Arterial Wall Inflammation and Increased Hematopoietic Activity in Patients With Primary Aldosteronism.
Adult
Aged
Arteries
/ diagnostic imaging
Arteritis
/ blood
Biomarkers
/ blood
Case-Control Studies
Cross-Sectional Studies
Female
Fluorodeoxyglucose F18
Gene Expression Profiling
Hematopoiesis
/ physiology
Humans
Hyperaldosteronism
/ blood
Inflammation
/ blood
Male
Middle Aged
Monocytes
/ metabolism
Netherlands
/ epidemiology
Positron Emission Tomography Computed Tomography
18F-FDG PET-CT
atherosclerosis
immune system
inflammation
mineralocorticoid
primary aldosteronism
Journal
The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362
Informations de publication
Date de publication:
01 05 2020
01 05 2020
Historique:
received:
01
11
2019
accepted:
24
12
2019
pubmed:
26
12
2019
medline:
10
2
2021
entrez:
26
12
2019
Statut:
ppublish
Résumé
Primary aldosteronism (PA) confers an increased risk of cardiovascular disease (CVD), independent of blood pressure. Animal models have shown that aldosterone accelerates atherosclerosis through proinflammatory changes in innate immune cells; human data are scarce. The objective of this article is to explore whether patients with PA have increased arterial wall inflammation, systemic inflammation, and reprogramming of monocytes. A cross-sectional cohort study compared vascular inflammation on 2'-deoxy-2'-(18F)fluoro-D-glucose; (18F-FDG) positron emission tomography-computed tomography, systemic inflammation, and monocyte phenotypes and transcriptome between PA patients and controls. This study took place at Radboudumc and Rijnstate Hospital, the Netherlands. Fifteen patients with PA and 15 age-, sex-, and blood pressure-matched controls with essential hypertension (EHT) participated. PA patients displayed a higher arterial 18F-FDG uptake in the descending and abdominal aorta (P < .01, P < .05) and carotid and iliac arteries (both P < .01). In addition, bone marrow uptake was higher in PA patients (P < .05). Although PA patients had a higher monocyte-to-lymphocyte ratio (P < .05), systemic inflammatory markers, cytokine production capacity, and transcriptome of circulating monocytes did not differ. Monocyte-derived macrophages from PA patients expressed more TNFA; monocyte-derived macrophages of healthy donors cultured in PA serum displayed increased interleukin-6 and tumor necrosis factor-α production. Because increased arterial wall inflammation is associated with accelerated atherogenesis and unstable plaques, this might importantly contribute to the increased CVD risk in PA patients. We did not observe inflammatory reprogramming of circulating monocytes. However, subtle inflammatory changes are present in the peripheral blood cell composition and monocyte transcriptome of PA patients, and in their monocyte-derived macrophages. Most likely, arterial inflammation in PA requires interaction between various cell types.
Identifiants
pubmed: 31875423
pii: 5686861
doi: 10.1210/clinem/dgz306
pmc: PMC7105350
pii:
doi:
Substances chimiques
Biomarkers
0
Fluorodeoxyglucose F18
0Z5B2CJX4D
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© Endocrine Society 2019.
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