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| | | Year : 2011 | Volume : 54 | Issue : 1 | Page : 170-172 | | | Naturally occurring anti M complicating ABO grouping | | | Safoorah Khalid1, Roelyn Dantes2, Sunu Varghese2, Imadeddin Al Hakawati2
1 Royal Darwin Hospital, NT, Australia
2 Dr. Sulaiman Al Habib Medical Center, Olaya, Riyadh, Saudi Arabia
Click here for correspondence address and email | Date of Web Publication | 7-Mar-2011 | | |      | |  Abstract | | | Anti M is considered a naturally occurring antibody that is usually active at temperatures below 37°C and is thus of no clinical significance. This antibody, if present in an individual, can lead to a discrepancy between forward and reverse ABO grouping and thus creates diagnostic difficulties for blood bank staff. We report a case of a 58-year-old lady who had an unexpected reaction in reverse grouping due to anti M that posed a problem for us in the interpretation of results of her blood group. We also reviewed the literature to find out the significance of such discrepancy in blood grouping. Keywords: ABO discrepancy, anti M, blood grouping, naturally occurring antibody How to cite this article:
Khalid S, Dantes R, Varghese S, Al Hakawati I. Naturally occurring anti M complicating ABO grouping. Indian J Pathol Microbiol 2011;54:170-2 |
| Introduction | |  |
Anti M is a naturally occurring saline agglutinin that was first identified by Wolff and Johnson in 1933. [1],[2] It is the most commonly encountered antibody of the MNS system. [1] Most examples of anti M are reactive at temperatures below 37°C, with an optimum temperature of 4°C, and are considered to be clinically insignificant. [3] However, rarely, the antibody agglutinates red cells at 37°C or at the antiglobulin phase of testing and can lead to hemolytic transfusion reactions and hemolytic disease of the newborn (HDN). [1],[4],[5],[6]
In our experience, this is the first case of anti M that was encountered during routine ABO/Rh typing and complicated the interpretation of our results. We identified the antibody after excluding the possibility of subgroup of A.
| Case Report | | |
A blood sample of a 58-year-old female was received for ABO/Rh typing. Blood grouping was performed by conventional test tube technique and gel technique (DiaClon ABO/D + reverse grouping for patients, Diamed-ID Microtyping system, Cressier Sur Morat, Switzerland) by two operators. The result is shown in [Figure 1] and it can be seen that there is an extra reaction with A cells in reverse grouping. Testing on the fresh sample also revealed the same results. At this time, the patient was also inquired about her past and present history. She was a Filipino lady and married with three successful and uneventful pregnancies. She never received any blood transfusion.
After excluding the possibility of technical errors, further testing was employed. The red cells were tested with anti A1 lectin; however, agglutination of red cells with anti A1 excluded the possibility of subgroup of A. Direct antiglobulin test and autocontrol were negative, ruling out the presence of autoantibody. Antibody screening was then performed with four cell panel (ID-DiaScreen I, II, III, 1V; Diamed-ID Microtyping system) and was found to be positive (+3) with screening cells I, II and IV. Screening was also done by manual method and it revealed the positive results with same cells at immediate spin. Subsequently, antibody identification (ID-DiaPanel, Diamed-ID Microtyping system) was carried out and the antibody identified after crossing out was anti M [Table 1]. We then tried to remove the antibody from the serum by incubating at room temperature with known M-positive red cells that demonstrated dosage. Reverse grouping was performed after this procedure and agglutination was observed with B cells only, and thus forward grouping now correlated with reverse grouping.
The antibody was reactive at temperatures below 37 ° C and thus regarded as clinically insignificant.
| Discussion | | |
Despite the introduction of methods to avoid interference with the results of pretransfusion testing, cold alloantibodies still yield unexpected reactions in ABO/Rh typing and create a nuisance for blood group serologists. Majority of these antibodies including anti M antibodies are IgM antibodies that are not active at 37°C and the discrepancy can be resolved by performing the testing at strict warm temperatures. [1] Thus, these are not clinically significant and can be ignored in transfusion practice. However, sometimes, anti M is reactive at 37°C and at the antihuman globulin phase; in this case, the importance of these antibodies cannot be ignored because of the potential to cause hemolytic transfusion reactions and HDN. [4],[5],[6] Hence, the test results must be interpreted cautiously.
Anti M shows dosage effect and this was noted in our patient also, stronger reaction with homozygous cells (M+N-) than cells (M+N+). [1] These antibodies are also pH dependent and have an optimum pH of 6.5. Below this pH, these are inactive and therefore nonspecific.
The frequency of anti M in routine blood donors is 1 in 2500 to 5000. [7] Because of the rarity of these antibodies, only case reports and case series have been published. The largest series is reported from Severance hospital during 1985-1992 and there were 20 patients with naturally occurring anti M antibodies. [8] There was no evidence of HDN or hemolytic transfusion reaction in these patients. However, HDN has been reported as a result of anti M and even intrauterine deaths have been reported. [6],[9],[10] Delayed hemolytic transfusion reactions have also been observed in association with anti M antibodies. [4],[5] Fortunately, in our patient, the antibody was clinically insignificant and there was no history of HDN in any of the three pregnancies.
Based on the rare significance of these antibodies, it is extremely important to carefully interpret the results of blood grouping and pretransfusion testing in laboratories and it is wise not to release any discrepant results without resolution and confirmation.
| References | | |
| 1. | Brecher ME, editor. AABB Technical Manual. 14 th ed. Bethesda: American Association of Blood Banks; 2005. 
| | 2. | Wolff E, Johnson B. Studien uber die untergruppen A1 and A2 mit besonderer berucksichtigung der paternitasuntersuchungen. Dtsh Ztschr Gerichtl Med 1933;22:65-85.
| | 3. | Tondon R, Kataria R, Chaudhry R, Anti M. Report of two cases and review of literature. Asian J Transfus Sci 2008;2:81-3.
[PUBMED]  | | 4. | Alperin JB, Riglin H, Branch DR, Gallagher MT, Petz LD. Anti M causing delayed transfusion reaction. Transfusion 1983;23:322-4
| | 5. | Sancho JM, Pujol M, Fernandez F, Soler FM, Manzano P, Felio E. Delayed hemolytic transfusion reaction due to anti M antibody. Br J Haematol 1998;103:268-9.
| | 6. | Duguid JK, Bromilow IM, Entwistle GD, Wilkinson R. Hemolytic disease of the newborn due to anti M. Vox Sanguinis 1995;68:195-6.
[PUBMED] | | 7. | Klein HG, Anstee DJ. Othere red cell antigens. In: Klein HG, Anstee DJ, editors. Mollison's Blood transfusion in Clinical Medicine. 11 th ed. London: Blackwell Science; 2005. p. 209-52.
| | 8. | Kim HO, Choi MJ, Hong SG, Kwon OH. Anti M antibody identified in patients- 20 cases. Kor J Blood Transf 1992;3:173-7.
| | 9. | Furukawa K, Nakajima T, Kogure T, Yazaki K, Yoshida M, Fukashi T, et al. Example of a woman with multiple intrauterine deaths due to anti M who delivered a live child after plasmapheresis. Exp Clin Immunogenetics 1993;10:161-7.
| | 10. | Kanra T, Yuce K, Ozcebe IU. Hydrops fetalis and intrauterine deaths due to anti M. Acta Obstet Gynecol Scand 1996;75:415-7.
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Correspondence Address:
Safoorah Khalid
Department of Pathology, Royal Darwin Hospital, PO Box 41326, Casuarina, NT 0811
Australia
  | 4 |
DOI: 10.4103/0377-4929.77394 PMID: 21393909
[Figure 1]
[Table 1] | |
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