Primary Aldosteronism and Cerebrovascular Diseases

Chen, Zheng Wei; Hung, Chi Sheng; Wu, Vin-Cent; Lin, Yu Hung

doi:10.3803/enm.2018.33.4.429

Cited by 25 publications

(18 citation statements)

References 48 publications

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“…Therefore, in situ aldosterone excess could also result in cellular senescence, possibly in a paracrine or autocrine fashion, with increased oxidative stress damages inflicted in the same manner as cortisol in CPAs [ 18 , 19 ], particularly in KCNJ5 -mutated tumors. On the other hand, aldosterone excess was reported to damage heart, kidney, vessels and brain as direct aldosterone effects towards MR activation/oxidative stress, independently of blood pressure status [ 11 , 43 , 44 , 45 ]. In addition, this aldosterone-induced cellular senescence has already been reported in human and rat kidney proximal tubular cells with an oxidative stress/p53/p21-dependent pathway stimulated by mineralocorticoid receptor activation [ 46 , 47 ].…”

Section: Discussionmentioning

confidence: 99%

Cellular Senescence in Human Aldosterone-Producing Adrenocortical Cells and Related Disorders

et al. 2021

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In situ cortisol excess was previously reported to promote cellular senescence, a cell response to stress, in cortisol-producing adenomas (CPA). The aim of this study was to explore senescence pathways in aldosterone-producing cells and related disorders, and the influence of aldosterone overproduction on in situ senescence. We analyzed 30 surgical cases of aldosterone-producing adenoma (APA), 10 idiopathic hyperaldosteronism (IHA) and 19 normal adrenals (NA). CYP11B2 and senescence markers p16 and p21 were immunolocalized in all those cases above and results were correlated with histological/endocrinological findings. In the three cohorts examined, the zona glomerulosa (ZG) was significantly more senescent than other corticosteroid-producing cells. In addition, the ZG of adjacent non-pathological adrenal glands of APA and IHA had significantly higher p16 expression than adjacent non-pathological zona fasciculata (ZF), reticularis (ZR) and ZG of NA. In addition, laboratory findings of primary aldosteronism (PA) were significantly correlated with p21 status in KCNJ5-mutated tumors. Results of our present study firstly demonstrated that non-aldosterone-producing cells in the ZG were the most senescent compared to other cortical zones and aldosterone-producing cells in PA. Therefore, aldosterone production, whether physiological or pathological, could be maintained by suppression of cell senescence in human adrenal cortex.

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Section: Discussionmentioning

confidence: 99%

Cellular Senescence in Human Aldosterone-Producing Adrenocortical Cells and Related Disorders

et al. 2021

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“…Owing to the development of the current diagnostic methods, PA is the most common cause of secondary hypertension, with a prevalence rate of 5-15% for patients with hypertension. 7 Furthermore, it can cause cerebrovascular diseases, hypertension, electrolyte imbalance, and cardiovascular changes structurally and functionally. The increased stroke rate in PA may be related to the excessive aldosterone effects on blood vessels and direct damage from hypertension.…”

Section: Discussionmentioning

confidence: 99%

Pearls & Oy-sters: Cerebral Microbleeds Caused by Adrenocortical Adenoma-Related Primary Aldosteronism

Lee

Choi²,

Lee³

et al. 2021

Neurology

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“…Often, patients complain of headaches of varying intensity, which is due to hyperhydration of the brain and increased intracranial pressure. Recently, the issue of PHA associated with intracranial hypertension is discussed (14,15). Such patients complain of headache, increased BP in the range up to 160/90 mmHg, visual impairment (reduced visual acuity).…”

Section: Pha Symptomsmentioning

confidence: 99%

Characteristics and features of clinical manifestations of primary hyperaldosteronism (literature review)

Shidlovskyі¹,

Shidlovskyi²,

Шеремет³

et al. 2019

Ro J Med Pract.

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Introduction. Primary hyperaldosteronism as a cause of secondary arterial hypertension ranges from 4.6 to 13.0%, and among patients with refractory hypertension to medication therapy is about 20%. Meanwhile, its detectability among patients with arterial hypertension in centers of primary health care is from 6 to 13%, and in secondary care centers-from 23 to 30%. The high frequency of life-threatening cardiovascular complications dictates the need for early and timely diagnosis of primary hyperaldosteronism in the stages of the primary and secondary units of medical care. In addition, studies conducted in German and Italian hospitals among general practitioners showed a low level of knowledge about primary hyperaldosteronism. Objective. To promote the knowledge of general practitioners about clinical symptoms and clinical features of primary hyperaldosteronism. Results. Therefore, the main task of the work is the systematization and dissemination of knowledge for general practitioners about the symptoms and peculiarities of the clinical course of primary hyperaldosteronism. Such signs as an inadequate response to hypotensive therapy of a combination of three drugs, a manifestation of arterial hypertension under the age of 30, a rapid increase in blood pressure even in the elderly and/or the loss of efficacy of antihypertensive therapy, apnea in dream are distinguished in its non-specific clinical picture, without indicating priority. In the literature, there are recommendations to separate classical and secondary clinical manifestations. Classical include arterial hypertension, hypokalemia, hypervolemia, metabolic alkalosis, and minor ones such as headache, retinopathy, neuromuscular symptoms (paresthesia's, convulsions, general weakness), carbohydrate metabolism disorders, arrhythmias, early onset of hypertrophy and fibrosis of the heart muscle and smooth muscle vessels, hypokalemia and moderate hypernatremia. Conclusions. In the clinical course of the disease, the cardiovascular, neuromuscular, renal and metabolic syndromes are distinguished, or in combination of several of them, in each particular case, the primary hyperaldosteronism may appeared (or manifested).

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Primary Aldosteronism and Cerebrovascular Diseases

Cited by 25 publications

References 48 publications

Cellular Senescence in Human Aldosterone-Producing Adrenocortical Cells and Related Disorders

Cellular Senescence in Human Aldosterone-Producing Adrenocortical Cells and Related Disorders

Pearls & Oy-sters: Cerebral Microbleeds Caused by Adrenocortical Adenoma-Related Primary Aldosteronism

Characteristics and features of clinical manifestations of primary hyperaldosteronism (literature review)

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