but not before the operation when the serum K was low. The K content of the muscles was markedly decreased and that of Na significantly raised., Pre-operatively the ecg showed the typical hypopotassaemic changes. Post-operatively these changes persisted for several weeks with a normal serum K level. The blood sugar curve after loading showed a delayed fall, which is attributed to the concurrence of the effect of the K depletion and the direct effect of increased aldosterone production. As the blood pressure fell rapidly after the operation while the intracellular metabolism did not recover for several weeks, it is probable that the hypertension in primary aldosteronism is a direct cause of the increased aldosterone production. The post-operative investigations indicate a very gradual recovery of the intracellular abnormalities.Keywords
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