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Next Article 
Quantification of plasma factor XIIa-Cl(-)-inhibitor and kallikrein-Cl(-
)-inhibitor complexes in sepsis
JH Nuijens, CC Huijbregts, AJ Eerenberg-Belmer, JJ Abbink, RJ Strack van Schijndel, RJ Felt-Bersma, LG Thijs and CE Hack
Central Laboratory, The Netherlands Red Cross Blood Transfusion Service,
Amsterdam.
Considerable evidence indicates that activation of the contact system of
intrinsic coagulation plays a role in the pathogenesis of septic shock. To
monitor contact activation in patients with sepsis, we developed highly
sensitive radioimmunoassays (RIAs) for factor XIIa-Cl(- )-inhibitor
(Cl(-)-Inh) and kallikrein-Cl(-)-Inh complexes using a monoclonal antibody
(MoAb Kok 12) that binds to a neodeterminant exposed on both complexed and
cleaved Cl(-)-Inh. Plasma samples were serially collected from 48 patients
admitted to the intensive care unit because of severe sepsis. Forty percent
of patients on at least one occasion had increased levels of plasma factor
XIIa-Cl(-)-Inh (greater than 5 x 10(-4) U/mL) and kallikrein-Cl(-)-Inh
(greater than 25 x 10(- 4) U/mL), that correlated at a molar ratio of
approximately 1:3. Levels of factor XII antigen in plasma and both the
highest as well as the levels on admission of plasma factor XIIa-Cl(-)-Inh
in 23 patients with septic shock were lower than in 25 normotensive
patients (P = .015: factor XII on admission; P = .04: highest factor
XIIa-Cl(-)-Inh; P = .01: factor XIIa-Cl(-)-Inh on admission). No
significant differences in plasma kallikrein-Cl(-)-Inh or prekallikrein
antigen were found between these patients' groups. Elevated Cl(-)-Inh
complex levels were measured less frequently in serial samples from
patients with septic shock than in those from patients without shock (P
less than .0001). Based on these results, we conclude that plasma Cl(-)-Inh
complex levels during sepsis may not properly reflect the extent of contact
activation.
Volume 72,
Issue 6,
pp. 1841-1848,
12/01/1988
Copyright © 1988 by The American Society of Hematology
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