Proinflammatory mediator activity, endogenous antagonists and the systemic inflammatory response in intra-abdominal sepsis. Scottish Sepsis Intervention Group.
BACKGROUND
Severe intra-abdominal sepsis continues to carry a high mortality rate. The physiological response to sepsis in this condition and its relationship with proinflammatory mediators and their endogenous antagonists require further clarification.


METHODS
Fifty-seven patients were stratified by Acute Physiology And Chronic Health Evaluation (APACHE) II score at the time of admission to an intensive care unit (group 1, score of less than 20; group 2, score of 20 or more). Serial measurements of clinical and immunological variables were made.


RESULTS
Non-survivors from group 2 had a raised acute physiology score (P = 0.01), a higher peak serum interleukin (IL) 6 concentration (P = 0.03) and a depressed level of endogenous immunoglobulin (Ig) G class antiendotoxin core antibody (P = 0.005). In group 1, although organ failure score increased progressively in non-survivors, physiology score and peak IL-6 level were similar to those in survivors, and endogenous IgG class antiendotoxin core antibody titre rose (P = 0.02). In both groups IL-1 and tumour necrosis factor alpha were detected infrequently, but their natural antagonists were present in much higher concentrations in both survivors and non-survivors. Levels of C-reactive protein were raised in both but were not significantly different between survivors and non-survivors.


CONCLUSIONS
During the development of organ failure and death, the pattern of proinflammatory mediators and their endogenous antagonists can vary markedly and may in part be determined by the extent of the initial physiological disturbance.
University Department of Surgery, Royal Infirmary, Edinburgh, UK.
C H
CH
Wakefield
G R
GR
Barclay
K C
KC
Fearon
A S
AS
Goldie
J A
JA
Ross
I S
IS
Grant
G
G
Ramsay
J C
JC
Howie
D000210:Acute-Phase Reaction; D000907:Antibodies, Bacterial / Q000276:immunology; D002097:C-Reactive Protein / Q000378:metabolism*; D004378:Duodenal Diseases / Q000378:metabolism / Q000382:microbiology; D004731:Endotoxins / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D018123:Receptors, Interleukin / Q000037:antagonists & inhibitors; D012044:Regression Analysis; D013272:Stomach Diseases / Q000378:metabolism / Q000382:microbiology; D016019:Survival Analysis; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000907:Antibodies, Bacterial; D004731:Endotoxins; D015850:Interleukin-6; D018123:Receptors, Interleukin; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein