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一名 RhD 阳性孕妇体内的自身免疫性抗-D:病例报告。

Autoimmune anti-D in an RhD-positive pregnant woman: A case report.

作者信息

Kurniawan Samantha, Gerhardy Laura, Hull Sue, Janus Melanie, Dhondy Nina, Clarke Lisa

机构信息

Department of Haematology, Liverpool Hospital, Sydney, Australia.

Australian Red Cross Lifeblood, Sydney, Australia.

出版信息

Obstet Med. 2025 Jun 12:1753495X251346056. doi: 10.1177/1753495X251346056.

Abstract

BACKGROUND

Anti-D is usually alloimmune and develops in exposed RhD-negative individuals with potential for haemolytic disease of the fetus and newborn (HDFN). However, autoimmune anti-D is rare with limited understanding of its haemolytic risk to the fetus and mother.

CASE REPORT

A 30-year-old woman previously typed as B RhD positive was found to have an autoimmune anti-D on antenatal screening in her third pregnancy. RHD genotyping confirmed RhD positivity without D variants. Anti-D titres remained elevated at 1:512 throughout pregnancy with normal Doppler monitoring and no maternal haemolysis. The neonate was born at 38 weeks and 3 days of gestation with no evidence of haemolysis.

CONCLUSION

Autoimmune anti-D in pregnancy is rare and requires a multidisciplinary approach to management. Strategies include RHD genotyping to exclude D variants, close monitoring for HDFN, and careful selection of Rh phenotype matched blood for transfusion if required to avoid alloimmunisation for future pregnancies.

摘要

背景

抗-D通常是同种免疫性的,在暴露于RhD阴性且有胎儿及新生儿溶血病(HDFN)风险的个体中产生。然而,自身免疫性抗-D很罕见,对其对胎儿和母亲的溶血风险了解有限。

病例报告

一名先前血型为B RhD阳性的30岁女性在第三次怀孕的产前筛查中被发现有自身免疫性抗-D。RHD基因分型证实为RhD阳性且无D变异体。整个孕期抗-D效价持续升高至1:512,多普勒监测正常,且无母体溶血。新生儿于妊娠38周零3天出生,无溶血迹象。

结论

孕期自身免疫性抗-D罕见,需要多学科方法进行管理。策略包括进行RHD基因分型以排除D变异体,密切监测HDFN,以及在需要时仔细选择Rh表型匹配的血液进行输血,以避免未来妊娠发生同种免疫。

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本文引用的文献

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Intern Med. 2016;55(16):2253-8. doi: 10.2169/internalmedicine.55.6564. Epub 2016 Aug 15.
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Evaluation of non-invasive prenatal RHD genotyping of the fetus.胎儿无创性产前RHD基因分型的评估
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Autoimmune hemolytic anemia caused by anti-D.由抗-D引起的自身免疫性溶血性贫血。
Transfusion. 1973 Jul-Aug;13(4):214-8. doi: 10.1111/j.1537-2995.1973.tb05476.x.
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