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Research On The Forming Mechanism Of The Red Blood Cell Alloantibody To E Antigen And The Influence On DHTR And HDN

Posted on:2015-04-23Degree:DoctorType:Dissertation
Country:ChinaCandidate:P XuFull Text:PDF
GTID:1314330428475201Subject:Clinical Laboratory Science
Abstract/Summary:PDF Full Text Request
Red blood cell (RBC) alloantibodies might be responsible for adverse transfusion reactions and haemolytic disease of the newborn. Foreign antigens expressed on the RBCs of donors or fetus may stimulate the immune system, lead to erythrocyte alloimmunisation then form RBC alloantibodies to foreign antigens, and RBC alloantibody to E antigen is often the most frequently identified alloantibodiy.The management or treatment on the adverse transfusion reactions and haemolytic disease of the newborn always relay on the recognization, but it's easy ignored or misdiagnosed, which may enfluence the patients' therapy, even lead to severe consequence. To prevent it, in the practice of transfusion, only minor institution may apply antigen matching transfusion for those whose RBC alloantibody had been formed. However, this method isn't popular for exertion, time consuming, adding the healthy cost and requesting professional staff. Until now, no efficient prophylaxis for haemolytic disease of the newborn resulting from RBC alloantibody to E antigen was found.According to these shortages, this study aims to explore the forming mechanism of RBC alloantibody and provide the science data for prophylaxis and therapy on adverse transfusion reactions and haemolytic disease of the newborn resulting from the RBC alloantibody.Part1Risk and mechanism of adverse transfusion reactions and haemolytic disease of newborn resulting from the RBC alloantibody to E antigenBackgroud and Objective:To explore the risk and mechanism of adverse transfusion reactions and haemolytic disease of the newborn resulting from the RBC alloantibody to E antigen by surveying the prevalence, specificity and risk of red blood cell alloantibodies among hospitalised Han Chinese patients? Methods:Antibody screening was conducted among42,517hospitalised Hubei Han Chinese individuals using column agglutination technology. Samples that were positive in antibody screening were subjected to antibody identification by the tube test. Clinical data, including gender, age, race, transfusion history and records of alloantibody detection, transfusion reactions or haemolytic disease of the newborn, were collected to analyse the prevalence and specificity of alloantibodies and complications associated with them.Results:A total of212patients with alloantibodies were identified among42,517patients, yielding a prevalence of0.50%in this study. Significantly different prevalence rates were observed according to age and sex. The most frequently identified alloantibodies were anti-E (87/212,41.0%), anti-D (45/212,21.2%), anti-M (41/212,19.3%) and a combination of anti-E and anti-c (13/212,6.1%). Haemolytic disease was observed in13infants with anti-D, three infants with anti-E and one infant with anti-Fya alloantibodies. Delayed haemolytic transfusion reactions occurred in four patients with alloantibodies.Conclusions:In hospitalised Han Chinese individuals, the overall prevalence of alloantibodies was0.50%, with anti-E, anti-D and anti-M being the most frequently identified alloantibodies. These results indicate that anti-D and anti-E alloantibodies were major risk factors for haemolytic disease of the newborn or delayed haemolytic transfusion reactions in this study population. Part2Risk and influence assessment on the anti-E forming result from foreign RBC E antigen stimulatingBackgroud and Objective:Anti-E alloantibody has been one of the most frequently detected clinically significant alloantibodies in previous studies, then the risk and influence on the anti-E forming result from foreign RBC E antigen stimulating were explored in the present study.Methods:We picked out258patients at risk of exposure to foreign E antigen among1239patients who received1306donors RBC transfusions and monitored the development of anti-E during the duration of their hospital stay.Results:Approximately1/4of patients had a risk of exposure to foreign E antigen during RBC transfusion. Although nearly half of the patients had histories of previous transfusion and/or pregnancy, even30of whom had received multiple previous transfusions and/or pregnancies and12had additional multiple exposures to foreign E antigen, no anti-E or any other alloantibody was found in this study.Conclusions:In this study population, the risk of exposure to foreign E antigen was high while receiving RBC transfusions, which was one initiating mechanism of anti-E forming, but not all maight produce anti-E. Part3Influence and mechanism of the development of anti-E resulting from the immune regulation gene TRIM21Backgroud and Objective:To explore the influence and mechanism of the development of anti-E resulting from the immune regulation gene TRIM21by analyzing the mutation of rs660in TRIM21gene among different sex and age groups in patients with red blood cell alloantibody to E antigen, and the cellular and humoral immune function among different allele of rs660in TRIM21gene.Methods:The mutation of rs660in TRIM21gene were detected by gene sequencing in49patients with red blood cell alloantibody to E antigen and35control individuals without red blood cell alloantibody to E antigen, then the allele distribution of rs660in TRIM21gene among different sex and age groups were analyzed and compared to explore the influence and mechanism. The cellular and humoral immune function among different allele of rs660in TRIM21gene were simultaneous determined in20patients with red blood cell alloantibody to E antigen and15control individuals.Results:31were detected with allele T of rs660in TRIM21gene and18with allele C in patients with red blood cell alloantibody to E antigen. The allele distribution of rs660in TRIM21gene wasn't remarkablly different between different sex groups among patients with red blood cell alloantibody to E antigen (P>0.05).26were detected with allele T of rs660in TRIM21gene and9with allele C in control individuals without red blood cell alloantibody to E antigen. The allele distribution of rs660in TRIM21gene wasn't remarkablly different between different sex groups among control individuals without red blood cell alloantibody to E antigen (P>0.05). The allele distribution of rs660in TRIM21gene wasn't remarkablly different between patients and control groups (P>0.05). Among different sex and age groups in patients and control individuals, none of the allele distribution of rs660in TRIM21gene was remarkablly different.In the less than five years old group with red blood cell alloantibody to E antigen,9were detected with allele T of rs660in TRIM21gene and5with allele C. In the five to ten years old group,11were detected with allele T and5with allele C. In the more than ten years old group,13were detected with allele T and6with allele C. The allele distribution of rs660in TRIM21gene wasn't remarkablly different among the different age groups with red blood cell alloantibody to E antigen (P>0.05)The cellular and humoral immune function among different allele of rs660in TRIM21gene weren't remarkablly different in patients and controls.Conclusions:The allele T frequency of rs660in TRIM21gene was higher than allele C in both patients with red blood cell alloantibody to E antigen and controls without red blood cell alloantibody to E antigen. The allele distribution of rs660in TRIM21gene wasn't remarkablly different among different sex and age groups (P>0.05). Among different allele of rs660in TRIM21gene, the cellular and humoral immune function weren't remarkablly different. No influence was observed on the development of red blood cell alloantibody to E antigen resulting from the rs660mutation of TRIM21gene.
Keywords/Search Tags:RBC alloantibodies, Delayed haemolytic transfusion reactions, Haemolyticdisease of the newborn, Han ChineseRBC allo immunization, Anti-E alloantibody, RBC transfusionRed blood cell alloantibody to E antigen, Immune regulation, TRIM21, Gene mutation
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