PMID- 9504573
OWN - NLM
STAT- MEDLINE
DCOM- 19980326
LR  - 20201209
IS  - 0090-3493 (Print)
IS  - 0090-3493 (Linking)
VI  - 26
IP  - 3
DP  - 1998 Mar
TI  - Immunoglobulin E and eosinophil counts are increased after sepsis in trauma 
      patients.
PG  - 465-9
AB  - OBJECTIVES: To determine the time course of plasma immunoglobulin E (IgE) 
      concentration increases after traumatic injury, if increased IgE concentrations 
      were related to clinical events or complications, and if increased peripheral 
      eosinophil counts could be related to trauma, sepsis, or organ-specific 
      complications. DESIGN: Data relating to severity of injury, clinical 
      complications, plasma concentrations of IgE, and peripheral eosinophil counts 
      were prospectively collected. SETTING: Trauma service, tertiary-care medical 
      center. PATIENTS: One hundred adult trauma patients admitted to the intensive 
      care unit. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Plasma IgE 
      concentrations increased in most patients. However, the greatest increases were 
      observed in patients with sepsis (p = .03), renal dysfunction (p = .04), or 
      pneumonia (p = .02). IgE increases were not related to severity or mechanism of 
      injury, allergy history, or age. The day of highest observed IgE concentration 
      was related to the day of onset of sepsis (p = .012, r = .39), and occurred a 
      mean of 3.8 days after sepsis. Most patients had increased peripheral eosinophil 
      counts and eosinophil percentages of white blood cells during their intensive 
      care unit stays. Eosinophil counts were greater in patients with sepsis (p < 
      .0001), severe sepsis (p < .0001), or pneumonia (p < .002). CONCLUSIONS: 
      Increased IgE concentrations and eosinophil counts were found after sepsis and do 
      not appear to be related to the initial injury. Since IgE and eosinophil 
      production are enhanced by interleukin-4 and interleukin-5, respectively, these 
      findings suggest that T-helper lymphocyte type 2 cytokines are activated in 
      response to sepsis after traumatic injury.
FAU - DiPiro, J T
AU  - DiPiro JT
AD  - University of Georgia College of Pharmacy, the Medical College of Georgia, 
      Athens, USA.
FAU - Howdieshell, T R
AU  - Howdieshell TR
FAU - Hamilton, R G
AU  - Hamilton RG
FAU - Mansberger, A R Jr
AU  - Mansberger AR Jr
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Crit Care Med
JT  - Critical care medicine
JID - 0355501
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - *Eosinophils
MH  - Female
MH  - Humans
MH  - Immunoglobulin E/*blood
MH  - *Leukocyte Count
MH  - Male
MH  - Pneumonia/complications/immunology
MH  - Prospective Studies
MH  - Respiratory Distress Syndrome/etiology/immunology
MH  - Sepsis/complications/*immunology
MH  - Wounds and Injuries/complications/*immunology
EDAT- 1998/03/21 03:21
MHDA- 2001/03/28 10:01
CRDT- 1998/03/21 03:21
PHST- 1998/03/21 03:21 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1998/03/21 03:21 [entrez]
AID - 10.1097/00003246-199803000-00016 [doi]
PST - ppublish
SO  - Crit Care Med. 1998 Mar;26(3):465-9. doi: 10.1097/00003246-199803000-00016.