Endocrine Abstracts

Objective: Clinical and histopathological assessment of a consecutive series of Munich patients operated between 2016 and 2018 for unilateral primary aldosteronism (PA).Background: Unilateral PA is the most common surgically curable form of hypertension mainly caused by an aldosterone-producing adenomas (APA). Somatic mutations in KCNJ5, CACNA1D, ATP1A1 or ATP2B3drive the aldosterone excess in the majority of APAs. Genetic variants in <...

BackgroundUnilateral forms of primary aldosteronism (PA) are usually surgically treated to remove the source of aldosterone excess. After adrenalectomy, aldosteronism persists in a subset of patients indicating abnormal aldosterone production from the unresected gland.ObjectiveTo retrospectively analyze histopathology and post-surgical outcomes in a 3-year prospective cohort of patients diagnosed with unilate...

Background: The role of ferroptosis – a regulated form of cell death – in the pathophysiology of aldosterone-producing adenomas (APA) is unclear.Objective: To identify mechanisms of ferroptosis in human adrenal cells and translate these findings to APA pathophysiology.Methods: Cell death detection, lipid ROS generation and mRNA sequencing were performed on HAC15 cells treated with the specific ferroptosis inducer RSL3 (1,...

Objective: Aldosterone-producing adenomas (APA) are a major cause of primary aldosteronism. Somatic mutations explain the excess aldosterone production in the majority of patients with APA with mutations in KCNJ5 encoding a potassium channel the most prevalent in most reported populations. Mechanisms driving cell proliferation are largely undefined.Design and method: Quantitative transcriptome analysis using RNA-seq was used to identify differen...

Rationale: Endothelial dysfunction (ED) is a hallmark of primary aldosteronism and paves the way for subsequent atherosclerotic disease. Past research has confirmed that one factor involved in ED is disturbed nitric oxide (NO) signalling. Since defects in NO release alone cannot explain the whole effect, we set out to address the role of endothelial CYP-expoygenase products (epoxyeicosatrienoic acids, EETs) in aldosterone-mediated endothelial dysfunction.<p class="abstext"...