Abstract
ln order to investigate the possible involvement of the plasma kallikrein-kinin system (K-K system) in Crow-Fukase syndrome, high molecular weight kininogen (HMWK), low mclecular weight kininogen (LMW-K), plasma prekallikrein (P.KaI), kininaseI (KI), kininaseII (KII) andFactor XII levels were measured in the plasma of 7patients.
Factor XI Ievels in the plasma of all patients assayed were significantly Iower than that of normal control (between20%and70% of normal control).A downward value in HMW-K level was also observed, while no significant change in the levelsofLMW-K, P.KalandKI was observed. On the other hand, markedly decreasedKII level was obsen/ed in the plasma of 6 patients (between 30% and 70% of normal control).
Judging from these results, a following possible hypothesis which suggests the involvement of the K-K system in this syndrome could be proposed. Namely, the activation of Factor XII by some reasons would occure and the generated Factor XIIa activated P. Kal. Then, the generated kallikrein selectively acted on HMW-K and liberated bradykinin from HMW-K molecule. Kallikrein also acted on Factor XII and the consumption of Factor XII wouldl be accelerated.therefore kinin would play important roles in this syndrome, such as edema formatlon etc. Decreased KII level would facilitate the kinin action.
ln our present studies no significant change ofP. Kal level and not so much altera- tion of HMW-K level were observed, so further details are now being studied to make sure the involvement of the K.K system in this syndrome.
