However, most of the times, these patients have history of multiple transfusions making phenotyping of patients unreliable. patient’s self-antigens and evidence of anemia. Many a times, anemia is severe enough to warrant reddish cell component transfusion. Warm-reactive autoantibodies interfere in the pretransfusion screening. These red blood Acitretin cell (RBC) autoantibodies present in patient’s serum potentially react with all the cells of antibody identification panel giving pan-reactive picture and making alloantibody identification complex. However, identifying the alloantibodies in these cases is usually important to prevent the occurrence of severe hemolytic reaction. In untransfused patients, the estimated incidence of alloantibody formation after blood transfusion ranges from 0.5% to 1%.[1] In chronically transfused patients, this risk increases to 20%C60%.[2] Likewise in AIHA patients, over one-third to one-half of patients have underlying alloantibody(s).[3] Patients of -thalassemia major are dependent on regular blood transfusion for entire lifetime. The development of antibodies against RBC antigen which may be alloantibody or autoantibody further complicates the transfusion therapy. It is in these patients with autoantibodies that this transfusion requirements are also high. Many a occasions, these patients do not get appropriately matched blood models and get access to Rabbit Polyclonal to GALK1 only partially compatible or incompatible blood for transfusion. The problem is usually that autoantibodies mask underlying alloantibodies and failure to recognize alloantibody(s) may cause hemolytic transfusion reactions which may be at times even life threatening and also limit the availability of subsequent safe transfusion(s). Finding the compatible blood models in thalassemia patients with existing antibody(s) is usually a tedious and complex process and needs immunohematological expertise and specialized reagents in a well-equipped immunohematology (IH) laboratory. In this statement, we present our approach in a thalassemia patient presented Acitretin with 5.8 g hemoglobin with AIHA. Case Statement A 23-year-old male known case of -thalassemia major presented with severe anemia and was denied compatible blood at other hospitals before being referred to our hospital. He was admitted in hemato-oncology unit for blood transfusion since his hemoglobin was 5.8 at admission and experienced marked pallor and other symptoms of anemia. Antibody screen was pan reactive. With this clinical information, the sample was sent to our IH reference laboratory for workup. Initial immunohematology workup Forward blood grouping was AB positive, while in reverse grouping, there was 3+ agglutination reaction with all reagent cells (A, B, and O cells). Antibody screen was repeated and found to be pan reactive with evidence of hemolysis. Auto-control and direct antiglobulin test (DAT) was 3+ positive. This picture of anemia Acitretin with positive DAT and auto-control was suggestive of possible AIHA. Blood grouping was carried out by conventional tube technology (CTT), and DAT was carried out on polyspecific antihuman globulin (AHG) column agglutination card (Ortho Clinical Diagnostics; Mumbai, India). Repeat forward grouping (warm saline washes) Forward grouping in CTT was repeated after washing the reddish cells of the patient three times with warm normal saline as per Departmental Standard Operating Procedure. The blood group of the patient was now confirmed as O Rh D unfavorable Acitretin (instead of initial false-positive typing as AB positive). Monospecific direct antiglobulin test DAT was repeated Acitretin using monospecific card (IgG, C3d, and Control; Ortho Clinical Diagnostics; Mumbai, India) to identify the type of sensitization. Results showed IgG positive and C3d unfavorable. Control was unfavorable which validated the results. This picture was suggestive of warm type of AIHA. Direct antiglobulin test-IgG dilution and IgG subclasses On IgG dilution studies, anti-IgG titer of 1000 was recognized. This titer was clinically relevant indicating risk of hemolysis and necessity to do IgG subclasses. Patient’s reddish cells were treated to identify responsible IgG subclass for sensitization. IgG1 and IgG3 were positive. Elution Acid elution (Bag Systems; Germany) was performed to free the IgG.