 Abstract | | |
The P blood group system was introduced in 1927 by Landsteiner and Levine. About 75% of the population possesses P1 phenotype. P2 simply implies P1 negative and there is no P2 antigen. Individuals with P2 may have anti-P1 antibodies in there serum are cold-reacting antibodies which are clinically insignificant and occasionally active at 20°C or higher temperatures. However, in certain cases, anti-P1 is clinically significant and may cause acute intravascular hemolytic transfusion reactions. Our case report confirms the complexity and difficulty in the diagnosis of anti-P1. In India, very few cases are reported regarding clinical significant anti-P1. Here, we report a case of IgM type of antibody anti-P1 which was reactive at 37°C and AHG phase in a 66-year-old female planned for Whipple's surgery, who had grouping discrepancies in reverse typing and incompatibility during routine crossmatch.
Keywords: Anti-P1, blood group discrepancy, blood transfusion, patient blood management
How to cite this article:
Thulasiram N, Sahoo D, Basavarajegowda A. Clinical significant anti-P1 antibody with wide thermal amplitude: A tale of successful blood management. Asian J Transfus Sci 2023;17:125-7 |
How to cite this URL:
Thulasiram N, Sahoo D, Basavarajegowda A. Clinical significant anti-P1 antibody with wide thermal amplitude: A tale of successful blood management. Asian J Transfus Sci [serial online] 2023 [cited 2023 Mar 21];17:125-7. Available from: https://www.ajts.org/text.asp?2023/17/1/125/356867 |
| Introduction | |  |
Landsteiner and Levine introduced P blood group system in 1927.[1] For many reasons, the terminology is confusing and now it was called as P1, not P. The antigen P is the only antigen of the GLOB system. Every P1 and P2 population has the antigen P on their red cells. Majority of the population are either P1 (about 75% of the English population) or P2, P2 simply implies P1 negative, and there is no P2 antigen.[2] Mostly, P2 population has anti-P1 in their serum as a cold reacting agglutinin which is occasionally active at 20°C or higher temperatures. P is formed by the action of a beta-1,3-GalNAc transferase, whereas P1 is formed by the action of an alpha 1,4 Gal transferase (A4GALT), so these antigens are genetically different.[3]
P1 was found on platelets, lymphocytes, and fibroblasts. Strains for certain organisms with adhesions specific for disaccharides agglutinate red cells from peoples of blood groups P1, P2 but not P. P1 has nonhuman origin present in echinococcus cyst fluid which can stimulate the production of anti-P1 in humans with hydatid disease. The P1 phenotype is present in 79% of Caucasians, 94% of African Americans, and 20% of Cambodians and Vietnamese.[4]
Anti-P1 antibody is frequently present in P2 individuals and most often naturally occurring. Nearly two out of three unselected P2 individuals possessing anti-P agglutinins were found in the serum. Normally, these agglutinins were very weak and active only at low temperatures.[5] P2 pregnant women, the anti-P1 frequency approximately 90% but no evidence was reported that was connected with alloimmunization in pregnancy.[6],[7] In men who had never had injections or transfusions of blood, the most potent anti-P1 sera was obtained.[8] The clear-cut immediate hemolytic transfusion reaction due to anti-P1 has been reported by Moureau (1945). Anti-P1 was undoubtedly reported for a delayed hemolytic transfusion reaction, with fall in packed cell volume and rise in serum bilirubin, in a patient whose plasma has a potent IgG anti-P1 active over a wide thermal range.[9]
Here, we report a case of IgM type of antibody, anti-P1 in a 66-year-old female, who had grouping discrepancy and cross match incompatible.
| Case Report | | |
A 66-year-old female was admitted to our hospital with diagnosis of periampullary carcinoma of the pancreas. Surgical management of malignancy was scheduled electively and submitted blood samples for routine typing and screening in the transfusion medicine department. Blood grouping was done by conventional tube technique. During forward grouping, it showed agglutination reaction to anti-B and anti-D anti sera just like a normal B positive blood group. However, during reverse grouping, the patient's sample showed strong agglutination reaction with A, B, and O group cells [Table 1]. Hence, a discrepancy was noted between forward and reverse grouping. Antibody Screening and Identification tests were done using commercially available 3- cell and 11- cell panels (Ortho Clinical Diagnostics, USA). In 3- cell panel, no reaction was seen in panel 1, while panel 2 and 3 showed positive reactions. In 11 cell panel, all panels were reactive except panel 5 and 10 [[Table 2] and 3]. Direct Coombs test and Auto Control test were negative. We observed that antibody might be IgM type because pan reactivity was given in reverse grouping, then the patient serum was evaluated through indirect antiglobulin test, against a panel of cells at 4°C, 24°C immediate spin, incubating for 10 min at 24°C and 37°C followed by AHG phase [Table 3]. The existence of anti-P1 antibody was confirmed with ruling in, ruling out which had stronger reaction at 4°C. The strength of reaction came down gradually from 4°C to 37°C which suggests that, it was a IgM type of antibody. Phenotyping of patient showed negative to P1 antigen and in view of surgical management of blood loss requested packed red blood cell (PRBC) to reserve during procedure. Five PRBC bags were cross matched. Three were found incompatible. Two bags which were compatible were phenotyped and found P1 antigen negative. Remaining incompatible PRBC bags were phenotyped and found to be P1 antigen positive. Postoperatively, the patient needed blood transfusion and two units of PRBC transfused. The transfusion was uneventful, patients hemoglobin improved, and subsequently she was discharged.
| Discussion | | |
About 67% of P2 individuals' posses anti-P1 antibody in their serum and most of them are naturally occurring. Two out of three P2 individuals will have anti-P1 agglutinins in their serum. In individuals with P2 phenotype with anti-P1 antibody, routine pretransfusion workup can be challenging and complex.[4] In reverse typing, it shows strong reaction with A, B, and O group cells. During antibody identification, this antibody reacts with all panel cells through a wide thermal range except the auto control and direct agglutination test. The routine antibody screening methods that are used to detect IgG antibodies have the potential to miss clinically significant IgM antibodies, particularly antibodies of lower strength. Smith et al. reported case of HTR mediated by IgM anti-P1 reactive at 37°C.[4] While anti-P1 is usually clinically insignificant and reactive at <25oC and can reactive at 37°C also.[2] Since the diagnostic workup of individuals with P1 phenotype is complex, these individuals can easily be misdiagnosed; our case report shows the meticulous workup toward ruling out anti-P1 antibodies.
| Conclusion | | |
Our case report confirms the complexity and difficulty in the diagnosis of anti-P1 which can be naturally occurring auto antibody-P1 reacting at wide thermal range. For elective procedures, all stakeholders must discuss and formulate the strategy well in advance for surgical management of blood loss.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 2. | Klein H, Anstee D, Mollison P. ABO, H, LE, P1PK, GLOB, I and FORS blood group systems. In: Mollison's Blood Transfusion in Clinical Medicine. Oxford: Wiley-Blackwell; 2014. |
| 3. | Thuresson B, Westman JS, Olsson ML. Identification of a novel A4GALT exon reveals the genetic basis of the P1/P2 histo-blood groups. Blood 2011;117:678-87. |
| 4. | Smith D, Aye T, Er LS, Nester T, Delaney M. Acute hemolytic transfusion reaction due to anti-P1: A case report and review of institutional experience. Transfus Med Hemother 2019;46:380-3. |
| 5. | Henningsen K. On the heredity of blood factor P. Acta Pathol Microbiol Scand 1949;26:769-85. |
| 6. | Cutbush M, Mollison PL. Relation between characteristics of blood-group antibodies in vitro and associated patterns of redcell destruction in vivo. Br J Haematol 1958;4:115-37. |
| 7. | Thakral B, Bhattacharya P, Agnihotri N, Sharma RR, Marwaha N, Gopalan S. Acute hemolytic transfusion reaction by anti-P1 antibody in pregnancy. Am J Hematol 2005;78:163-4. |
| 8. | Arndt PA, Garratty G, Marfoe RA, Zeger GD. An acute hemolytic transfusion reaction caused by an anti-P1 that reacted at 37 degrees C. Transfusion 1998;38:373-7. |
| 9. | DiNapoli JB, Nichols ME, Marsh WL, Warren D, Mayer K. Hemolytic transfusion reaction caused by IgG anti-P1. Transfusion 1978;18:383. |
Correspondence Address:
Nallagondla Thulasiram
Department of Transfusion Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Puducherry
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ajts.ajts_165_21
[Table 1], [Table 2], [Table 3], [Table 1], [Table 2], [Table 3] |
