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Diagnosis and genetic analysis of severe neonatal anemia caused by α-Thalassemla combined with cold IgG anti-M
- Source :
- Zhongguo shuxue zazhi, Vol 35, Iss 12, Pp 1266-1269 (2022)
- Publication Year :
- 2022
- Publisher :
- Institute of Blood Transfusion of Chinese Academy of Medical Sciences, 2022.
-
Abstract
- Objective To investigate the family inheritance of α-Thalassemla gene and the risk of severe anemia in neonates caused by cold IgG anti-M. Methods ABO, Rh, MN blood groups and the specificity of unexpected antibody were identified by blood group serology. The IgG subtype and antibody titer of anti-M antibody were detected. The etiology of neonatal hemolytic disease was identified by three tests and α-Thalassemla gene diagnosis. Results Family investigation showed that father was B, CCDee, MN with no α-Thalassemla gene detected; Mother B, CcDee, NN, carrying α-Thalassemla gene; both the proband and his brother were B, CCDee, MN, carrying α-Thalassemla gene. Cold IgG anti-M was present in plasma of both the mother and the proband. The titer of the mother was 128 and that of the proband was 64. The subtype of IgG anti-M was IgG1 and IgG3. The direct anti-globulin test, release test and free test of the proband and his brother were negative, and the diagnosis was severe anemia and hemolysis caused by α-Thalassemla combined with cold IgG anti-M. Conclusion The direct antiglobulin test of neonatal hemolytic disease caused by IgG anti-M can be negative or weakly positive, and α-Thalassemla gene could be hereditary in families. The presence of α-Thalassemla gene can cause anemia, hemolysis and splenomegalysis in neonates, which could be aggravated when accompanied by cold-type IgG anti-M. In the presence of high-valency IgG antibody in plasma, blood exchange combined with transfusion can improve the curative effect.
Details
- Language :
- Chinese
- ISSN :
- 1004549X and 1004549x
- Volume :
- 35
- Issue :
- 12
- Database :
- Directory of Open Access Journals
- Journal :
- Zhongguo shuxue zazhi
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.f96a4ee5ba664bcaa06e99d6b7fec606
- Document Type :
- article
- Full Text :
- https://doi.org/10.13303/j.cjbt.issn.1004-549x.2022.12.019&lang=en