Letter to the Editor Vox Sang 1992;63:238
A .J . M . de Mana B.A. vun Dijk" G. L. Daniels' "
"
Blood Transfusion Service, University Hospital, Nijmegen, The Netherlands; Medical Research Council Blood Group Unit, London, UK
Antibodies to the Anton antigen were first mentioned in 1972 by Boorman and Tippett [1] and anti-Wj was first reported in 1983 by Marsh et al [2]. It subsequently became apparent that anti-Anton and anti-Wj were antibodies detecting the samc determinant [3,4], and in 1986 the new name AnWj was given to both Anton and Wj [S]. AnWj is a high-incidence antigen phenotypically related to the Lutheran blood group system. The antigen is absent o r has weak expression on Lu (a-b-) red cells of persons with the dominant inhibitor gene In(Lu). Antibodies to AnWj have been found to be of no clinical significance [6]. In this report we describe an example of an anti-AnWj causing haemolytic transfusion reactions. A 64-year-old male with a known paraproteinaemia (Waldenstrom's macroglobulinaemia), receiving 5 mg prednisone daily, required therapeutic red cell transfusions. In pre-transfusion testing a non-specific alloantibody was found reactive by indirect antiglobulin techniques with all red cells tcstcd except the patient's own cells. Blood transfusions were given with group 0, rr, K-, Wr (a-) red cells. At three separate occasions, the patient developed severe transfusion reactions with high body temperature, shaking fever and haemoglobinurea. L D H and bilirubin were increased. No lymphocytotoxic antibodies could be detected. Also, no other allo-antibodies to red cclls were detected after absorption of the patient's serum with red cells of different phenotypes. The patient's red cells were grouped as follows: 0,MMSs, Pl(+). rr(cde/cde), Lu (a-b+), K-k+, Kp ( a - b f ) , Le (a-b+), Fy (a+b-), Jk (a+b+). A"Cr-survival test was performed with 20 ml of weakly cross-match-incompatible red cells which underwent significant destruction; the 1- and 2.5-hour samples showcd 65 and 58% survival. respectively. The disappearance of
An Example of Anti-AnWj Causing Haemolytic Transfusion
the red cells is described by a two-component curve. The first component has a calculated half-life of 0.5 h; the second component has a half-life of 50 h. Again, the patient had a transfusion reaction. T h e antibody reacted with all cells of common Lutheran phenotypes tested, but did not react with Lu (a-b-) samples of the In(Lu) type o r with cord red cell samples. It reacted with Lu (a-bf) red cells treated with papain, trypsin, chymotrypsin, pronase o r 2-aminoethylisothiouroniumbromide; a pattern of reactions typical of anti-AnWj but not of antibodies to Lutheran system antigens which are destroyed by trypsin, chymotrypsin o r 2-aminoethylisothiouroniumbromide [6]. The antibody dit not react with AnWjnegative red cellsobtained from a member of the only reported family demonstrating inheritance of the AnWj-negative phenotype [7]. The patient's red cells were AnWj-negative as determined by one human allo-antiAnWj and two murine monoclonal antiAnWj. Red cells of the patient's sister and 3 brothers were AnWj-positive. Anti-AnWj has been detected in individuals with either acquired o r inherited AnW,j-negative phenotypes [4,7], but it has not been possible to ascertain the background of the AnWj-negative phenotype of the patient described here.
.............................................. References I Boorman KE, Tippett P: Unpublished ohservations. 1972; cited i n : Blood groups in man. Oxford, Blackwell. 1975, pp 274-275. 2 Marsh WL. Brown PJ, Dinapoli J, et al: AntiWj: An autoantibody that defines a high-incidence antigen modified by the In (Lu) gene. Transfusion 1983:23: 128-130. 3 Poole J, Giles C: Anton and Wj, are they related? Transfusion 1985;25:443. 4 Mannessier L, Rouger P, Johnson CL, Mueller KA. Marsh WL: Acquired loss of red-cell Wj antigen in a patient with Hodgkin's disease. Vox Sang 1986;50:240-244. 5 The Working Party on Terminology of Red Cell Surface Antigens. Int Soc Blood Transfus Newslett 1987;34:5. 6 Daniels G: Blood Group Systems: Duffy, Kidd and Lutheran. Arlington. American Association of Blood Banks, 1988. 7 Poole J, Levene C. Bennett M, Sera R, van Alphen L. Spruell PJ: A familiy showing inhcritance ofthe Anton blood group antigen AnWj and independence of AnWj from Lutheran. Transfus Med 1991;1:245-251.
Acknowledgement We thank the Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, forconfirmationof our initial serological findings.
A.J.M. de Men. PliD Blood Transfwion Service University Hospital Nijmegrn. PB 9101 NL6500 HB Nijmegen (The Netherlands)
0 1992 S. Karger AG. Basel ~X~~2~91H~7/92/11~33~23X 52.75/(1
A .J . M . de Mana B.A. vun Dijk" G. L. Daniels' "
"
Blood Transfusion Service, University Hospital, Nijmegen, The Netherlands; Medical Research Council Blood Group Unit, London, UK
Antibodies to the Anton antigen were first mentioned in 1972 by Boorman and Tippett [1] and anti-Wj was first reported in 1983 by Marsh et al [2]. It subsequently became apparent that anti-Anton and anti-Wj were antibodies detecting the samc determinant [3,4], and in 1986 the new name AnWj was given to both Anton and Wj [S]. AnWj is a high-incidence antigen phenotypically related to the Lutheran blood group system. The antigen is absent o r has weak expression on Lu (a-b-) red cells of persons with the dominant inhibitor gene In(Lu). Antibodies to AnWj have been found to be of no clinical significance [6]. In this report we describe an example of an anti-AnWj causing haemolytic transfusion reactions. A 64-year-old male with a known paraproteinaemia (Waldenstrom's macroglobulinaemia), receiving 5 mg prednisone daily, required therapeutic red cell transfusions. In pre-transfusion testing a non-specific alloantibody was found reactive by indirect antiglobulin techniques with all red cells tcstcd except the patient's own cells. Blood transfusions were given with group 0, rr, K-, Wr (a-) red cells. At three separate occasions, the patient developed severe transfusion reactions with high body temperature, shaking fever and haemoglobinurea. L D H and bilirubin were increased. No lymphocytotoxic antibodies could be detected. Also, no other allo-antibodies to red cclls were detected after absorption of the patient's serum with red cells of different phenotypes. The patient's red cells were grouped as follows: 0,MMSs, Pl(+). rr(cde/cde), Lu (a-b+), K-k+, Kp ( a - b f ) , Le (a-b+), Fy (a+b-), Jk (a+b+). A"Cr-survival test was performed with 20 ml of weakly cross-match-incompatible red cells which underwent significant destruction; the 1- and 2.5-hour samples showcd 65 and 58% survival. respectively. The disappearance of
An Example of Anti-AnWj Causing Haemolytic Transfusion
the red cells is described by a two-component curve. The first component has a calculated half-life of 0.5 h; the second component has a half-life of 50 h. Again, the patient had a transfusion reaction. T h e antibody reacted with all cells of common Lutheran phenotypes tested, but did not react with Lu (a-b-) samples of the In(Lu) type o r with cord red cell samples. It reacted with Lu (a-bf) red cells treated with papain, trypsin, chymotrypsin, pronase o r 2-aminoethylisothiouroniumbromide; a pattern of reactions typical of anti-AnWj but not of antibodies to Lutheran system antigens which are destroyed by trypsin, chymotrypsin o r 2-aminoethylisothiouroniumbromide [6]. The antibody dit not react with AnWjnegative red cellsobtained from a member of the only reported family demonstrating inheritance of the AnWj-negative phenotype [7]. The patient's red cells were AnWj-negative as determined by one human allo-antiAnWj and two murine monoclonal antiAnWj. Red cells of the patient's sister and 3 brothers were AnWj-positive. Anti-AnWj has been detected in individuals with either acquired o r inherited AnW,j-negative phenotypes [4,7], but it has not been possible to ascertain the background of the AnWj-negative phenotype of the patient described here.
.............................................. References I Boorman KE, Tippett P: Unpublished ohservations. 1972; cited i n : Blood groups in man. Oxford, Blackwell. 1975, pp 274-275. 2 Marsh WL. Brown PJ, Dinapoli J, et al: AntiWj: An autoantibody that defines a high-incidence antigen modified by the In (Lu) gene. Transfusion 1983:23: 128-130. 3 Poole J, Giles C: Anton and Wj, are they related? Transfusion 1985;25:443. 4 Mannessier L, Rouger P, Johnson CL, Mueller KA. Marsh WL: Acquired loss of red-cell Wj antigen in a patient with Hodgkin's disease. Vox Sang 1986;50:240-244. 5 The Working Party on Terminology of Red Cell Surface Antigens. Int Soc Blood Transfus Newslett 1987;34:5. 6 Daniels G: Blood Group Systems: Duffy, Kidd and Lutheran. Arlington. American Association of Blood Banks, 1988. 7 Poole J, Levene C. Bennett M, Sera R, van Alphen L. Spruell PJ: A familiy showing inhcritance ofthe Anton blood group antigen AnWj and independence of AnWj from Lutheran. Transfus Med 1991;1:245-251.
Acknowledgement We thank the Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, forconfirmationof our initial serological findings.
A.J.M. de Men. PliD Blood Transfwion Service University Hospital Nijmegrn. PB 9101 NL6500 HB Nijmegen (The Netherlands)
0 1992 S. Karger AG. Basel ~X~~2~91H~7/92/11~33~23X 52.75/(1
