| Literature DB >> 28815406 |
Xiuzhang Xu1,2, Lin Li3, Wenjie Xia1, Haoqiang Ding1, Dawei Chen1, Jing Liu1, Jing Deng1, Yangkai Chen1, Zhiming He3, Jiali Wang1, Yuan Shao1, Sentot Santoso1,2, Xin Ye4, Qun Fang5.
Abstract
Cases of CD36 deficiency are not rare in Asian populations, foetal and neonatal alloimmune thrombocytopenia (FNAIT) caused by anti-CD36 isoantibodies appears more frequent than other HPA alloantibodies. However, little is known about the treatment of anti-CD36 mediated FNAIT in this region. A Chinese male foetus, whose mother had a history of multiple intrauterine foetal demise and/or hydrops, was diagnosed with severe FNAIT at 27 weeks of gestational age. Immunological analysis revealed total absence of CD36 on platelets and monocytes from mother, caused by a 329-330delAC mutation of the CD36 gene. Anti-CD36 and anti-HLA class I antibodies were detected in the maternal serum, whereas only anti-CD36 isoantibodies were detectable in the foetal blood sample. Serial intrauterine transfusions with red blood cells (RBC) and platelets from a CD36null donor were performed to improve the severe anaemia and thrombocytopenia. The baby (2250 g; Apgar scores 10) was delivered vaginally at 32 weeks of gestation with normal haemoglobin (186 g/L) but low platelet count (48 × 109/L). After 2 days the platelet count rose to 121 × 109/L. This report suggests that intrauterine transfusions with compatible RBC and CD36null platelets are useful in preventing the deleterious clinical effects of anti-CD36-mediated severe FNAIT.Entities:
Keywords: Anti-CD36 antibody; Foetal anaemia and hydrops; Foetal and neonatal alloimmune thrombocytopenia; Intrauterine transfusion
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Year: 2017 PMID: 28815406 DOI: 10.1007/s12185-017-2310-5
Source DB: PubMed Journal: Int J Hematol ISSN: 0925-5710 Impact factor: 2.490