Background Besides phagocyte-derived oxidative autoaggression, proteolytic
destruction of functional proteins in the peritoneal cavity may also be inv
olved in the pathomechanism of secondary peritonitis. To evaluate the patte
rn of proteolysis, 43 patients undergoing initial operation for acute perit
onitis (n = 30) or scheduled abdominal lavages (Etappenlavage) for resoluti
on of persistent peritonitis (n = 13) and 16 surgical patients with abdomin
al exudation without peritonitis were enrolled in our study.
Materials and methods Thirty blood samples and purulent exudates were taken
simultaneously in each peritonitis group at the surgical interventions. Si
xteen clear exudates were obtained li om patients with post-operative non-i
nfectious irritations. The following parameters were measured: (a) elastase
(from neutrophils) and cathepsin B (from monocytes/ macrophages); (b) alph
a(1)-proteinase inhibitor (alpha(1)PI) and overall cysteine proteinase inhi
bitor capacity; and (c) opsonic activity and degradation products of fibrin
ogen, complement C3 and immunoglobulin IgG.
Results Circulating levels of phagocyte proteinases and of alpha(1)PI were
significantly elevated, whereas antigen concentrations and opsonic activity
of C3 and IgG were slightly reduced in peritonitis patients compared to he
althy volunteers. No degradation products were detectable in patients' bloo
d. Discharge of phagocyte proteinases was even more pronounced in both type
s of peritonitis exudates. Although most of the elastase was complexed with
alpha(1)PI, active elastase and its specific fibrinogen split product was
found along with significantly reduced inhibitory capacity for elastase and
cysteine proteinases. Local opsonic activity was dramatically diminished b
ecause of proteolytic degradation of C3 and IgG. Despite some phagocyte pro
teinase release, no destruction of functional proteins was seen in clear ex
udates.
Conclusions Higher values of extracellularly released phagocyte proteinases
concomitant with lower opsonin activity in exudates from patients with per
sistent peritonitis can be taken as a further hint of the involvement of lo
cal proteolysis-induced pathomechanisms in the development of lethal multip
le organ failure, which occurred more frequently in patients with persisten
t peritonitis (54%) than in those with acute peritonitis (27%).