Kallikrein and prekallikrein levels in a large number of congenital clotting deficiencies and abnormalities.
Kallicrein (K) and prekallicrein (PK) were assayed in a large number of cases with congenitial clotting factor defects. Patients with factor XII deficiency were separated from other clotting abnormalities. The results were compared with a control group of normal subjects. We found significantly reduced PK activity levels in the factor XII deficient group. Although less evident, the reduction of PK activity in the group of other clotting defects was modest, however, not due to a factor VII defect. In our study we found that in the absence of factor XII, PK is not activated. Further studies will be necessary to show if PK activation is altered or reduced in other congenital clotting abnormalities.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001777:Blood Coagulation; D001778:Blood Coagulation Disorders / Q000097:blood / Q000151:congenital / Q000201:enzymology*; D002648:Child; D002675:Child, Preschool; D005174:Factor XII / Q000378:metabolism; D005175:Factor XII Deficiency / Q000151:congenital / Q000201:enzymology; D005260:Female; D005342:Fibrinolysis; D006801:Humans; D007223:Infant; D007610:Kallikreins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011288:Prekallikrein / Q000097:blood*
D005174:Factor XII; D011288:Prekallikrein; D007610:Kallikreins