ArticleHeart and vessels2015
Implications of pentraxin 3 levels in patients with acute aortic dissection.
Article in Heart and vessels, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Establishment of a nomogram model based on immune-related genes using machine learning for aortic dissection diagnosis and immunomodulation assessment.International journal of medical sciences · 2025Article
- Blood biomarker panel recommended for personalized prediction, prognosis, and prevention of complications associated with abdominal aortic aneurysm.The EPMA journal · 2019Article
- Article
- Association of Plasma Pentraxin-3 Levels on Admission with In-hospital Mortality in Patients with Acute Type A Aortic Dissection.Chinese medical journal · 2016Article
- Dynamic monitoring of platelet activation and its role in post-dissection inflammation in a canine model of acute type A aortic dissection.Journal of cardiothoracic surgery · 2016Article
- Is pentraxin 3 a biomarker, a player, or both in the context of coronary atherosclerosis and metabolic factors?Heart and vessels · 2015Article
- Possible association between serum alkaline phosphatase concentration and thoracicacute aortic dissection.International journal of clinical and experimental medicine · 2015Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute aortic dissection (AAD) causes transient inflammation with occasional pleural fluid (PF) accumulation. Although pentraxin 3 (PTX3) is a vascular inflammation-related biomarker, little is known about PTX3 levels in patients with AAD. We explored the serial changes in plasma PTX3 levels and the association of peak levels with the amount of PF accumulation. Consecutive patients (n = 41) with Stanford type B AAD were enrolled, and blood samples for the measurements of serum albumin, plasma PTX3 and high-sensitivity C-reactive protein (CRP) were collected daily until 7 days after symptom onset. PF accumulation on computed tomography imaging on the third hospital day was divided into 3 grades (I: none or slight, II: mild in the uni- or bilateral pleural cavity, III: moderate or more). PTX3 and CRP levels were analyzed after logarithmic transformation because of their skewed distributions. Peak PTX3 and CRP levels were observed at 4.3 ± 2.1 and 4.7 ± 2.0 days after symptom onset, and their values were 12.2 [interquartile range (IQR), 8.2-20.9] ng/mL and 12.0 (IQR, 8.6-15.2) mg/dL, respectively. On univariate analysis, the peak level of PTX3 had a negative correlation with the minimum level of serum albumin, and a positive correlation with PF grade and duration of intensive care unit stay. On multivariate analysis, the peak level of PTX3 was correlated with PF grade (P = 0.037). In conclusion, the peak level of PTX3 in patients with AAD was associated with the amount of transient PF accumulation, which may be associated with inflammatory vascular permeability.
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