title: Human pentraxin 3 (PTX3) as a novel biomarker for the diagnosis of pulmonary arterial hypertension.
abstract: BACKGROUND
  Although inflammation is an important feature of pulmonary arterial hypertension (PAH), the usefulness of local inflammatory markers as biomarkers for PAH is unknown. In this study, we tested whether plasma concentrations of human pentraxin 3 (PTX3), a local inflammatory marker, would be a useful biomarker for detecting PAH.
  
  
  METHODS
  Plasma PTX3 concentrations were evaluated in 50 PAH patients (27 with idiopathic PAH, 17 with PAH associated with connective tissue disease (CTD-PAH), and six with congenital heart disease), 100 age and sex-matched healthy controls, and 34 disease-matched CTD patients without PAH. Plasma concentrations of B-type natriuretic peptide (BNP) and C-reactive protein (CRP) were also determined.
  
  
  RESULTS
  Mean PTX3 levels were significantly higher in all PAH patients than in the healthy controls (4.40±0.37 vs. 1.94±0.09 ng/mL, respectively; P<0.001). Using a threshold level of 2.84 ng/mL, PTX3 yielded a sensitivity of 74.0% and a specificity of 84.0% for the detection of PAH. In CTD-PAH patients, mean PTX3 concentrations were significantly higher than in CTD patients without PAH (5.02±0.69 vs. 2.40±0.14 ng/mL, respectively; P<0.001). There was no significant correlation between plasma levels of PTX3 and BNP or CRP. Receiver operating characteristic (ROC) curves for screening PAH in patients with CTD revealed that PTX3 (area under the ROC curve 0.866) is superior to BNP. Using a PTX3 threshold of 2.85 ng/mL maximized true-positive and false-negative results (sensitivity 94.1%, specificity 73.5%).
  
  
  CONCLUSIONS
  Plasma concentrations of PTX3 may be a better biomarker of PAH than BNP, especially in patients with CTD.
authors.affiliation: Department of Cardiology, Keio University School of Medicine, Tokyo, Japan. u1@ta-mu.net
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Tamura
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Ono
authors.forename: Masataka
authors.initials: M
authors.lastname: Kuwana
authors.forename: Kenji
authors.initials: K
authors.lastname: Inoue
authors.forename: Makoto
authors.initials: M
authors.lastname: Takei
authors.forename: Tsunehisa
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Takashi
authors.initials: T
authors.lastname: Kawakami
authors.forename: Jun
authors.initials: J
authors.lastname: Fujita
authors.forename: Masaharu
authors.initials: M
authors.lastname: Kataoka
authors.forename: Kensuke
authors.initials: K
authors.lastname: Kimura
authors.forename: Motoaki
authors.initials: M
authors.lastname: Sano
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Daida
authors.forename: Toru
authors.initials: T
authors.lastname: Satoh
authors.forename: Keiichi
authors.initials: K
authors.lastname: Fukuda
mesh_terms: D019540:Area Under Curve; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D065627:Familial Primary Pulmonary Hypertension; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood* / Q000175:diagnosis; D008297:Male; D008875:Middle Aged; D012372:ROC Curve; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins