Correspondence

DOUGLAS W. HUESTIS, M.D., Editor

Tucson. Arizonia

Anti-IgA in Blood Donors

To tbe Editor: Anaphylactoid transfusion reactions are very

rare (one per 20,000-50,000 transfusions), but are potentially lethal. Reports from multiple centers now agree that such reactions may result from the interaction of immunoglobulin A (IgA) in donor plasma with antibodies to IgA in recipient plasma. Subsequent transfusions in patients with proven susceptibility to reactions with donor IgA must be with compatible components. Red blood cells after very thorough washing, can usually be safely transfused into such patients although occasional patients react even when given previously frozen red blood cells deglycerolized by standard tech- niques. For such patients, and for all patients who require plasma components after having an anaphylactoid reaction caused by anti-IgA, components must be provided from blood donors whose plasma totally lacks IgA. Fortunately, such donors are easily found. On the average, ap- proximately one of every 900 apparently healthy blood donors lack IgA. IgA deficiency is easily de- tected by a simple gel diffusion technique. However, 26 per ceht of those samples which showed no precipitin lines on gel diffusion have measurable levels of IgA by more sensitive tech- niques such as hemagglutination inhibition or radioimmunoassay. The absence of IgA (aIgA) must be verified by one of these more sensitive techniques. The first registry of aIgA donors was established in San Francisco. More recently, registries have been established by the American National Red Cross, in Canada, in Denmark and in Finland.

It is clearly recognized that aIgA individuals are easily immunized to IgA. Usually such anti- bodies are class-specific; i.e., they react with red blood cells coated with all or almost all mo- noclonal IgA globulins. These antibodies are usually present in the absence of any obvious his- tory of stimulation such as transfusion, gamma globulin injection or pregnancy. Obviously, the aIgA blood donors themselves are at risk of form- ing antibodies to IgA. If the antibodies are strong, it appears reasonable to assume that these indi- viduals are also at risk of a serious transfusion reaction should they ever need a blood transfu-

sion. Blood centers which have detected donors with strong antibodies to IgA have an obligation to notify these donors of this potential risk. The blood centers should recommend that these donors carry with them at all times (on a bracelet or wallet card) notice that transfusion of blood components containing IgA may result in a serious reaction.

We define “strong” antibodies as those with a titer of at least 256 by hemagglutination assay. We know of no serious reactions in patients with class-specific anti-IgA with a titer lower than this. It could be argued that all aIgA donors should be notified of the potential transfusion reaction prob- lem, whether or not they have detectable anti- bodies at that time. The individual’s right to be told about anything which may have bearing on his future health needs to be balanced, however, with the risk of unnecessarily alarming large numbers of normal persons. At the present time, it is probably premature to make any recommenda- tions regarding aIgA donors who do not have strong antibodies.

For completeness, it should also be pointed out that anaphylactoid reactions have also been caused by anti-IgA in patients with normal levels of IgA. In those instances, the antibody has limited specificity, being directed at an IgA de- terminant which is the product of a genetic allele not possessed by the patient. In the four proven cases, reactions were attributed to anti-AZm( l), and could be avoided by transfusing either aIgA plasma or normal plasma with IgA of the AZm(- 1) phenotype. Antibodies to IgA-coated red blood cells are not uncommon in the general population, and detection of anti-IgA of limited specificity in a patient with normal IgA levels does not, in most instances, indicate a likelihood of transfusion reactions.

The clinical significance of anti-IgA of limited specificity remains unclear and no allotypes of the major gamma-Al subclass of human IgA have yet been defined. Therefore, further studies on anti- IgA of limited specificity are urgently needed. Nonhemolytic transfusion reactions should be carefully investigated to distinguish the roles of antibodies to IgA, IgG, other plasma protein, platelets and leukocytes. Comparison of pre- and posttransfusion antibody titers will be particularly

289 Transfusion May-JuZe 1976

Volume 16 Number 3

290 CORRESPONDENCE Transfusion May-June 1976

helpful in proving the clinical role of antibodies de- tected.--(;. N. Vyas and H. A . Perkins, Depart- ment of Laboratory Medicine, University of California and the Irwin Memorial Blood Bank, Son Francisco, California.

Bombay Phenotype

To the Editor:

Race and Sanger’s latest edition of Blood Groups in Man has a table on page 25 which lists Bombay (0,) and para-Bombay phenotypes found in various ethnic groups. Since they indicate that

there are no references in the medical literature describing these phenotypes in blacks, we wish to report the following case which is unremarkable except for race. In March, 1974, a nine-year-old American black girl admitted to Henry Ford Hos- pital for orthopedic surgery was found to have blood of the rare Bombay phenotype OR. The child was a ward of the court and had been placed in a foster home. The court refused to divulge family identity. In this case, the possibility of her being the result of a consanguineous mating could only be speculated on.-Kathryn M . Beattie. MT(ASCP)SBB, and Sheikh M . Saeed, M.D. . Red Cross Blood Center and Henry Ford Hos- pital, Detroit Michigan.

Announ cement The Center for Immunology, State University of New York a t Buffalo, announces

the Fifth International Convocation on Immunology to be held June 7-10, 1976 a t Grand Island, New York. The theme of the program “Human Blood Groups” will in- clude presentation of papers by distinguished scientists internationally recognized as experts on the topics: red blood cell antigen-antibody interactions; chemistry of blood group antigens; blood group soluble antigens; ABH subgroups and variants; Ii blood group antigens; expansion of the Lutheran and Kell blood group systems; blood group antigens affecting the erythrocytic membrane; and red cell antigens on other cells. Further information may be obtained by contacting Dr. James F. Mohn, Direc- tor, The Center for Immunology, Room 210 Sherman Hall, State University of New York a t Buffalo, Buffalo, New York 14214.