title: Activation of the contact system by filtration of platelet concentrates with a negatively charged white cell-removal filter and measurement of venous blood bradykinin level in patients who received filtered platelets.
abstract: BACKGROUND
  Several recent reports have described hypotensive transfusion reactions in patients receiving platelet concentrates (PCs) filtered through white cell-reduction filters. It is well known that a negatively charged surface activates the contact system, consisting of factor XII, prekallikrein, and high-molecular-weight kininogen.
  
  
  METHODS
  To clarify the mechanisms of these hypotensive reactions, the possibility that white cell-reduction filtration activates the contact system was examined. Venous blood plasma bradykinin levels were also measured in patients receiving PC transfusions through filters.
  
  
  RESULTS
  None of the measured values were changed by filtration through a positively charged filter. However, filtration through a negatively charged filter resulted in a decrease in the amounts of prekallikrein and an increase in the amount of bradykinin generated, which indicated the activation of the contact system. The bradykinin level was inversely related to the activity of angiotensin-converting enzyme (ACE) in the PCs and was elevated by addition of an ACE inhibitor. Although the venous blood plasma bradykinin level did not change in two patients with a normal ACE activity during PC transfusion through the negatively charged filter, two patients who had decreased ACE activity, showed a significant increase in bradykinin during the transfusion.
  
  
  CONCLUSIONS
  These results suggest that the generation of a large amount of bradykinin by filtration of PCs through a negatively charged filter might cause hypotensive reactions in patients with decreased ACE activity. The clinical significance of bradykinin generation requires further study.
authors.affiliation: Department of Research, Japanese Red Cross Central Blood Center, Tokyo, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Shiba
authors.forename: K
authors.initials: K
authors.lastname: Tadokoro
authors.forename: M
authors.initials: M
authors.lastname: Sawanobori
authors.forename: K
authors.initials: K
authors.lastname: Nakajima
authors.forename: K
authors.initials: K
authors.lastname: Suzuki
authors.forename: T
authors.initials: T
authors.lastname: Juji
mesh_terms: D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001792:Blood Platelets / Q000737:chemistry; D001920:Bradykinin / Q000097:blood; D002216:Captopril / Q000494:pharmacology; D003174:Complement C1 Inactivator Proteins / Q000032:analysis; D006224:Cricetinae; D005260:Female; D005374:Filtration / Q000295:instrumentation; D006801:Humans; D007022:Hypotension / Q000209:etiology; D007704:Kininogens / Q000097:blood; D007937:Leukapheresis / Q000295:instrumentation; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D017713:Platelet Transfusion; D011288:Prekallikrein / Q000032:analysis; D065227:Transfusion Reaction; D000511:alpha-Macroglobulins / Q000032:analysis
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D003174:Complement C1 Inactivator Proteins; D007704:Kininogens; D000511:alpha-Macroglobulins; D011288:Prekallikrein; D002216:Captopril; D007703:Peptidyl-Dipeptidase A; D001920:Bradykinin