LETTERS to the EDITORC1-esterase inhibitor substitution in sepsis
References (3)
- et al.
Elevated plasma levels of the anaphylatoxins C3a and C4a are associated with a fatal outcome in sepsis
Am J Med
(1989)
Cited by (59)
Biological activities of C1 inhibitor
2008, Molecular ImmunologyCitation Excerpt :Experience with the use of C1 inhibitor in human sepsis remains somewhat limited. In the early 1990s, it was reported that C1 inhibitor treatment of small numbers of patients with septic shock suppressed activation of both the complement (decreased C3a and C5a) and contact (increased factor XII and prekallikrein) systems (Hack et al., 1993, 1992). A single double-blind, placebo-controlled trial has been reported (Caliezi et al., 2002).
Disseminated intravascular coagulation in sepsis
2005, ChestCitation Excerpt :However, less microvascular thrombosis was found in the treated animals.9092 Two uncontrolled studies117118 in which C1-Inh was administered to septic patients demonstrated less need for vasopressor medications, possibly due to attenuation of complement and contact-phase activation. In a randomized, double-blind, placebo-controlled pilot study,93 C1-Inh was administered to patients with severe sepsis or septic shock.
The Biological Role of the C1 Inhibitor in Regulation of Vascular Permeability and Modulation of Inflammation
2004, Advances in ImmunologyCitation Excerpt :These data suggest, therefore, that C1INH contributes to protection from gram-negative endotoxin shock via three mechanisms: inhibition of excessive complement activation, which would limit the amount of C5a generated (Czermak et al., 1999; Laudes et al., 2002; Strachan et al., 2000); inhibition of contact system activation, which would limit the amount of activated plasma kallikrein, factor XIIa, and bradykinin generated (Caliezi et al., 2001; Colman, 1999); and direct inhibition of endotoxin binding to macrophages, which thereby suppresses macrophage activation (Liu et al., 2003). Experience with the use of C1INH in patients with sepsis has been limited (Caliezi et al., 2001, 2002; Fronhoffs et al., 2000; Hack et al., 1992, 1993, 1994; Marx et al., 1999; Zeerleder et al., 2003). In the only randomized, double-blind study, patients with sepsis secondary to a variety of organisms were treated with C1INH every 12 h for 36 h (Caliezi et al., 2002).
Recent advances in the use of C1 inhibitor as a therapeutic agent
2003, Molecular ImmunologyMechanisms of C1-inhibitor deficiency
2002, ImmunobiologyC1-esterase inhibitor in ischemia and reperfusion
2002, Immunobiology