Dr. Kaplan has raised some objections to our letter published in Indian Pediatrics(1). Referring to his own study(2), he states: "............. We stand by our conclusions that G-6-PD deficiency associated neonatal hyper-bilirubinemia, in the population we studied, commences in the immediate perinatal period". Dr. Kaplan takes great pains to explain that in his study he had not implied that bilirubin rise in G-6-PD deficient neonates starts in utero, but rather in the "perinatal period". Referring to our letter, he says: "The authors (i.e., Drs. Murki and Dutta) conclude that their data negates that of a previous study of ours that jaundice in G-6-PD deficient infants commences most likely in utero".

We would like to clarify certain facts by quoting verbatim from the relevant articles. In the discussion section of his own article(2), Dr. Kaplan stated "Although umbilical cord blood sampling undoubtedly would have offered a more accurate representation of the in utero status, for logistical reasons and because of difficulties in coordinating the study with the delivery room staff, we chose to obtain samples from the infants within 3 hours of delivery to reflect the in utero situation. Although we cannot exclude categorically a very early postnatal onset of the bilirubinemia, we are confident that this method of sampling reliably reflected the in utero state". Later in the same article he writes: "In the current study, already immediately after birth, most likely reflecting the in utero status, the G-6-PD-deficient neonates had significantly higher serum bilirubin values than control participants."

All that Dr. Murki and I did in our study was to examine the cord blood bilirubin among G6PD deficient babies, something which Dr. Kaplan himself admits is a more accurate representation of the in utero state. Having found no difference between G-6-PD deficient babies and normal controls, we concluded: "Our study negates the possibility raised by Kaplan et al that in G-6-PD deficient neonates jaundice commences most likely in utero."(l) We had, by no means, negated Dr. Kaplan’s study as a whole. We had restricted ourselves to negating the possibility of in utero rise of bilirubin, which Dr. Kaplan had raised in his article. We have no contest with anything else that Dr. Kaplan has concluded. We fully agree that mutational differences between Sephardic Jews and Indians may account for some of the differences between his study and ours.