title: Intravenous immunoglobulin improves sepsis-induced coagulopathy: A retrospective, single-center observational study.
abstract: BACKGROUND
  Inflammation and coagulation are closely interrelated processes in the pathogenesis of sepsis. This study aimed to determine whether intravenous immunoglobulin (IVIg) could improve the hyperinflammatory state and coagulation/fibrinolysis abnormalities in patients with sepsis.
  
  
  METHODS
  Forty-one patients with sepsis were included. Nineteen patients were treated with IVIg (IVIg group; 5.0 g daily for 3 days within 2 days after hospitalization), and 22 patients were not (non-IVIg group). Inflammatory and coagulation/fibrinolysis molecular markers, Japanese Association for Acute Medicine disseminated intravascular coagulation score, and the Sequential Organ Failure Assessment score were evaluated in each group.
  
  
  RESULTS
  On admission, patients in the IVIg group had a significantly more severe condition. In the IVIg group, after treatment, C-reactive protein, procalcitonin, and interleukin-6 levels significantly decreased relative to values on admission. Also, compared with admission, the various coagulation/fibrinolysis molecular markers decreased after treatment. Moreover, the Japanese Association for Acute Medicine disseminated intravascular coagulation score and the Sequential Organ Failure Assessment score also significantly decreased after treatment. In contrast, in the non-IVIg group, only interleukin-6 level and thrombin-antithrombin complex levels significantly decreased. The 28-day mortality rate of the IVIg group was approximately one third of the value of the non-IVIg group (IVIg: 5.3% vs non-IVIg: 18.2%).
  
  
  CONCLUSIONS
  Intravenous immunoglobulin treatment significantly improved hemostatic abnormalities along with the hyperinflammatory state in patients with sepsis. Accordingly, IVIg treatment should be classified as an adjunctive therapy for patients complicated with sepsis-induced coagulopathy.
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Ishikura
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Nakamura
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Yasumasa
authors.initials: Y
authors.lastname: Kawano
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Junichi
authors.initials: J
authors.lastname: Tanaka
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Mariko
authors.initials: M
authors.lastname: Mizunuma
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Daiki
authors.initials: D
authors.lastname: Ohta
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Nishida
authors.affiliation: Department of Emergency and Critical Care Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
authors.forename: Akira
authors.initials: A
authors.lastname: Murai
mesh_terms: D000369:Aged, 80 and over; D000990:Antithrombin III; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D001778:Blood Coagulation Disorders / Q000097:blood / Q000209:etiology / Q000628:therapy*; D002097:C-Reactive Protein / Q000378:metabolism; D002116:Calcitonin / Q000097:blood; D015740:Calcitonin Gene-Related Peptide; D005260:Female; D006487:Hemostasis; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000627:therapeutic use*; D007155:Immunologic Factors / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D063305:Organ Dysfunction Scores; D010447:Peptide Hydrolases; D011498:Protein Precursors / Q000097:blood; D012189:Retrospective Studies; D018805:Sepsis / Q000097:blood* / Q000150:complications
chemical_list: D015415:Biomarkers; C000606589:CALCA protein, human; D016756:Immunoglobulins, Intravenous; D007155:Immunologic Factors; D015850:Interleukin-6; D011498:Protein Precursors; C046193:antithrombin III-protease complex; D000990:Antithrombin III; D002116:Calcitonin; D002097:C-Reactive Protein; D010447:Peptide Hydrolases; D015740:Calcitonin Gene-Related Peptide
keywords: Coagulation; Coagulopathy; Disseminated intravascular coagulation (DIC); Inflammation; Intravenous immunoglobulin (IVIg); Sepsis