Clinical study
Endotoxin, prekallikrein, complement and systemic vascular resistance: Sequential measurements in man

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Abstract

Eighteen patients were studied prior to and again within 6 hours after transurethral resection or cystoscopy. In addition to hemodynamic measurements, detection of endotoxin by limulus assay and bacteriologic sampling; prekallikrein, C3, C3 proactivator and lysosomal enzyme levels were measured. In five patients limulus assays were positive, and in one, gram-positive bacteremia developed but limulus assay remained negative. All six had significant decreases in prekallikrein, C3 or C3 proactivator. Systemic vascular resistance fell in all six. Four additional patients who had a decrease in systemic vascular resistance were not endotoxemic or bacteremic; one of these had a decrease in prekallikrein only. In the remaining eight patients with neither bacteremia nor endotoxemia, systemic vascular resistance did not change or increase after Instrumentation. One had a decrease in C3 proactivator, another in prekallikrein. There was no significant difference in age, disease, antibiotic therapy or bacteremla hi the two groups of patients. Four of the five resectional procedures were performed in the group that showed decreases in systemic vascular resistance. The data suggest that acute endotoxemia or gram-positive bacteremia in man is associated with depletion of prekallikrein, decreased peripheral resistance and, in some instances, activation of the complement system.

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    The latter effect appears specific, because no significant change in factor XII or kininogen levels is noted. Endotoxic shock is associated with depletion of contact activation proteins (Hirsch et al., 1974; Mason et al., 1970; O'Donnell et al., 1976; Robinson et al., 1975), and serial HK levels have prognostic value because a drop to near zero usually indicates a fatal outcome, as do lower prekallikrein levels (O'Donnell et al., 1976). A monoclonal antibody to factor XII markedly diminished the mortality by 50% in a baboon model of endotoxic shock (Pixley et al., 1992, 1993), largely due to effects on hypotension and its sequelae.

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    The contact-phase (ie, the factor XII-kallikrein) system has been shown to be activated on bacterial surfaces, suggesting an important way that both coagulation abnormalities and the release of vasodilating substances might occur in septic shock.125 Consumption of prekallikrein, HMWK, or both, has been shown to occur in patients with sepsis.126-129 Consumption of functional prekallikrein also has been shown to occur in human volunteers challenged with a small dose of LPS.130

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This study was presented in part at the Annual Meeting of the American Federation for Clinical Research, Southern Section, January 24, 1974.

1

From the Immunology and Cardiology Research Sections, Veterans Administration Hospital, Hines, Illinois; and Department of Medicine, Loyola University Stritch School of Medicine, Maywood, Illinois.

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