Indian Journal of Pathology and Microbiology

: 2011  |  Volume : 54  |  Issue : 4  |  Page : 851--852

Hydrops fetalis due to maternal anti Jk b

MP Chacko1, A Mathan1, M Kumar2, R Jose3,  
1 Department of Transfusion Medicine and Immunohaematology, Christian Medical College and Hospital, Vellore, Tamil Nadu, India
2 Department of Neonatology, Christian Medical College and Hospital, Vellore, Tamil Nadu, India
3 Department of Obstetrics and Gynecology, Christian Medical College and Hospital, Vellore, Tamil Nadu, India

Correspondence Address:
M P Chacko
Department of Transfusion Medicine and Immunohaematology, Christian Medical College and Hospital, Vellore - 632 004, Tamil Nadu

How to cite this article:
Chacko M P, Mathan A, Kumar M, Jose R. Hydrops fetalis due to maternal anti Jk b.Indian J Pathol Microbiol 2011;54:851-852

How to cite this URL:
Chacko M P, Mathan A, Kumar M, Jose R. Hydrops fetalis due to maternal anti Jk b. Indian J Pathol Microbiol [serial online] 2011 [cited 2022 May 25 ];54:851-852
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Full Text


In India, antenatal screening for blood group antibodies that may lead to hemolytic disease of the newborn (HDN) is frequently limited to screening for anti D. However, screening panels that can detect a range of clinically significant minor blood group antibodies are available. The following case illustrates the importance of antenatal screening for minor blood group antibodies and also highlights the entity of severe haemolytic disease of the foetus in the clinical spectrum of anti Jk b.

A 32 year old woman presented in our centre as gravid3, para1, living1. She had undergone a term cesarean section during her first pregnancy. Her second pregnancy terminated in an abortion, of which details are unavailable. During her first two visits at 18 weeks + 6 days, and at 29 weeks gestational age, she was clinically well, and uterine size corresponded to gestational age. Her blood group was A positive, Hb 10.5 g%, and infectious markers negative. However, at her second visit, ultrasonography revealed gross foetal ascites and pericardial effusion. The pregnancy was terminated and a male foetus weighing 1.34 kg was delivered normally and expired shortly after birth. The foetus showed hydrops and low set posteriorly placed ears, brachycephaly and anti mongoloid slant.

Investigations at this stage showed maternal indirect coombs test (ICT) positivity of 3+ with a titer of 1:64. Maternal direct coombs test (DCT) was negative. Using commercial typing sera the maternal red cell phenotype was resolved as D+C-E+c+e+ K- Jka+ Jk b -. Employing a commercial 3 cell antibody screening panel and an in- house 11 cell antibody identification panel, the antibody was identified as anti Jk b.

One year later, the mother presented as a fourth gravida at 35 weeks + 4 days. ICT was still 3+ and cell panels again identified anti Jk b. Ultrasonography suggested fetal hydrops. Lower segment cesarean section (LSCS) was performed and a 2.06 kg baby girl was delivered. The baby was severely anemic (hemoglobin 9.8 g%) and jaundiced (total bilirubin 5.8 mg%, direct 0.5 mg%). Reticulocyte count was elevated (7.04%), DCT was 3+ positive, and red cell phenotyping showed the baby to possess Jk b (4+). The baby was transfused and administered intensive phototherapy. Over the following two days bilirubin increased (peaking at 10.7 mg%), then decreased. The baby was discharged on the fifth day.

Most reported cases of HDN due to anti Jk b have been clinically mild. [1] However a few exceptions have been reported. [2],[3],[4] The latter were generally gravida 3 or more. Thakral et al. have described HDN due to anti Jk b in the baby of a seventh gravida mother with 4 previous missed abortions and 2 inta-uterine deaths, one of which showed congenital malformations. [4] In the third pregnancy we described as well as in another fatal case (Ferrando et al.), hydrops was detected not earlier than the late second trimester, and till then fetal growth corresponded to age. Antibody titre in both instances was 1/64 - significant, though not usually associated with intra-uterine death. In our case, external anomalies were described, suggesting the possibility of a non immune cause contributing to severity. While the fourth pregnancy had a better outcome, the role of timely diagnosis and intervention here must be emphasized.


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