Complement, neutrophil, and macrophage activation in women with severe preeclampsia and the syndrome of hemolysis, elevated liver enzymes, and low platelet count.

Activation of complement, neutrophils, and macrophages was studied in 14 women with severe preeclampsia, 11 of whom had the syndrome of hemolysis, elevated liver enzymes, and low platelet count; in 14 women with normal pregnancies; in seven normal pregnant women undergoing cesarean deliveries; and in 15 healthy nonpregnant women. Activation of complement, neutrophils, and macrophages was measured by plasma determinations of complement split products, polymorphonuclear (PMN) elastase, and neopterin, respectively. Women with severe preeclampsia had increased levels of C5a, terminal complement complex, PMN elastase, and neopterin at delivery and 1 day postpartum as compared with the normal pregnant group. One week postpartum, neopterin remained higher in preeclamptic women, whereas the complement components and PMN elastase had returned to normal. Cesarean delivery after normal pregnancy did not increase the levels of complement split products, PMN elastase (except for one value), or neopterin. The nonpregnant women had normal PMN elastase and neopterin levels. Accordingly, complement, neutrophils, and macrophages are activated in women with severe preeclampsia at delivery. The plasma levels of PMN elastase correlated positively to the formed terminal complement complexes in vivo. An in vitro study was performed to elucidate further the connection between complement and leukocyte activation. Recombinant C5a incubated in whole blood and in a neutrophil cell suspension gave a dose-dependent release of PMN elastase. Both the clinical and the in vitro results indicate that activation of the complement system may affect the function of neutrophils. This study supports the theory that the pathologic manifestations of severe preeclampsia may be explained by complement-induced release of biologically active substances from activated leukocytes.

Terminal complement complexes and anaphylatoxins in septic and ischemic patients.

Terminal complement complex (TCC) and anaphylatoxin formation in 18 patients with sepsis and 20 patients with acute limb ischemia were studied before the start of treatment and seven days later. The septic or ischemic patients had elevated levels of plasma TCC before start of therapy. In successfully treated patients these concentrations were within the normal range one week later. Similarly, the plasma anaphylatoxin level was increased before therapy and returned to the normal range within seven days. Escherichia coli incubated in vitro in fresh human serum at body temperature started formation of TCC in a dose-related manner. As complement will induce cellular lysis via TCC and edema via anaphylatoxins, anemia and impaired respiration in these patients may be influenced by increased concentrations of terminal complement complexes and of C3a and C5a.