Maintaining inventories of plasma with low titer anti-T 

A colleague at a blood center in Wisconsin wonders if any blood centers in USA maintain an inventory of low titre anti-T plasma, and if so, how do they screen donors to identify those with low titre anti-T?

The following comments have been received.

ADDENDA Mar. 5, 2004

1. A colleague in Colorado reports that in the last few years they seem to have had an 'outbreak' of patients who have become T- or Tk- activated (and even an acquired B!). They attribute this to a heightened awareness of screening septic patients among their intensive care and neonatal physicians. They utilize washed red cells and platelets for these patients. When the use of fresh frozen plasma cannot be avoided, they attempt to perform minor crossmatching from integral unit segments in the effort to select 'least incompatible' units. The Colorado colleague states that in Applied Blood Group Serology, 4th ed., Issitt references Nancy Heddle as reporting the uneventful transfusion of plasma-containing products to three premature infants with necrotizing enterocolitis (NEC) and T-activated red blood cells. If one makes the effort to screen, some degree of T- or Tk- activation will be found in most infants with NEC. In the Colorado colleague's opinion, observation of a greater degree of severity of T-activation, demonstrating polyagglutination and red cell hemolysis, would be the situation in which one would proceed with extreme caution with the administration of fresh frozen plasma. That is of course problematic because septic children frequently have accompanying coagulopathies.
   
   
2. A transfusion medicine physician at an academic center in New Mexico comments that in his opinion, many case reports over the past 50 years have erroneously suggested that T activation CAUSES hemolysis and that plasma used for infants with T activation should be screened for anti-T.
   
   A n exhaustive review of this topic is available in the first reference below (Crookston KP et al), along with experimental data supporting the argument that when hemolysis is seen it is not immune-mediated. The New Mexico colleague adds that another study (Boralessa, H et al., Transfusion, 2000) also suggested that there is no need for a low-titer anti-T inventory.
   
   He adds that in his opinion, the best studies ever done on the topic were published in Danish in a PhD dissertation by Poulsen (Poulsen, MPE, 1961. Polyagglutinabilitet og T-omdannelse. Medicine. Copenhagen, Denmark, University of Copenhagen: 186 pages.) This contains over one hundred tables of experimental evidence and also the data from two papers he published in the journal Nature in 1954. This work is also summarized in the first reference below by Crookston et al. but has been otherwise ignored in the English literature. That said, if clinicians are really worried, you can satisfy them by doing a simple minor crossmatch.
   
   The first two of the above-mentioned references are provided here
   • Crookston KP, Reiner AP et al. (2000). "RBC T activation and hemolysis: implications for pediatric transfusion management." Transfusion 40(7): 801-12 (no abstract).
   • Boralessa, H, Modi N et al. (2002). "RBC T activation and hemolysis in a neonatal intensive care population: implications for transfusion practice." Transfusion 42(11): 1428-34.

ADDENDA May 16, 2007

3. Editors' note: The Blood First Edition Paper by Jozsi M, et al. Anti-factor H autoantibodies block C-terminal recognition function of factor H in hemolytic uremic syndrome prepublished online May 10, 2007 may be germane to this discussion.

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