Abstract
Inflammation, edema and local vascular permeability changes are essential features of the complex regional pain syndrome type I (CRPS I). The role of kallikrein-kinin system components as the major mediators in the development of these symptoms is poorly investigated.
 The objective: to investigate the role of kallikrein-kinin system in pathophysiologic mechanisms of CRPS I.
 Patients and methods. We have investigated level of prekallikrein (PK), activity of fast-reacting (FRI) and time-dependent (TDI) inhibitors of plasma kallikrein, and blood plasma proteolytic activity (BPPA) in 45 patients with CRPS I and 15 healthy volunteers.
 Results. Analysis of kininogenesis activity and sympathetic-adrenal system revealed their close interdependence. Our data corresponds well with the literature information about depressive effect of sympathetic nervous system on kininase activity. This leads to the accumulation of vasoactive peptides in the injures segment of the extremity. Decrease of neurogenic effects at the later stages of CRPS I leads to the fall of the basal kininogenesis level.
 Conclusion. Local humoral factors such as the components of kallikrein-kinin system play an important role in CRPS I pathophysiologic mechanisms and are dependent on sympathetic-adrenal system activity.
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