Twin blood group chimerism seems to be very rare in humans. The 30–40 previously reported cases usually were found by mere coincidence during routine blood grouping in hospitals or blood banks. Usually in these cases frank blood group mixtures of, for example, 50/50%, 25/75%, or 5/95% at most were seen. Smaller percentages are very difficult to notice during routine work‐up. Using a sensitive fluorescence technique (sensitivity >0.01%) we detected blood group chimerism in 32/415 (8%) twin pairs and 12/57 (21%) triplet pairs, respectively, which is a higher incidence than reported previously. © 1996 Wiley‐Liss, Inc.

We studied the value of leukocyte depletion of platelet transfusions for the prevention of secondary human leukocyte antigen (HLA)- alloimmunization in patients with a high-risk of prior immunization induced by pregnancies. Seventy-five female patients with hematologic malignancies (mostly acute leukemia) and a history of pregnancy were randomized to receive either standard random single-donor platelet transfusions (mean leukocytes, 430 x 10(6) per transfusion) or leukocyte-depleted random single-donor platelet transfusions. Leukocyte depletion to less than 5 x 10(6) leukocytes per platelet transfusion (mean leukocytes, 2 x 10(6) per transfusion) was achieved by filtration. Of the 62 evaluable patients, refractoriness to random donor platelets occurred in 41% (14 of 34) of the patients in the standard group and in 29% (8 of 28) of the patients in the filtered group (P = .52); anti-HLA antibodies developed in 43% (9 of 21) of individuals in the standard group and 44% (11 of 25) of cases in the filtered group. The time toward refractoriness and development of anti- HLA antibodies was similar for both groups. We conclude that leukocyte depletion of random single-donor platelet products to less than 5 x 10(6) per transfusion does not reduce the incidence of refractoriness to random donor platelet transfusion because of boostering of anti-HLA antibodies.

943. 9. Mitsuishi Y, Urlacher A, Mayer S, Tongio MT. DNA-RFLP studies of the 72 core cell lines selected for the Southern blot protocol. In: Histocompatibility testing 1987. (Immunology of HLA. Vol. 1.) New York: Springer, 1989; 916. 10. Long EO, Wake CT, Gorski J, Mach B. Complete sequence of an HLA-DRB chain deduced from a cDNA clone and identification of multiple non-allelic DRB chain genes. EMBO J 1983; 2: 289 11. Auffray C, Lillie JW, Korman AJ, et al. Structure and expression of HLA-DQ and -DX genes: intrallelic alternate splicing of the HLA-DQ gene and functional splicing of the HLA-DX gene using a retroviral vector. Immunogenetics 1987; 26: 63. 12. Sheldon EL, Kellogg DE, Watson R, Leverson CH, Erlich HA. Use of nonisotopic M13 probes for genetic analysis: application to HLA class II loci. Proc Natl Acad Sci USA 1986; 83: 9085 13. Roux-Dosseto M, Auffray C, Lillie W, et al. Genetic mapping of a human class II antigen B-chain cDNA to the SB region of the HLA-complex. Proc Natl Acad Sci USA 1983; 80: 6036 14. Erlich H, Stetler D, Sherg-Dong R, Saiki R. Analysis by molecular cloning of the human class II genes. Fed Proc 1984; 43: 15. 15. Terasaki PI, Bernoco D, Par MS. Microdroplet testing for HLA-A, B, and D antigens. Am J Clin Pathol 1978; 69: 103 16. Dupont B, Brown DW, Yunis EJ, Carpenter CB. HLA-D by cellular typing. In: Terasaki PI, ed. Histocompatibility testing 1980. Los Angeles: UCLA Tissue Typing Laboratory, 1980. 17. Martell RW, Oudshoorn M, May RM, Du Toit ED. Restriction fragment length polymorphism of HLA-DRw53 detected in South African blacks and individuals of mixed ancestry. Hum Immunol 1989; 26: 237. 18. Kaminski ER. How important, is histocompatibility in bone marrow transplantation? Bone Marrow Transplant 1989; 4: 439. 19. Anasetti C, Amos D, Beatty PG, et al. Effect of HLA compatibility on engraftment of bone marrow transplantations in patients with leukemia or lymphoma. N Engl J Med 1989; 320: 197. 20. AL-Daccak R, Loiseau P, Soulie A, et al. HLA-DP genotyping in HLA-A,B, and DR identical intrafamilial bone marrow trans plantation. Leukemia 1990; 4: 222. 21. Pawelec G, Ehniger G, Schmidt H, Wernet P. HLA-DP matching and graft-versus-host disease in allogenic bone marrow trans plantation. Transplantation 1986; 42: 558. 22. Oaks MK, Carmer DV. The genetics of bone marrow transplanta tion in the rat. Transplantation 1985; 39: 69. 23. Beatty PG, Clift RA, Mickelson EM, et al. Marrow transplantation from related donors other than HLA-identical siblings. N Engl J Med 1985; 313: 765. 24. Kaminski E, Hows J, Man S, et al. Prediction of graft versus host disease by frequency analysis of cytotoxic T cells after unrelated donor bone marrow transplantation. Transplantation 1989; 48: 608. 25. Kaminski E, Sharrock C, Hows J, et al. Frequency analysis of cytotoxic T lymphocyte precursors: possible relevance to HLAmatched unrelated donor bone marrow transplantation. Bone Marrow Transplant 1988; 3: 149. 26. Howard MR, Hows JM, Gore SM, et al. Unrelated donor marrow transplantation between 1977 and 1987 ...

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Analysis of erythrocyte populations, using red blood cell antigen differences between host and donor as marker, was performed with a sensitive fluorescent microsphere assay to monitor marrow engraftment and mixed red cell chimaerism after allogeneic bone marrow transplantation (BMT). An adapted transfusion policy, using marker negative erythrocyte transfusions, was required for this analysis. In all patients the marrow graft was depleted of lymphocytes by counterflow centrifugation. Thirty-seven patients were evaluable for donor repopulation at one or more points in the first 6 months after BMT. At 0.5 month donor erythrocytes were detectable in 19 out of 22 patients. At 6 months donor erythrocytes were detectable in 100% of the evaluable patients. In the first 3 months after BMT the average donor erythrocyte repopulation in recipients of major ABO mismatched transplantations was delayed. Thirty-eight patients were evaluable for chimaerism at 6 months or later after BMT. A high incidence of mixed red cell chimaerism was observed varying from 50% to 71% at different points of analysis. Mixed red cell chimaerism with low percentages (less than 1%) of host cells was not related with relapse, nor did high percentages (greater than 10% of host cells necessarily indicate relapse.

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This article reports the first case of immune hemolytic anemia possibly associated with the ingestion of suprofen. The patient suffered from massive hemoglobinuria and acute renal failure. Serologic studies of the patient's serum revealed suprofen-dependent red cell antibodies. However, tolmetin-dependent antibodies were also found in the serum, showing the same properties as the suprofen antibodies and an even higher titer. The patient not only had drug-dependent antibodies in the serum, but also had developed autoantibodies, a phenomenon that has been described for several other drugs. The working mechanism by which suprofen and tolmetin caused immune hemolysis had properties of both the immune complex model and the induction of autoimmunity. Although it was unclear whether the immune hemolytic anemia was the result of suprofen, tolmetin, or cross-reacting antibodies, we feel that suprofen should be added to the list of nonsteroidal anti-inflammatory drugs associated with a positive direct antiglobulin test.

The purpose of this study was to determine the predictive value and reliability of using a 'critical titre' when assessing the ability of red cell alloantibodies to cause haemolytic disease of the newborn. Titration studies and clinical follow-up of 418 antenatal cases where the mothers had red cell antibodies were studied retrospectively. The antibody specificities were anti-D (n = 359), anti-c (n = 34), anti-E (n = 19) and anti-K (n = 6). Depending on the titre being lower or higher than 16 in the indirect antiglobulin test, the severity of disease was established on the given therapy. Anti-D antibodies with a titre 16 were present in 20% of all cases associated with transfusion need of the child; for anti-c, -E and -K the figure was 4%. Titres> or = 16 resulted in both groups in 50% of the cases in phototherapy only, or no therapy at all. Titres are therefore not reliable indicators for predicting the severity of haemolytic disease of the newborn. Neither should they be used as a guide to whether or not antenatal intervention is indicated. Alternative quantitative or functional assays that measure cytotoxic lysis or phagocytosis or a combination of both should be performed instead.