Correspondence Address:
Neelam Marwaha
Department of Transfusion Medicine, PGIMER, Chandigarh - 160 012
India

Full Text

Sir,

A male infant weighing 2.75kg was born by normal vaginal delivery at 38 weeks to an O Rh (D)-positive multigravida (gravida 3) mother after an uneventful pregnancy. At 36 h of life, the baby was noticed to be deeply icteric. Investigations revealed total serum bilirubin (TSB) of 20.0mg/dL, packed cell volume (PCV) of 34% with peripheral blood smear showing mild anisopoikilocytosis with polychromasia. ABO Rh (D) typing and a direct antiglobulin test (DAT) were performed on the patient sample. The infant was A 1 Rh (D) positive with DAT positive using polyspecific antihuman globulin (anti-IgG + anti-C 3 d). With monospecific antihuman globulin, only anti-IgG was found to be positive and anti-C 3 d was negative. Possibility of ABO hemolytic disease of newborn (HDN) with or without presence of other irregular antibodies was considered. Newborn, maternal and paternal blood groups were found to be A 1 Rh (D) positive, O Rh (D) positive and A 1 Rh (D) positive, respectively. Antibody screen using a 0.8% commercial three-cell panel (Diacell, Switzerland) by column agglutination technology was negative on maternal serum, infant's serum and eluate from the newborn's red cell. Newborn's serum and eluate from its red blood cells demonstrated presence of anti-A, which confirmed the diagnosis of ABO HDN. Maternal serum had high titer anti-A (IgG titer 1:2048) after dithiothretiol treatment by the tube technique. TSB of the infant increased to 21.0 mg/dL and he received a double volume exchange transfusion (DVET) using O Rh (D)-positive peripheral red blood cells (PRBC) along with AB blood group plasma followed by intravenous immunoglobulin (IVIg) at a dose of 1mg/kg body weight. After DVET and IVIg, the TSB dropped to 10.1mg/dL. [Figure 1] shows the course of post-natal stay of the child in the neonatal nursery. The child was under phototherapy till post-natal day 6 of life and was discharged on day 7 of life.

ABO incompatibility between the mother and the baby occurs in 15-20% of all pregnancies, which produces HDN in 10% of these cases. [1] As compared with the other ABO blood groups that have predominantly IgM antibodies, 40-93% of the group O mothers also have IgG anti-A and anti-B antibodies. [2] Factors known to affect the severity of ABO HDN include not only the quantity of maternal anti-A or anti-B that cross the placenta but also the Ig subclass as each has different biological properties affecting their lytic potential. [3] Our case highlights the fact that ABO incompatibility is not always a benign condition and should be considered in all babies who have hemolysis and whose mothers are group O, even in the presence of a negative DAT. Asians and blacks have a higher prevalence of DAT-positive ABO HDN than Caucasians. [4] In ABO HDN, newborns with A and, especially, A 1 blood groups have more severe disease as compared with B or A 2 blood group newborns. [5] In the present case, the infant was typed as A 1 positive with anti-A 1 lectin.

It is therefore important to recognize that ABO HDN, although an often mild disease, can have an unexpectedly severe course and we need to be conscious of this so that appropriate intervention can be employed promptly to prevent serious complications.

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