{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T04:43:00Z","timestamp":1782276180189,"version":"3.54.5"},"reference-count":35,"publisher":"Institute of Physiology of the Czech Academy of Sciences","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiol Res"],"published-print":{"date-parts":[[2016,4,29]]},"abstract":"<jats:p>Primary aldosteronism (PA) is the most common cause of endocrine hypertension with a high frequency of cardiovascular complications. The unfavorable cardiometabolic profile may be due to aldosterone-mediated activation of inflammatory cells, circulatory cytokines and activation of collagen synthesis in the vessel wall. Aim of our study was to evaluate differences in the levels of hsCRP, IL-6, TNF-\u03b1 and N-terminal propeptide of collagen I (PINP) in patients with PA and essential hypertension (EH) as a control group, and between the subtypes of PA (aldosterone producing adenoma \u2013 APA, idiopathic hyperaldosteronism \u2013 IHA). We studied 28 patients with PA (IHA \u2013 10 patients, APA \u2013 12 patients, 6 unclassified) and 28 matched patients with EH. There were no differences in the levels of inflammatory markers between the followed groups [EH vs. PA: TNF-\u03b1 (5.09 [3.68-6.32] vs. 4.84 [3.62-6.50] pg\/ml), IL-6 (0.94 [0.70-1.13] vs. 0.97 [0.71-1.28] pg\/ml), hsCRP (0.53 [0.25-1.54] vs. 0.37 [0.31-0.61] mg\/l), leukocytes (6.35\u00b11.42 vs. 5.97\u00b11.29 109 l); APA vs. IHA: TNF-\u03b1 (4.54 [3.62-7.03] vs. 5.19 [4.23-5.27] pg\/ml), IL-6 (0.96 [0.63-1.21] vs. 0.90 [0.65-1.06] pg\/ml), hsCRP (0.34 [0.29-0.47] vs. 0.75 [0.36-1.11] mg\/l), leukocytes (6.37\u00b11.41 vs. 5.71\u00b11.21 109 l)]. Significant differences in the levels of PINP between PA and EH group were observed (35.18 [28.46-41.16] vs. 45.21 [36.95-62.81] \u03bcg\/l, p\u22640.003). No differences in inflammatory markers were observed between the followed groups, we confirmed higher levels of PINP in patients with PA.<\/jats:p>","DOI":"10.33549\/physiolres.932994","type":"journal-article","created":{"date-parts":[[2020,2,13]],"date-time":"2020-02-13T11:50:19Z","timestamp":1581594619000},"page":"229-237","source":"Crossref","is-referenced-by-count":11,"title":["Inflammatory Markers in Primary Aldosteronism"],"prefix":"10.33549","author":[{"given":"Z.","family":"\u0160OML\u00d3OV\u00c1","sequence":"first","affiliation":[{"name":"Third Department of Internal Medicine, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"O.","family":"PETR\u00c1K","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"ROSA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B.","family":"\u0160TRAUCH","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"INDRA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T.","family":"ZELINKA","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M.","family":"HALUZ\u00cdK","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"V.","family":"ZIK\u00c1N","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R.","family":"HOLAJ","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"J.","family":"WIDIMSK\u00dd","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"19169","published-online":{"date-parts":[[2016,4,15]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"AN SJ, BOYD R, ZHU M, CHAPMAN A, PIMENTEL DR, WANG HD: NADPH oxidase mediates angiotensin II-induced endothelin-1 expression in vascular adventitial fibroblasts. 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