Inflammatory cytokine response in patients with septic shock secondary to generalized peritonitis.
OBJECTIVE
The aims of this study were the following: a) to assess the proinflammatory cytokine (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1, and IL-6) response in patients with septic shock secondary to generalized peritonitis; and b) to evaluate the influence of bacteremic status, type of peritonitis (acute perforation or postoperative), and peritoneal microbial status (mono- or polymicrobial) on cytokine expression and mortality.


METHODS
Prospective study.


METHODS
Surgical intensive care unit of a university hospital.


METHODS
Fifty-two consecutive patients with septic shock caused by generalized peritonitis.


METHODS
Routine blood tests, blood cultures, and cytokine assays were performed during the first 3 days after onset of shock.


RESULTS
Serum TNF-alpha and IL-6 concentrations were measured by using a radioimmunoassay, and IL-1 concentrations were measured by using ELISA. Median serum concentrations on day 1 were: TNF-alpha, 90 pg/mL; IL-1, 7 pg/mL; and IL-6, 5000 pg/mL. TNF-alpha and IL-6 concentrations decreased significantly between the first and third days of septic shock (p = .0001), whereas IL-1 concentrations remained low. The decrease in IL-6 tended to be more pronounced in the survivors group (p = .057). Median TNF-alpha serum concentrations were higher in bacteremic compared with nonbacteremic patients (151 vs. 73 pg/mL, p = .003). TNF-alpha, IL-1, and IL-6 serum concentrations and mortality were not different between acute perforation vs. postoperative peritonitis and mono- versus polymicrobial peritonitis.


CONCLUSIONS
The systemic release of TNF-alpha and IL-6 during septic shock caused by generalized peritonitis was maximal on day 1 and decreased rapidly during the next days. No systemic release of IL-1 was observed. IL-6 serum concentrations remained higher in patients who subsequently died. Among the different features of peritonitis studied, only bacteremia influenced the systemic cytokine response (higher TNF-alpha).
Riché
F C
FC
Department of Anesthesiology, Hôpital Lariboisière, Paris, France.
Cholley
B P
BP
Panis
Y H
YH
Laisné
M J
MJ
Briard
C G
CG
Graulet
A M
AM
Guéris
J L
JL
Valleur
P D
PD
D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016470:Bacteremia / Q000150:complications* / Q000382:microbiology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D016469:Fungemia / Q000150:complications* / Q000382:microbiology; D017052:Hospital Mortality; D006801:Humans; D007375:Interleukin-1 / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010538:Peritonitis / Q000150:complications* / Q000382:microbiology; D011183:Postoperative Complications / Q000382:microbiology; D011446:Prospective Studies; D011863:Radioimmunoassay; D012772:Shock, Septic / Q000097:blood / Q000276:immunology* / Q000382:microbiology* / Q000401:mortality; D016019:Survival Analysis; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha