Incompatible crossmatch: First sign of a hemolytic transfusion reaction due to out-of-group platelet transfusion.

Platelet (PLT) transfusion is undertaken in a variety of clinical settings with thrombocytopenia, with or without bleeding. Since PLTs are most often stored in donor plasma, group-specific PLT transfusions are preferred to out-of-group transfusions. PLTs adsorb ABO antigens over their surface from the plasma. In major ABO-incompatible PLT transfusions, anti-A/B from the patient plasma react with the ABO antigens on transfused PLTs and can potentially cause adverse reactions or PLT refractoriness. Transfusion of PLTs with major ABO incompatibility, though effective in preventing clinical bleeding, is associated with reduced posttransfusion PLT count increments. In minor incompatible PLT transfusion transfused, anti-A/B can cause hemolytic transfusion reaction (HTR) which is not always related to a high titer of anti-A/B in the donor. Although attempts are made to practice ABO identical PLT transfusion, most centers practice out-of-group random donor platelets (RDPs) as well as single-donorplatelets (SDP) transfusion. The limited PLT shelf life does not always permit ABO identical PLT transfusion. At our center, ABO-specific PLT transfusions are practiced where possible, and in case of minor ABO-incompatible transfusions, antibody titers are not done. Here, we report a case of HTR due to out-of-group SDP transfusion, detected in the laboratory after an incompatible red blood cell (RBC) crossmatch.

Clinical and laboratory profile of anti-M.

CONCLUSIONS: Anti-M is a frequently detected naturally occurring antibody that has been reported in various clinical settings and also in voluntary donors. We describe here the clinical and laboratory findings of 11 cases with anti-M detected at our center. This report is a retrospective study in which we reviewed our immunohematology laboratory records for cases involving anti-M. Both donor and patient data from a 28-month period (September 2014 to December 2016) were reviewed. During this period, 11 examples of anti-M were detected (8 patients, 1 voluntary whole blood donor, and 1 hematopoietic stem cell donor. Anti-M was also detected in one external quality assessment scheme sample received during this period. In conclusion, anti-M can be detected in various clinical settings. This antibody can be clinically significant; in the laboratory, it can present as a serologic problem such as an ABO group discrepancy or an incompatible crossmatch. After detection, management and course of action is determined by both the antibody characteristics and the clinical setting.

Blood Group Discrepancy-First Sign of Autoimmune Hemolytic Anemia after Hematopoietic Stem Cell Transplantation in a Child.

A 12-year-old male child was presented in the emergency with features of anemia and mild icterus on day+67 of HSCT. The child was suffering from Fanconi anemia and undergone HSCT from ABO-matched, fully HLA matched sibling donor. The diagnosis of mixed type AIHA due to cytomegalovirus reactivation was made in the immunohematology laboratory and blood group discrepancy was the first sign of AIHA in this patient. Though the cold agglutinin titer was not significant but the clinical symptoms and laboratory evidences were suggestive of significant hemolysis due to underlying IgG autoantibody. In addition the high complement avidity of IgM autoantibody might also be a contributing factor for clinically significant hemolysis in this case. The patient was successfully treated with phenotype matched blood transfusion, rituximab and oral steroid therapy.

Warm autoimmune hemolytic anemia with mimicking anti-e specificity causing intravascular hemolysis in a chronic ITP patient.

A 12-year-old male child presented to the emergency room with three days history of cola-colored urine, mild icterus, dyspnea, palpitation and fatigue. He had a history of chronic ITP two years ago and had since been on steroid for maintenance of platelet count. He was subsequently diagnosed as a case of warm autoimmune hemolytic anemia. Laboratory investigations were suggestive of intravascular hemolysis, and on immuno-hematological evaluation it was diagnosed that the patient had autoantibody with mimicking anti-e specificity. The specificity of autoantibody was further confirmed by adsorption study. The patient was successfully managed by transfusion of Rh(e)-negative red cells,steroid and rituximab therapy. So an autoantibody with mimicking anti-e specificity was identified in this case, which was significant in clinical point of view.