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Year : 2014  |  Volume : 3  |  Issue : 2  |  Page : 128-129

Severe hemolytic disease of fetus and newborn due to Anti-S antibodies

Department of Neonatology, King Edward Memorial Hospital for Women, Subiaco, Perth, WA 6008, Australia

Date of Web Publication18-Jun-2014

Correspondence Address:
Vudum Sridhar Reddy
Department of Neonatology, King Edward Memorial Hospital for Women, 374 Bagot Road, Subiaco, Perth, WA 6008
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4847.134719

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How to cite this article:
Reddy VS, Kohan R. Severe hemolytic disease of fetus and newborn due to Anti-S antibodies. J Clin Neonatol 2014;3:128-9

How to cite this URL:
Reddy VS, Kohan R. Severe hemolytic disease of fetus and newborn due to Anti-S antibodies. J Clin Neonatol [serial online] 2014 [cited 2021 Jun 12];3:128-9. Available from: https://www.jcnonweb.com/text.asp?2014/3/2/128/134719


The relative proportion of hemolytic disease of fetus and newborn (HDFN) caused by non-D antibodies (Abs) has increased with the introduction of anti-D prophylaxis. Anti-S/s Abs constitute 2% of the alloantibodies detected in antenatal women. [1] S antigen is one of the 46 antigens constituting MNS blood group system (M, N, S, s, and U being clinically relevant high prevalence antigens). [2] Immunoglobulin G anti-S alloantibodies causing HDFN result from exposure to alloantigen through prior blood transfusion or fetomaternal hemorrhage. Anti-S Abs are a rare cause of HDFN and generally are thought to cause mild hemolytic jaundice. [3] Severe cases requiring multiple exchange transfusions [4] or resulting in fetal/neonatal deaths have been reported. [3]

A term 2.7 kg baby was born to a mother with the following antenatal history - 27-year-old G2P1, blood group A RhD positive, Kidd typing Jk (a + b−) S phenotype: s + s+, Ab screen positive for anti-Jk b and anti-S at titers 1:1 and 1:512 at the first antenatal visit and 1:1 and 1:256 respectively at 28 weeks. Ab titer remained at that level until delivery. Her partner's blood group was A RhD negative Jk (a+b+) S phenotype: S+ s + with a 50% chance of fetus inheriting the target antigens. Close antenatal monitoring with biophysical profile and middle cerebral artery peak systolic velocity (MCA-PSV) estimation was started at 24 weeks gestation. MCA-PSV hovered about 1.5 multiples of the median (MoM) reaching a maximum of 82.5 cm/s (just under 1.5 MoM) in the 38 th week suggesting possibility of mild fetal anemia. The mother was managed expectantly following the standard protocol. [5] Her Ab screen during her first pregnancy 4 years prior was positive for anti-S and anti-Jk b at titers 1:512 and 1:2 respectively. Her first baby developed only mild jaundice with negative direct antiglobulin test (DAT).

The second baby had severe anemia and jaundice at birth. Blood results in the first hour revealed the following - cord blood bilirubin 200 μmol/L (11.7 mg/dl), blood group: A negative, S phenotype S + s+, Kidd typing: Jk (a+b−); DAT positive, anti-S Abs eluted off cord red cells; hemoglobin (Hb) 81 g/L, white blood cells (WBC) 21.4 × 10 9 /L, platelets 68 × 10 9 /L, nucleated red blood cells (RBC) 191/100 WBC, retic count 34%; peripheral blood picture: Marked polychromasia, occasional fragmented and contracted red cells.

With a total bilirubin (TBil) of 260 μmol/L (15.2 mg/dl) at 4.5 h of life, a double volume exchange transfusion was performed with O negative blood (packed RBC). Postexchange, TBil was 162 μmol/L (9.5 mg/dl), Hb 199 g/L, platelet count 12 × 10 9 /L, international normalized ratio 1.2, prothrombin time 16.4 s, and activated partial thromboplastin time 36.5 s. He received platelet transfusion and in an effort to prevent the need for a second exchange transfusion, 1 g/kg intravenous immunoglobulin. Subsequently, TBil rose to a maximum of 272 μmol/L (15.9 mg/dl) on day 3 [Figure 1]. His conjugated bilirubin peaked at 68 μmol/L (3.97 mg/dl) on day 5 before declining. Phototherapy was continued at maximum intensity and withdrawn by day 5. Hearing screening with automated auditory brainstem response was normal. He developed late anemia with Hb of 81 g/L on day 38, which recovered with Iron and Folate supplementation.
Figure 1: Total serum bilirubin (mmol/L) plotted against time in hours after birth

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Antenatal monitoring by MCA-PSV did not predict the severity of the disease in this case. Continued vigilance is necessary when any Ab known to be associated with HDFN is detected in a mother, with prompt evaluation and treatment of the affected newborn.

  References Top

1.Dajak S, Stefanoviæ V, Capkun V. Severe hemolytic disease of fetus and newborn caused by red blood cell antibodies undetected at first-trimester screening (CME). Transfusion 2011;51:1380-8.  Back to cited text no. 1
2.Reid ME. MNS blood group system: A review. Immunohematology 2009;25:95-101.  Back to cited text no. 2
3.Griffith TK. The irregular antibodies: A continuing problem. Am J Obstet Gynecol 1980;137:174-7.  Back to cited text no. 3
4.Mayne KM, Bowell PJ, Green SJ, Entwistle CC. The significance of anti-S sensitization in pregnancy. Clin Lab Haematol 1990;12:105-7.  Back to cited text no. 4
5.Schenone MH, Mari G. The MCA Doppler and its role in the evaluation of fetal anemia and fetal growth restriction. Clin Perinatol 2011;38:83-102.  Back to cited text no. 5


  [Figure 1]

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