title: Circulating thymus- and activation-regulated chemokine/CCL17 is a useful biomarker for discriminating acute eosinophilic pneumonia from other causes of acute lung injury.
abstract: BACKGROUND
  The presentation of acute eosinophilic pneumonia (AEP) closely resembles that of acute lung injury (ALI)/ARDS, including its idiopathic form, acute interstitial pneumonia (AIP). AEP usually lacks peripheral eosinophilia at the acute phase; therefore, the establishment of serum biomarkers for AEP would be clinically useful.
  
  
  METHODS
  We measured the levels of thymus- and activation-regulated chemokine (TARC)/CCL17, eotaxin/CCL11, KL-6, and surfactant protein-D (SP-D) in serum for patients with acute parenchymal lung diseases including AEP (n = 17), AIP (n = 13), pneumonia-associated ALI/ARDS (n = 12), and alveolar hemorrhage (n = 7). To evaluate diagnostic ability, each marker was estimated by measuring the area under the receiver operating characteristic curve (AUC).
  
  
  RESULTS
  Serum TARC/CCL17 levels of AEP patients were much higher than those of patients in other disease groups. More importantly, high circulating TARC/CCL17 levels were observed in AEP even at acute phase when peripheral eosinophilia was absent. TARC/CCL17 showed the largest AUC, and the TARC/CCL17 levels with cutoff points from 6,259 to 7,039 pg/mL discriminated AEP from other syndromes with sensitivity and specificity of 100%. The KL-6 level was low in most patients with AEP, and the sensitivity was 81.6% in cutoff with 100% specificity. The AUC for eotaxin/CCL11 and SP-D was small, with values of 0.73 (95% confidence interval [CI], 0.60 to 0.86) and 0.53 (95% CI, 0.31 to 0.64), respectively.
  
  
  CONCLUSIONS
  This study indicates that the measurement of circulating TARC/CCL17 and KL-6 is useful for discriminating AEP from other causes of ALI.
authors.affiliation: Division of Pulmonary Disease, Department of Brain and Nerve Science, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama-machi, Oita 879-5593, Japan. eishida@med.oita-u.ac.jp
authors.forename: Eishi
authors.initials: E
authors.lastname: Miyazaki
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Nureki
authors.forename: Emiko
authors.initials: E
authors.lastname: Ono
authors.forename: Masaru
authors.initials: M
authors.lastname: Ando
authors.forename: Osamu
authors.initials: O
authors.lastname: Matsuno
authors.forename: Tetsujiro
authors.initials: T
authors.lastname: Fukami
authors.forename: Takuya
authors.initials: T
authors.lastname: Ueno
authors.forename: Toshihide
authors.initials: T
authors.lastname: Kumamoto
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000951:Antigens, Neoplasm / Q000097:blood; D015415:Biomarkers / Q000097:blood; D054413:Chemokine CCL11; D054414:Chemokine CCL17; D019742:Chemokines, CC / Q000097:blood*; D003937:Diagnosis, Differential; D018450:Disease Progression; D005260:Female; D006470:Hemorrhage / Q000150:complications / Q000175:diagnosis*; D006801:Humans; D017563:Lung Diseases, Interstitial / Q000150:complications / Q000175:diagnosis*; D008297:Male; D008875:Middle Aged; D018396:Mucin-1; D009077:Mucins / Q000097:blood; D011657:Pulmonary Eosinophilia / Q000097:blood* / Q000150:complications / Q000175:diagnosis*; D037663:Pulmonary Surfactant-Associated Protein D / Q000097:blood; D012128:Respiratory Distress Syndrome / Q000150:complications / Q000175:diagnosis* / Q000209:etiology; D012189:Retrospective Studies; D012680:Sensitivity and Specificity
chemical_list: D000951:Antigens, Neoplasm; D015415:Biomarkers; C515456:CCL11 protein, human; C106230:CCL17 protein, human; D054413:Chemokine CCL11; D054414:Chemokine CCL17; D019742:Chemokines, CC; C060192:MUC1 protein, human; D018396:Mucin-1; D009077:Mucins; D037663:Pulmonary Surfactant-Associated Protein D