Clinical studyEndotoxin, prekallikrein, complement and systemic vascular resistance: Sequential measurements in man☆
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Cited by (60)
Formation of bradykinin: A major contributor to the innate inflammatory response
2005, Advances in ImmunologyCitation Excerpt :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.
Platelet-activating factor, eicosanoids, and bradykinin as targets for adjuvant therapies for sepsis
2001, Seminars in Pediatric Infectious DiseasesCitation Excerpt :Consumption of functional prekallikrein also has been shown to occur in human volunteers challenged with a small dose of LPS.130 In some of these studies, low circulating levels of HMWK, prekallikrein, or both, have been shown to be more common in patients with hypotension than in patients with uncomplicated sepsis,126,129,131 supporting the notion that activation of factor XII-dependent pathways and excessive production of BK contribute to the development of shock in sepsis. In addition, Nuijens et al24 have shown that sepsis is associated with proteolytic cleavage of C1-Inh to an inactive form, called iC1-Inh, and that high circulating levels of iC1-Inh portend a fatal outcome.
The intrinsic coagulation/kinin-forming cascade: Assembly in plasma and cell surfaces in inflammation
1997, Advances in ImmunologyStructural biology, cellular interactions and pathophysiology of the contact system
1993, Thrombosis Research
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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.
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From the Immunology and Cardiology Research Sections, Veterans Administration Hospital, Hines, Illinois; and Department of Medicine, Loyola University Stritch School of Medicine, Maywood, Illinois.