Neonatal Alloimmune Thrombocytopenia (NATP) Associated with Maternal-Fetal Incompatibility for Blood Group B.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 955-955
Author(s):  
Brian R. Curtis ◽  
Janice G. McFarland ◽  
Andrea Fick ◽  
Andrew J. Lochowicz ◽  
Robert H. Ball ◽  
...  

Abstract In most individuals, A and B blood group antigens are weakly expressed on platelets, allowing ABO incompatible platelets to be tolerated when transfused. However, in a minority of normal subjects (high expressers, H-Exp), platelets carry 10–20 times the usual number of A or B epitopes (up to 20,000/platelet, Blood2000;96:1574). Post-transfusion survival of incompatible H-Exp platelets has not been systematically studied. We recently encountered a family in which NATP in two infants appears to have been caused by maternal anti-B reacting with H-Exp fetal platelets inherited from a father with the group B H-Exp trait. The first two children (C1 and C2) born to a G4P2 group O mother and A2B father were positive for blood group B, and had neonatal thrombocytopenia (TP) (C1 = 33K/μL, C2 = 61K/μL), anemia, positive direct antiglobulin test, elevated reticuloytes and hyperbilirubinemia requiring phototherapy. C1 required 3 platelet transfusions and RBC transfusion, and C2 required RBC transfusion. Both recovered in the immediate neonatal period. A third child (C3) inherited blood group A2 from the father and was born with a normal platelet count. The parents were incompatible for HPA-2b and -3b, but no platelet-specific antibodies were detected in maternal serum. High titer IgG antibodies were detected in maternal serum against father’s platelets in both flow cytometry and modified antigen capture ELISA. This activity was completely removed by absorption with normal, washed group B RBCs. When tested by flow cytometry with monoclonal anti-B and anti-A, the father’s platelets were shown to carry 17 times the normal level of B antigen, and only trace amounts of A antigen. We previously showed that the potent glycosyltransferase activity associated with the H-Exp trait causes essentially all H antigen on platelets and RBCs to be converted to A and/or B antigen. Consistent with this, father’s platelets and RBCs were found to express no detectable H. Quantitation of B and H antigens on platelets and RBCs from C1 and C2 is pending receipt of samples. Findings made in this family indicate that maternal anti-B (and presumably anti-A) IgG antibodies can cause NATP in infants with the ABO “high expresser” trait. Maternal-fetal ABO incompatibility should be considered as a cause of NATP when maternal antibodies against platelet-specific antigens cannot be demonstrated. The possibility that ABO incompatibility can aggravate thrombocytopenia caused by antibodies against recognized platelet-specific antigens also deserves consideration.

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 20-20
Author(s):  
Connie M. Arthur ◽  
Harold Clifford Sullivan ◽  
Christian Gerner-Smidt ◽  
Nourine Ahmed-Kamili ◽  
Ashley Bennett ◽  
...  

Abstract Introduction: Anti-ABO antibodies represent the earliest recognized immunological barrier to transfusion and transplantation. However, despite Landsteiner's discovery of ABO blood group antigens over a century ago, the factors that regulate anti-ABO antibody formation remain relatively unknown. Anti-ABO antibodies develop spontaneously within the first few months of life, in the absence of a known antigenic exposure. However, antibody levels vary considerably between individuals suggesting that differences in exposure to environmental triggers may regulate anti-ABO antibody formation. As distinct microbes can stimulate very specific anti-carbohydrate antibodies, we hypothesized that variation in exposure to microbes that decorate themselves in ABO carbohydrates may regulate anti-blood group antibody formation. However, no model currently exists to examine the potential impact of microbial exposure on the development of naturally occurring anti-blood group antibodies. Methods: To examine the regulatory capacity of specific microbial exposure on naturally occurring antibody formation, we generated a model of ABO blood group antigens. As lower mammals do not express ABO antigens, we used recipients knocked out (KO) for the glycosyltransferase responsible for the synthesis of the carbohydrate B disaccharide (Bdis) antigen, an antigen very similar to the human blood group B antigen. Microbial flora was assessed in WT (Blood group B-like) or Bdis KO (Blood group O-like) by sequencing ribosomal DNA isolated from stool samples. Serum was assessed for Bdis reactivity at baseline and following Bdis+ microbial exposure using a glycan microarray. WT or Bdis KO recipients were transfused with Bdis+ RBCs followed by the evaluation of RBC clearance, antibody engagement and complement fixation by flow cytometry. Results: Similar to blood group O individuals, Bdis KO recipients spontaneously develop varied amounts of anti-Bdis antibodies within the first few weeks of life capable of inducing an acute hemolytic transfusion reaction following incompatible Bdis+ RBC transfusion. To determine whether specific microbial exposure is the primary regulating factor in anti-Bdis antibody formation, we separately housed Bdis KO recipients with low titer anti-Bdis antibodies, yielding an entire Bdis KO colony that never developed detectable anti-Bdis antibodies. Exposure of Bdis KO recipients that lacked detectable anti-Bdis antibodies to specific microbes that express the Bdis antigen induced robust anti-Bdis antibodies. However, the timing of microbial exposure was critical in dictating the likelihood of anti-Bdis antibody formation as younger mice produced anti-Bdis antibodies much more readily than adult mice following Bdis+ microbial exposure. Consistent with this, only Bdis KO recipients that experienced early Bdis+ microbial exposure possessed anti-Bdis antibodies with the capacity to induce an acute hemolytic transfusion reaction following Bdis+ RBC transfusion. Conclusions: These results demonstrate that Bdis KO recipients provide an attractive model to study naturally occurring antibody formation and suggest that anti-ABO antibodies are not an inevitable outcome of not expressing ABO blood group antigens. Instead, naturally occurring antibody formation appears to be temporally regulated by specific microbial exposure. As younger Bdis KO recipients developed antibody more readily than older Bdis KO recipients, in addition to Bdis+ microbial exposure, the actual timing of exposure appears to be a key regulator of anti-Bdis antibody formation. Thus variations in an individual's microbiota, particularly during early immunological development, likely dictate the level of anti-ABO antibody formation. As a result, intentional manipulation of an individual's microbial flora may provide a unique and previously unrecognized approach to prevent anti-ABO(H) antibody development in patients requiring transplantation or chronic transfusion. Disclosures No relevant conflicts of interest to declare.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4023-4023
Author(s):  
Jake Shortt ◽  
Mark N. Polizzotto ◽  
David Roxby ◽  
Geoff Magrin ◽  
Andrew Webb ◽  
...  

Abstract Passenger lymphocyte syndrome (PLS) is rare following solid organ transplantation. We describe 3 transplant recipients who developed severe hemolysis after receiving organs from a single donor with multiple red cell (RC) alloantibodies. The donor was a 54 y.o. male, blood group O Rh(D) negative (rr) with a positive antibody screen due to anti-D, anti-C and anti-k. His Cellano negative and RC alloantibody status was well characterized antemortem, given that he was a rare RC phenotype donor for the Australian Red Cross Blood Service (ARCBS). The lungs and the liver were offered for organ donation. The right single lung recipient was a 61 y.o. male with emphysema (blood group O Rh(D) positive [R2r]). From post transplant day (PTD) 0 to 10 his hemoglobin (Hb) fell from 126g/L to 69g/L without bleeding and with elevated hemolytic markers. A positive direct antiglobulin test (DAT) due to IgG was noted and anti-D eluted. Management included increased immunosuppression and transfusion of 2 RC units (rr, k positive). Ongoing hemolysis required a second transfusion at PTD 24. To facilitate tapering of corticosteroids, intravenous immunoglobulin (IVIG; 2g/kg in divided doses) was administered. The patient subsequently stabilized and 3 months post-transplant has mild compensated hemolysis with persisting anti-D. The left single lung recipient was a 59 y.o. female with emphysema (blood group O Rh(D) positive [R1r]). From PTD 0 to 10, Hb fell from 91g/L to 73g/L with elevated hemolytic markers. The antibody screen and elution demonstrated anti-D, and she was transfused with 2 RC units (rr, k positive). Three months post transplant she has ongoing evidence of mild compensated hemolysis with persisting anti-D. The liver recipient was a 45 y.o. male with Hepatitis B (blood group B Rh(D) positive [R1R1]). From PTD 0 to 13 Hb fell from 102g/L to 64g/L without bleeding. The DAT was positive (IgG) at day 4. Anti-D+B+C were detected in the plasma and anti-C+D+k+B were found in eluates. He was managed with increased immunosuppression and transfusion of 2 RC units (rr, k negative). Fresh Cellano negative units were accessed through the ARCBS rare RC register. The patient has subsequently also stabilized, despite ongoing seropositivity for anti-D (but not anti-k). These cases highlight the potential for severe hemolysis due to PLS following solid organ transplant. This is the first apparent description of PLS where anti-k has been implicated, with significant hemolysis in all recipients of organs from the same donor. We conclude that the identification of donor RC alloantibodies at the time of transplant should prompt close surveillance for development of PLS. Consideration of strategies to ameliorate hemolysis, such as early use of IVIG, is suggested. Where an antibody to a high incidence antigen (such as Cellano) is detected, early notification of central blood bank services may facilitate call up of phenotyped donors and provision of rare units.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1027-1027 ◽  
Author(s):  
Barbara Ghinassi ◽  
Maria Themeli ◽  
Kai-Hsin Chang ◽  
Gregory Halverson ◽  
Ghazala Hashmi ◽  
...  

Abstract Abstract 1027 Red blood cells (RBC) survive shear forces in the microvasculature because trans-membrane complexes embedded in the lipid bilayer attach their membrane to the cytoskeleton assuring its flexibility. The expression of clinically relevant red blood cell antigens present on these complexes is determined by genetic polymorphisms and their developmental regulation. Therefore, flow cytometry studies of blood group antigens may provide insights both on potential immunogenicity and on membrane structure of ex-vivo generated EBs. Blood group antigen profiles of EBs expanded ex vivo from one AB (three experiments), three CB, the H1 hESC line and one iPS line derived from mononuclear cells from a healthy donor were compared by flow cytometry using commercially available antibodies recognizing antigens present on proteins in the 4.1R [Duffy (Fya and Fy3), Kell (Kell prot, K/k, Kpa/Kpb, Jsb) and glycophorin C (GPC, Ge2)] and ankyrin R [glycophorin A (GPA, CD235a, M and EnaFS) RhAG and band 3 (Wrb)] complexes and on other important membrane proteins [glycophorin B (GPB, s and U), urea transporter (Kidd, Jk3), the complement receptor (CD35) and inhibitors of complement-mediated lysis (CD55 and CD59)]. Controls included DNA genotyping (CB, AB and H1-hESC) (HEA-Bead Chip, Immunocor, Norcross, GA) and immunophenotyping of blood red cells from the same AB and CB. Antigen expression similar to that observed on in vivo generated RBC was considered normal. EBs were generated from AB and CB at day 10 in HEMAser cultures whereas EBs from hESC and iPS were derived using previously optimized protocols. The maturation state was determined by morphological analyses and CD36/CD235a profiles. Irrespective of the stem cell source, the immunophenotype of ex-vivo expanded EBs was consistent with that predicted by genotyping. However, source specific differences in the magnitude of antigen expression and in the changes with maturation were observed (see Figure). Immature EBs from AB expressed normal levels of the antigens present on both the 4.1R (Duffy, Kell, GPC) and ankyrin R (GPA, M/N, EnaFS, RhAG and band 3) complexes. With maturation, expression of 4.1R-associated antigens remained normal while that of ankyrin R associated antigens varied (M decreased and RhAG increased). EBs from CB expressed normal levels of antigens present on the ankyrin R complex and of some of those present on the 4.1R complex (Duffy, Kell protein and GPA). However, expression of epitopes on Kell protein varied with some antigens expressed at normal levels (k and Jsb) and others (Kpa/Kpb) at levels 2x greater than normal. With maturation, CB-derived EBs maintained normal levels of ankyrin R associated antigens while those associated with complex 4.1R became barely detectable. EB from hESC expressed unbalanced levels of proteins associated with both ankyrin R (2x levels of GPA and barely detectable levels of RhAG) and 4.1R [3x levels of Duffy and 2x levels of Jsb (Kell) with normal levels of k and Kpb (Kell) antigens] complexes. The variegation in expression of different epitopes on the same protein observed with CB- and hESC-derived EBs likely reflect altered structural conformation of the complexes rather than differences in protein concentration on the membrane. EBs from iPS, as those from AB, expressed normal levels of antigens present on Ankyrin R and 4.1R complexes which increased with maturation. Irrespective of stem cell sources, EBs expressed normal levels of GPB and Kidd. EBs from AB expressed normal levels of the complement regulatory proteins tested which in the case of CD59 CD59 decreased with maturation. EBs from CB expressed normal levels of CD35 and CD59 but 2x levels of CD55 with expression of CD35 and CD55 decreasing with maturation. EBs from iPS expressed 2x levels of CD35 and CD55 and expression of these antigens was not affected by maturation. The observation that blood group antigenic profiles of ex-vivo generated EBs are consistent with those predicted by DNA-genotyping suggests that these cells are unlikely to be immunogenic for known epitopes. However, the antigen profiles of ankyrin R and 4.1R complexes were normal only for AB and iPS-derived EBs raising the possibility that antigenic deviations seen in EBs derived from CB and hESC may have immunologic or functional consequences in vivo. Disclosures: No relevant conflicts of interest to declare.


1991 ◽  
Vol 39 (4) ◽  
pp. 491-505 ◽  
Author(s):  
M Vierbuchen ◽  
G Uhlenbruck ◽  
F G Hanisch ◽  
W E Müller ◽  
M Ortmann ◽  
...  

We applied a peroxidase-antiperoxidase technique to study the distribution pattern and binding characteristics of the lectin from the marine sponge Geodia cydonium (Geodia cydonium agglutinin; GCA) in various human tissues. This lectin has been shown to possess a broad reactivity, but there was a distinct distribution of binding sites within the different organs. In the histochemical system GCA displayed no blood group specificity and labeled red blood cells, the vascular endothelium, and epithelial cells showing blood group antigen expression independent of the ABH blood group status. However, inhibition of GCA reactivity by simple sugars and complex carbohydrates demonstrated tissue-specific differences of lectin binding related to the ABH blood group status of the tissue and revealed information on the structural requirements of the histological lectin binding site. Tissues that totally lacked blood group antigens or that expressed only the H-antigen disclosed a GCA reactivity which was completely inhibited by lactose. In contrast, tissues that expressed blood group A- or blood group B-antigen exhibited a lactose-resistant lectin binding which was inhibited only by water-soluble blood group substance A from peptone A and by bovine glycophorin but not by other complex carbohydrates, including human glycophorin and human asialoglycophorin. Competitive inhibition studies in situ revealed that GCA binding was not inhibited by blood group type I/II carbohydrate sequence-specific lectins or by lectins with other sugar specificities. Inhibition by lactose of GCA binding to some histological sites indicates that the binding site consists of a beta-linked galactose-containing disaccharide. However, periodate oxidation of tissue sections had no effect on lectin binding, pointing to a subterminal location of the relevant sequence. The results obtained from inhibition studies with simple saccharides and complex carbohydrates in relation to the expression of ABH blood group antigens suggest a complex lectin combining site(s) in histological specimens. The lectin may possess either one binding site with a range of affinities for different carbohydrates (besides beta-linked disaccharides the GCA binding site accommodates to carbohydrate determinants carrying the blood group A or blood group B determinant), or may possess two different binding sites. Besides an acceptor site for beta-linked disaccharides, an additional binding site may exist accommodating to extended carbohydrate sequences related to A or B blood group structures. In conclusion, GCA represents a blood group-nonspecific lectin whose binding affinities are determined by the ABH blood group status of the tissue.


1965 ◽  
Vol 122 (6) ◽  
pp. 1075-1086 ◽  
Author(s):  
Sten Hammarström ◽  
Rutger Lagercrantz ◽  
Peter Perlmann ◽  
Bengt E. Gustafsson

Sera from patients with ulcerative colitis contain antibodies which hemagglutinate sheep red cells, sensitized with phenol-water extracts from. colon, cecum, or feces of germfree rats. Minor concentrations of such antibodies are also present in a certain fraction of normal human sera. Hemagglutination and hemagglutination inhibition experiments with human erythrocytes and with the rat extracts showed that the latter contained an antigen similar to human blood group A antigen. In contrast, a blood group B-like antigen could not be detected in these extracts. However, experiments with eel serum indicated that these extracts also contained an antigen similar to the H antigen of the human ABO system. Absorption of ulcerative colitis sera with human A1 erythrocytes but not that with B or O erythrocytes gave, in a few cases, a slight reduction of the hemagglutinating titers against rat cecum-sensitized sheep erythrocytes. In contrast, this treatment considerably reduced such titers when found in sera from healthy persons or from patients with unrelated diseases. It could be concluded that the rat extracts also contained a "colon" antigen, detected with antibodies, present at elevated titers, in the sera of ulcerative colitis patients, but not in those of the controls. This colon antigen is immunologically distinct from the blood group antigens studied. Hemagglutination inhibition experiments indicated that A, H and colon antigen were widely distributed throughout the gastrointestinal tract of the germfree rats. The colon antigen was found to be enriched in the extracts from colon, cecum, and feces. Fluorescent antibody staining provided evidence that both the colon antigen and the A antigen were present in similar sites of the colon and cecum mucosa, particularly in goblet cells of the crypts, and in the mucus.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Biruk Legese ◽  
Molla Abebe ◽  
Alebachew Fasil

Background. ABO and Rh blood group antigens are thought to be among genetic determinants of type 2 diabetes mellitus. Identification of blood group phenotypes are more associated with type 2 diabetes mellitus. It will be helpful for individuals who are susceptible blood groups to take care of themselves by avoiding other predisposing factors and taking preventive measures. Methods. Hospital-based comparative cross-sectional study was carried out from February to April 2019 at Felege Hiwot Comprehensive Referral Hospital. Sociodemographic and clinical data were collected with a semistructured pretested questionnaire. ABO and Rh Blood group were determined by slide and test tube methods. Biochemical parameters were determined with Mindray BS-200E fully automated clinical chemistry analyzer. Data were analyzed by IBM SPSS version 20 statistical software. Chi-square test and logistic regression analysis were employed for data analysis. A P value of < 0.05 was considered statistically significant. Results. From a total of 424 participants included for this study, blood group O was found higher in frequency with 74 (34.9%) and 97 (45.75%) for cases and healthy controls, respectively. ABO blood groups showed significant association with T2DM, a chi-square value of 12.163 and P value of 0.007. However, the Rh blood group was not associated with T2DM. Binary logistic regression analysis revealed that blood group B had a higher risk (OR: 2.12, 95% CI: 1.33-3.32) and blood group O had decreased risk (OR: 0.636, 95% CI: 0.43-0.94) of T2DM as compared to other blood groups. Conclusion. ABO blood group antigens showed significant association with type 2 diabetes mellitus. Blood group B was associated with an increased risk and O blood group with decreased risk of type 2 diabetes mellitus.


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 5159-5159
Author(s):  
Jitendra Mohan Khungar ◽  
Hara Prasad Prasad Pati ◽  
Manoranjan Mahapatra

Abstract Abstract 5159 Introduction: Auto Immune Hemolytic Anemia (AIHA) is one of the most common types of acquired hemolytic anaemias. Its main cause is auto antibody mediated rapid destruction of RBCs. Detection of these autoantibodies to erythrocytes is of fundamental importance for diagnosis. A number of methodologies have been tried for detection & evaluation of these autoantibodies. Demonstration of a positive Direct Antiglobulin Test (DAT) against these autoantibodies is an important serological assay in the diagnosis of auto immune hemolytic anemia (AIHA). This test is also considered as pathognomonic of immune-mediated hemolysis. This routinely used direct antiglobulin test (DAT) has the disadvantage of low sensitivity and does not detect low levels of red cell auto antibodies leading sometimes to false negative results. Flow cytometry can effectively diagnose such patients of auto immune hemolytic anemia with low levels of autoantibodies. Role of flow cytometry in the diagnosis of several non-malignant haematological disorders is being explored & present study has been conducted with the same objective. Aims & Objectives: This study was conducted with the following aims and objectives: •To assess the utility of flow-cytometry (FCM) in the diagnosis of suspected AIHA patients. •Compare the sensitivity of flow-cytometry (FCM) with Direct Antiglobulin Test (DAT) by Gel-card Test (GT). •To assess the positivity in DAT negative cases by flow-cytometry in suspected AIHA cases. Material & Methods: This was a prospective study, carried out in Haematology Deptt of All India Institute of Medical Sciences, where patients with suspected auto immune hemolytic anemia (AIHA) were studied during two years period. Blood samples of suspected patients of AIHA were tested by Gel Card Test as well as by Flow cytometry for detection of RBC bound IgG. Results: A total of 50 patients with suspected diagnosis of auto immune hemolytic anemia (AIHA) were studied by flow-cytometry as well as by Gel card test (GT) for detection of RBC bound IgG. Out of these 50 cases, 41 cases have turned out to be positive and 9 were negative by flow-cytometry. The quantification of positivity by flow-cytometry was obtained by calculating percentage fluorescence. The same 50 cases were also tested by Gel card test (GT). By Gel card test, out of 50 cases, 34 were positive & 16 were negative. Therefore, there were 7 cases which were negative for RBC bound IgG by Gel card test and these were positive by flow-cytometry. The flow cytometry figures of these cases will be shown & discussed in the presentation. Conclusions: Flow-cytometry is a reliable and sensitive method of detecting RBC-bound IgG antibodies for the diagnosis of auto immune hemolytic anemia. This can be used as a new routine diagnostic technique for auto immune hemolytic anemia. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
2005 ◽  
Vol 105 (12) ◽  
pp. 4693-4699 ◽  
Author(s):  
Stuart J. D. Neil ◽  
Áine McKnight ◽  
Kenth Gustafsson ◽  
Robin A. Weiss

Abstract ABO histo-blood group antigens have been postulated to modify pathogen spread through the action of natural antibodies and complement. The antigens are generated by a polymorphic glycosyl-transferase encoded by 2 dominant active and a recessive inactive allele. In this study we investigated whether ABO sugars are incorporated into the envelope of HIV-1 virions. HIV vectors derived from cells expressing ABO antigens displayed sensitivity to fresh human serum analogous to ABO incompatibility, and ABO histo-blood group sugars were detected on the viral envelope protein, glycoprotein 120 (gp120). Moreover, lymphocyte-derived virus also displayed serum sensitivity, reflecting the ABO phenotype of the host when cultured in autologous serum due to adsorption of antigens to cell surfaces. Serum sensitivity required both active complement and specific anti-ABO antibodies. Thus, incorporation of ABO antigens by HIV-1 may affect transmission of virus between individuals of discordant blood groups by interaction with host natural antibody and complement. (Blood. 2005;105:4693-4699)


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 26-26
Author(s):  
Yang Chen ◽  
Huiru Wang ◽  
Zimin Sun ◽  
Wen Yao ◽  
Huilan Liu ◽  
...  

Abstract Background:ABO incompatibility is not considered a main contraindication to allogeneic hematopoietic stem cell transplantation (aHSCT). However, it has been associated with a number of immunohematological complications. The effects of ABO incompatibility on aHSCT remain controversial.The change of isoagglutinin titers and early clinical outcomes were analyzed after unrelated cord blood transplantation (UCBT) with ABO-incompatibility donor. Methods:252 patients with hematological malignant diseases and other hematological disorders who underwent unrelated UCBT from January 2019 to April 2020 were retrospectively analyzed in this research. Patients were studied in identical, major, minor and bidirectional mismatch groups. Immunoglobulin m (IgM) isoagglutinin titers were tested one day before the transplant (-1 day), 2 weeks post-transplant, 4 weeks post-transplant and 6 weeks post-transplant. R esults:76 match,71 major mismatch, 70 minor mismatch and 35 bidirectional unrelated UCBT were identified. The median neutrophil, PLT and red blood cell (RBC) recovery days were 18, 38 and 22, respectively. ABO mismatch did not influence the neutrophil, PLT and RBC engraftment. The median of RBC transfusion in 30 days were 5 units and PLT were 6 units. There were no statisitcal difference in 0-30 days RBC and PLT transfusion after UCBT. 31-100 days transfusion was similar to in 30 days transfusion. No patients developed pure red cell anemia (PRCA). -1day IgM titers ≥1:16 did not develop higher risk of grade II-IV aGVHD when compared with titers≤1:8 group. However, we detected a marginal higher PLT transfusion in 30 days after transplant at antibody titers ≥1:16 group when compared with titers≤1:8 (P=0.051). In the major and bidirectional groups, we found that group O IgM anti-donor antibodies were displayed a significant higher than the group B anti-A titer (p&lt;0.001) in setting the time one day before the transplant, but no significant with group A. 2 weeks after the transplant, group B anti-A was still showed significant lower than the group O anti-A (p&lt;0.001). 4 weeks after the UCBT, we observed a modest, but no statistical significant lower titers of group B anti-A antibodies as compared with O group (P=0.097). 6 weeks after the transplant, there were no statistical significant among group O, A and B. In the multivariable Cox regression model, transfusion of ≥5 RBC units in 30 days after UCBT (HR=1.727, 95%CI=1.020-2.926, P=0.042) and PLT engraftment ≥38 days (HR=1.964, 95%CI=1.134-3.401, P=0.016) were correlated to greater risk of grade severe aGVHD. Conclusion:This study showed that ABO mismatch did not influence the neutrophil, PLT and RBC recovery time.Group O IgM anti-donor isoagglutinins in recepients showed a higher titers than the group B in setting with the time (-1 days pre-transplant, 2 weeks post-transplant, 4 weeks post-transpant). Pre-transplant higher anti-donor isoagglutinins were associated with more PLT transfusion requirements after UCBT. More RBC transfusion (≥5 units) and longer PLT recovery time (≥38 days) showed a higher incidence of severe aGVHD. Disclosures No relevant conflicts of interest to declare.


BioSight ◽  
2020 ◽  
Vol 1 (1) ◽  
pp. 21-25
Author(s):  
Sana Shahid ◽  
Syed Sadia Fatima ◽  
Seema Ghani

ABO blood group antigens have been identified as pathological agent in different disease conditions. For some time, the association of blood group with pregnancy associated conditions like pre-eclampsia is extensively under debate. Preeclampsia is a distressing condition of pregnancy which commonly causes maternal and fetal mortality around the globe. Multiple risk factors are found to be associated with preeclamptic occurrence. In this study our aim was to delineate a specific blood group which could be implicated as a risk factor for pre-eclampsia. Methods: This retrospective study was conducted in a tertiary care hospital of Karachi and retrieved obstetric data including blood group was from medical record files of 368 patients. Obtained data was analyzed by IBM SPSS version 21. Results: The prevalence of B group was recorded to be 41.3% as compared to O (26.1%), A (22.8%) and AB (9.8%). So, it can be concluded that women having blood group B are more prone to develop pre-eclampsia. Conclusion: Blood grouping of pregnant women in early weeks of pregnancy could assist in prediction or better management of pre-eclampsia.


Sign in / Sign up

Export Citation Format

Share Document