UNLABELLED: Since 1938 endolymphatic hydrops has generally been accepted as the basic histopathological substrate of Menière's disease. In animal studies it has been found that exogenous administration of aldosterone resulted in endolymphatic hydrops. Manifestations of Menière's disease are frequently observed in times of emotional stress. Mediated through the hypothalamus, stress leads to an increased secretion of adrenocorticotropic hormone from the anterior pituitary gland, followed by an increased adrenocortical production of glucocorticoids (cortisol and corticosterone) and mineralocorticoids (aldosterone). We addressed the question whether plasma aldosterone levels, like in guinea pigs, would be increased in patients with Menière's disease. As part of a diagnostic protocol a clinical prospective cohort study was therefore performed on 89 patients with Menière's disease to assess plasma aldosterone levels. Plasma aldosterone was not elevated in Menière patients compared to plasma aldosterone in a control group of 27 normal subjects. No statistically significant differences were found in plasma aldosterone between uni- and bilateral Menière's disease. Plasma aldosterone levels did not correlate with age, average hearing loss, duration or perceived severity of subjective complaints (vertigo, hearing loss, tinnitus and aural pressure). In this study plasma aldosterone was not elevated in patients with Menière's disease compared to normal subjects. Plasma aldosterone can thus not be used as a diagnostic tool for Menière's disease. IN CONCLUSION: No anomalous plasma aldosterone levels were found in Menière patients during an attack-free period. The question whether plasma aldosterone and cortisol levels show variations before, during and after an attack remains to be answered. If so, this might contribute to a better understanding of the pathophysiological mechanism of Menière's disease. Copyright 2001 S. Karger AG, Basel
UNLABELLED: Since 1938 endolymphatic hydrops has generally been accepted as the basic histopathological substrate of Menière's disease. In animal studies it has been found that exogenous administration of aldosterone resulted in endolymphatic hydrops. Manifestations of Menière's disease are frequently observed in times of emotional stress. Mediated through the hypothalamus, stress leads to an increased secretion of adrenocorticotropic hormone from the anterior pituitary gland, followed by an increased adrenocortical production of glucocorticoids (cortisol and corticosterone) and mineralocorticoids (aldosterone). We addressed the question whether plasma aldosterone levels, like in guinea pigs, would be increased in patients with Menière's disease. As part of a diagnostic protocol a clinical prospective cohort study was therefore performed on 89 patients with Menière's disease to assess plasma aldosterone levels. Plasma aldosterone was not elevated in Menière patients compared to plasma aldosterone in a control group of 27 normal subjects. No statistically significant differences were found in plasma aldosterone between uni- and bilateral Menière's disease. Plasma aldosterone levels did not correlate with age, average hearing loss, duration or perceived severity of subjective complaints (vertigo, hearing loss, tinnitus and aural pressure). In this study plasma aldosterone was not elevated in patients with Menière's disease compared to normal subjects. Plasma aldosterone can thus not be used as a diagnostic tool for Menière's disease. IN CONCLUSION: No anomalous plasma aldosterone levels were found in Menière patients during an attack-free period. The question whether plasma aldosterone and cortisol levels show variations before, during and after an attack remains to be answered. If so, this might contribute to a better understanding of the pathophysiological mechanism of Menière's disease. Copyright 2001 S. Karger AG, Basel