Protease-antiprotease levels and whole-blood chemiluminescence in acute peritonitis.
Whole-blood chemiluminescence and levels of leukocyte proteases and plasma protease inhibitors were studied in 43 patients with acute, generalized peritonitis. An almost three-fold increase in whole-blood chemiluminescence was found in acute peritonitis, which may indicate activation or "priming" of the leukocytes by blood-borne factors. High levels of leukocyte elastase and neutrophil proteinase 4(3) were found in plasma and peritoneal exudate. Patients with sepsis had higher plasma levels of both proteases than other patients. Large variations in the plasma levels among patients decreased their sensitivity as markers of infectious complications during the postoperative period. The plasma levels of the protease inhibitors followed three different patterns of reaction. The acute phase proteins alpha 1-proteinase inhibitor and C1-inactivator, increased during the first week of disease, to normalise later in its course. alpha 2-macroglobulin, antithrombin III and alpha 2-antiplasmin were all decreased from onset and normalised later in the course, while secretory leukocyte protease inhibitor showed a slow decrease throughout the course of disease. In peritonitis exudate, the levels of the main protease inhibitors, alpha 1-Proteinase Inhibitor and alpha 2-Macroglobulin, were decreased, probably due to complexation and subsequent elimination, as a part of the defense against liberated leukocyte proteases. The immunoreactive and especially functional levels of the protease inhibitors alpha 2-Antiplasmin, Antithrombin III and C1-Inactivator were also decreased in the exudate, indicating an increased turn-over of these proteins through activation of the cascade systems and/or break-down by leukocyte proteases. In contrast to the other inhibitors, secretory leukocyte protease inhibitor showed higher levels in exudate than in plasma, and unexpectedly high exudate/plasma-quotients were seen in cases with colonic perforations. Degradation of complement factor 3 (C3) and decreased "opsonic capacity" were found in exudate. The "opsonic capacity" could be correlated to the levels of leukocyte proteases in the exudate, which indicates that degradation of complement factor 3 may have been at least partly due to the action of leukocyte proteases. Further depletion of complement factors in exudates of long-standing peritonitis or abscesses may create a vicious circle of deficient opsonisation and clearance of bacteria, as earlier reported for chronic pleural exudates.
Bergenfeldt
M
M
Department of Surgery, Lund University, Malmö General Hospital, Sweden.
Ohlsson
K
K
D000208:Acute Disease; D000368:Aged; D001202:Ascitic Fluid / Q000201:enzymology; D001324:Autoantigens / Q000097:blood; D005260:Female; D006801:Humans; D019272:Leukocyte Elastase; D008163:Luminescent Measurements; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008875:Middle Aged; D053146:Myeloblastin; D009504:Neutrophils / Q000276:immunology; D010196:Pancreatic Elastase / Q000097:blood*; D010538:Peritonitis / Q000097:blood / Q000201:enzymology* / Q000276:immunology; D010587:Phagocytosis / Q000276:immunology; D011480:Protease Inhibitors / Q000097:blood*; D012697:Serine Endopeptidases / Q000097:blood*
D001324:Autoantigens; D011480:Protease Inhibitors; D012697:Serine Endopeptidases; D010196:Pancreatic Elastase; D019272:Leukocyte Elastase; D053146:Myeloblastin