title: Plasma levels of interleukin-1 receptor antagonist (IL-1ra) and severity of illness in patients with burns.
abstract: The present study was conducted to determine whether a plasma interleukin-1 receptor antagonist (IL-1ra) would reflect the severity of burn injury and to examine the relation between IL-1ra and the cytokines. We studied 24 burn patients in whom the total burn surface area (TBSA) accounted for at least 20% of the body surface, and in whom serial blood samples could be obtained beginning immediately after the burn injury. Plasma levels of IL-1ra were determined by enzyme-linked immunosorbent assay (ELISA). Plasma levels of tumor necrosis factor-alpha (TNF-alpha), IL-6, and IL-8 were also determined by ELISA. Endotoxin was measured by an endotoxin-specific synthetic substrate method. There was a significant correlation between the plasma levels of IL-1ra and TBSA during the first week following burn injury. The IL-1ra level was the highest immediately after the burn injury. The level decreased markedly thereafter, and again rose when infection occurred. The IL-1ra level was extraordinarily elevated in patients who developed concomitant sepsis, septic shock or the septic multiple organ dysfunction syndrome. The IL-1ra level on admission and the maximum IL-1ra level during the observation period were significantly higher in the patients who eventually died than in the survivors. There was a significant correlation between the level of IL-1ra and that of TNF-alpha, IL-6 or IL-8 during the observation period. No correlation was found between IL-1ra and endotoxin. The plasma IL-1ra level was closely correlated with the severity of inflammation and the clinical status of the burn patients, regardless of the infection. Results suggest that IL-1ra can serve as an index of the systemic inflammatory response syndrome (SIRS).
authors.affiliation: Critical Care and Emergency Center, Iwate Medical University, Morioka 020, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Endo
authors.forename: K
authors.initials: K
authors.lastname: Inada
authors.forename: Y
authors.initials: Y
authors.lastname: Yamada
authors.forename: T
authors.initials: T
authors.lastname: Kasai
authors.forename: T
authors.initials: T
authors.lastname: Takakuwa
authors.forename: H
authors.initials: H
authors.lastname: Nakae
authors.forename: Y
authors.initials: Y
authors.lastname: Kamei
authors.forename: T
authors.initials: T
authors.lastname: Shimamura
authors.forename: T
authors.initials: T
authors.lastname: Suzuki
authors.forename: S
authors.initials: S
authors.lastname: Taniguchi
authors.forename: M
authors.initials: M
authors.lastname: Yoshida
mesh_terms: D000328:Adult; D000368:Aged; D002056:Burns / Q000378:metabolism* / Q000401:mortality; D004731:Endotoxins / Q000097:blood / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D018123:Receptors, Interleukin / Q000037:antagonists & inhibitors*; D018805:Sepsis / Q000097:blood / Q000382:microbiology; D012795:Sialoglycoproteins / Q000097:blood / Q000378:metabolism*; D018746:Systemic Inflammatory Response Syndrome; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004731:Endotoxins; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D016209:Interleukin-8; D018123:Receptors, Interleukin; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha