title: Clinical Significance of Tissue Factor and CD13 Double-Positive Microparticles in Sirs Patients with Trauma and Severe Sepsis.
abstract: Activated immune cells such as monocytes are key factors in systemic inflammatory response syndrome (SIRS) following trauma and sepsis. Activated monocytes induce almost all tissue factor (TF) expression contributing to inflammation and coagulation. TF and CD13 double-positive microparticles (TF/CD13MPs) are predominantly released from these activated monocytes. This study aimed to evaluate TF/CD13MPs and assess their usefulness as a biomarker of pathogenesis in early SIRS following trauma and sepsis. This prospective study comprising 24 trauma patients, 25 severe sepsis patients, and 23 healthy controls was conducted from November 2012 to February 2015. Blood samples were collected from patients within 24 h after injury and diagnosis of severe sepsis and from healthy controls. Numbers of TF/CD13MPs were measured by flow cytometry immediately thereafter. Injury Severity Score (ISS) and Acute Physiology and Chronic Health Evaluation (APACHE) II and Sequential Organ Failure Assessment (SOFA) scores were calculated at patient enrollment. APACHE II and SOFA scores and International Society of Thrombosis and Haemostasis (ISTH) overt disseminated intravascular coagulation (DIC) diagnostic criteria algorithm were calculated at the time of enrollment of severe sepsis patients. Numbers of TF/CD13MPs were significantly increased in both trauma and severe sepsis patients versus controls and correlated significantly with ISS and APACHE II score in trauma patients and with APACHE II and ISTH DIC scores in severe sepsis patients. Increased numbers of TF/CD13MPs correlated significantly with severities in the acute phase in trauma and severe sepsis patients, suggesting that TF/CD13MPs are important in the pathogenesis of early SIRS following trauma and sepsis.
authors.affiliation: *Department of Traumatology and Acute Critical Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan †Laboratory for Clinical Investigation, Osaka University Hospital, Suita, Osaka, Japan.
authors.forename: Hisatake
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Kazuma
authors.initials: K
authors.lastname: Yamakawa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ogura
authors.forename: Taichin
authors.initials: T
authors.lastname: Koh
authors.forename: Naoya
authors.initials: N
authors.lastname: Matsumoto
authors.forename: Takeshi
authors.initials: T
authors.lastname: Shimazu
mesh_terms: D018806:APACHE; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood* / Q000378:metabolism; D018826:CD13 Antigens / Q000378:metabolism*; D055252:Cell-Derived Microparticles / Q000378:metabolism*; D005260:Female; D006801:Humans; D015601:Injury Severity Score; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018805:Sepsis / Q000097:blood* / Q000150:complications*; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood* / Q000209:etiology* / Q000378:metabolism; D013925:Thromboplastin / Q000378:metabolism*; D014947:Wounds and Injuries / Q000097:blood* / Q000150:complications* / Q000378:metabolism
chemical_list: D015415:Biomarkers; D013925:Thromboplastin; D018826:CD13 Antigens