Immunohematology最新文献

Variant D antigens can cause variable serologic results when typing with Anti-D reagents. There is limited information regarding the ability of Anti-D reagents to differentiate between D variants defined by RHD genotyping. This study was performed to determine if a panel of 20 U.S. Food and Drug Administration-licensed Anti-D reagents can identify molecularly defined D variants. Red blood cells from 119 donors carrying variant RHD alleles were tested at immediate spin (IS) and/or by the indirect antiglobuin test (IAT) using conventional test tube and/or column agglutination technology. Reaction strength at IS and IAT was reviewed to determine whether a pattern of reactivity could be correlated with a specific D variant. Agglutination results from each sample with each Anti-D reagent were combined to assess overall reactivity. The sample set consisted of 21 D variants, based on prior RHD genotyping. Of these variants, nine categories had three or more samples used for analysis (N = 102); 25 RHD*01W.1, 15 RHD*01W.2, 14 RHD*01W.3, 17 RHD*09.01, 14 RHD*09.03, 4 RHD*01W.4, 23 RHD*07, 4 RHD*10.05, and 6 reference allele RHD*01. As expected, IS showed more negative or weak reactions, and IAT produced more positive reactions with 3+/4+ agglutination strength. RHD*01W.3 samples showed strongest reactivity at IS and IAT. Greatest variation in reactivity was observed with RHD*01W.2, showing weakest overall reactivity at IS. All weak D types had at least one sample that yielded a negative result and one sample with 4+ agglutination at IS. Although there were general patterns of reactivity for each variant tested, no one pattern defined all samples carrying the same RHD allele. This study demonstrated that even with 20 different Anti-D reagents, serologic testing alone is insufficient to define weak or partial D types, characterize the risk for alloanti-D, or determine candidacy for Rh immune globulin. The results illustrate how multiple Anti-D reagents can be used to identify samples that should be reflexed to molecular testing.

A previously healthy 32-year-old male patient was admitted to hospital with malaise, dyspnea, anemia, thrombocytopenia, and leukopenia. Anemia and thrombocytopenia worsened during the third week. Considering the possible need for transfusion, routine ABO and D typing and an antibody detection test were performed. Antibody detection test was positive, necessitating fur ther immunohematologic investigation that revealed an antibody with Kell-related specificity and suppression/alteration of several high-prevalence Kell blood group system antigens. Autocontrols and direct antiglobulin tests (DATs) were negative in several samples during the disease course. Sequencing of the patient's KEL and XK genes did not reveal any mutations. Initial tentative diagnosis was myeloid neoplasm based on dyserythropoiesis in the bone marrow smear and no obvious biochemical signs of hemolysis. Azacitidine treatment was initiated, accordingly, but had to be interrupted when the patient's hemoglobin (Hb) dropped to 4.6 g/dL in 3 days, and he experienced more severe anemia symptoms (fatigue, nausea, and heart palpitations). Platelet concentrates, and 3 very rare Kell_null packed RBC concentrates, imported from abroad, were transfused. However, no increase in Hb was achieved. Platelet autoantibodies were not detected. Suspecting an autoimmune etiology, intravenous immunoglobulin and high-dose glucocorticoids were given. The patient responded to the latter treatment; he felt much better and regained his daily activity, and his Hb value and platelet count normalized on day 45. The steroid dose was tapered during the next 6 months until it was discontinued. His RBCs had normal Kell antigen expression, and the antibody was undetectable on day 105. Therefore, we concluded that an autoimmune etiology was the most plausible cause for the patient's condition despite a negative DAT. The immunohematologic investigation showed disease-related transient loss and/or alteration of several Kell system high-prevalence antigens and a Kell-related antibody that appeared to recognize a unique high-prevalence Kell antigen with a not-yet fully defined epitope.

Anti-IH is a common cold agglutinin that is typically clinically insignificant. We present a case that resulted in hemolysis. A 32-year-old male patient with transfusion-independent beta-thalassemia intermedia presented with symptomatic anemia. His blood sample typed as group B, D+ and demonstrated multiple alloantibodies and cold autoantibodies. He was transfused uneventfully, but re-presented 10 days later with recurrent, worsening anemia. At this time, transfusion of group O, phenotype-matched red blood cells (RBCs) resulted in an acute hemolytic reaction. While anemia was initially attributed to drug-mediated bone marrow toxicit y and subsequently to a delayed hemolytic reaction, further evaluation revealed Mycoplasma pneumoniae infection and a cold agglutinin (anti-IH specificity), indicating a likely autoimmune-mediated anemia due to an infectious etiology. Subsequent transfusion of 2 group B, phenotype-matched RBC units using a blood warmer was uneventful. Anti-IH is only rarely associated with hemolytic transfusion reactions, which may be exacerbated when transfusing group O RBC units to group B patients. M. pneumoniae infection likely led to cold agglutinin-mediated hemolysis of endogenous and transfused RBCs. The patient was successfully managed with intravenous immunoglobulin, steroids, rituximab, erythropoietin, hydroxyurea, and amoxicillin clavulanate/azithromycin. This case illustrates the importance of infectious disease evaluation in patients with unexplained anemia, the potential clinical significance of autoanti-IH, and the value of providing type-specific RBC units in these circumstances.

Distinguishing anti-D, anti- C, and anti-G specificities is particularly essential in antenatal cases to ensure proper patient management. The clinical management as well as Rh immune globulin (RhIG) prophylaxis depend on the accurate identification of these distinct antibodies. D- pregnant women with anti-G, but without anti-D, in their serum need RhIG prophylaxis at 28 weeks of gestation, at delivery if the infant is D+, and when clinically indicated to prevent the formation of anti-D and potential hemolytic disease of the fetus and newborn (HDFN). We present two cases in which determining the antibody specificities determined the course of the patient's treatment. In one case, a 30-year-old, gravida-1, para-0 woman with blood group A, D- and with no previous RhIG administration had the presence of anti-D, -C, and -G in her plasma. Because she had already been alloimmunized and developed anti-D, RhIG prophylaxis was not necessary. In another case, a 37-year-old, gravida-2, para-1 woman with blood group A, D- and no prior RhIG administration had anti-C and anti-G in her plasma. Because she was not sensitized to D, she needed RhIG prophylaxis. In conclusion, pregnant women can develop anti-C and/or anti-G in the absence of anti-D. Therefore, studies should be conducted to differentiate anti-D, -C, and -G in pregnant women who are presumptively identified as having anti-D and anti-C when their medical history (RhIG prophylactic therapy) suggests that anti-D may not actually be present. In the absence of anti-D, pregnant women should receive prophylaxis with RhIG to prevent alloimmunization to D. For pregnant women who are already sensitized to D, RhIG prophylaxis is not needed.

Red blood cell (RBC) alloimmunization can occur because of exposure to various sensitizing factors and poses a constant threat in transfusion. Assisted reproductive technology (ART) involves manipulation of sperm, ova, or embryos in vitro with the goal of producing a pregnancy. We present an interesting case of ART-induced maternal alloimmunization (AIMA) due to anti-c in a woman carrying a twin pregnancy. A 35-year-old primigravida, whose blood sample typed as group B, D+ and showed anti-c in her plasma, delivered twins by cesarean section. The spouse's blood group was also B, D+. The blood groups of twins I and II were confirmed to be B, D+ and AB, D+, respectively. The RBCs of twin I were c+, but those of twin II and the spouse were c-. On enquiry, history of ART with donor sperm insemination was noted. Because there were no previous sensitizations, antigenic inheritance from the sperm donor to twin I could be the possible sensitizing factor for maternal alloimmunization. To the best of our knowledge, this case is the first report of ART-induced maternal RBC alloimmunization in the literature. History of ART exposures should be documented, and appropriate RBC phenotyping of the parent as well as potential ART donors will help in timely detection or prevention of hemolytic disease of the fetus and newborn or other AIMA-related complications.

Rare donor programs are critically important for those patients with rare phenotypes who have produced the associated alloantibodies that necessitate the provision of rare blood components. We describe the American Rare Donor Program (ARDP) and its establishment, members, and policies. The specific phenotypes meeting the ARDP criteria for inclusion are described. Data on the number of rare donors registered by year, and the number of requests for rare blood components received and fulfilled over the 25 years of the program (1998-2023) are provided, along with a description of some notable cases and discussion of how the program supports patients with sickle cell disease.