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The Primary Aldosteronism Foundation [36] is a patient-driven initiative committed to creating the paradigm shift that will lead to optimum diagnosis and treatment of primary aldosteronism by raising awareness, fostering research, and providing support to patients and healthcare professionals worldwide.
Primary aldosteronism (hyporeninemic hyperaldosteronism) is most often caused by bilateral idiopathic (micronodular) adrenal hyperplasia (almost 70% of cases) [4] and adrenal adenoma (Conn's syndrome) (about 30% of cases). [4] These cause hyperplasia of aldosterone-producing cells of the adrenal cortex resulting in primary hyperaldosteronism.
Glucocorticoid remediable aldosteronism also describable as aldosterone synthase hyperactivity, is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient. It is a cause of primary hyperaldosteronism. [1]
The Randomized Aldactone Evaluation Study (RALES) trial is a landmark clinical study that assessed the impact of spironolactone, an aldosterone antagonist, on morbidity and mortality in patients with severe heart failure due to systolic dysfunction. [1] The findings from this trial significantly influenced the treatment guidelines for heart ...
Adrenocortical adenomas are classified as ACTH-independent disorders, and are commonly associated with conditions linked to hyperadrenalism such as Cushing's syndrome (hypercortisolism) or Conn's syndrome (hyperaldosteronism), which is also known as primary aldosteronism. [1]
The cutoff normal individuals from those with primary hyperaldosteronism is significantly affected by the conditions of testing, such as posture and time of day. On average, an ARR cutoff of 23.6 ng/dL per ng/(mL·h), expressed in alternative units as 651 pmol/L per μg/(L·h), has been estimated to have a sensitivity of 97% and specificity of 94%. [2]
Hyperaldosteronism is caused by the adrenal gland's overproduction of the hormone aldosterone. The excess production of the adrenal gland, specifically the zona glomerulosa, is the cause of primary hyperaldosteronism. Excessive renin-angiotensin-aldosterone system activation results in secondary hyperaldosteronism. [29]
A mineralocorticoid receptor antagonist (MRA or MCRA) [1] or aldosterone antagonist, is a diuretic drug which antagonizes the action of aldosterone at mineralocorticoid receptors. This group of drugs is often used as adjunctive therapy, in combination with other drugs, for the management of chronic heart failure .