Dear Diane, I am glad you brought up the topic, because the issue is quite
complicated. Last year I had a FT newborn patient from an Israeli family
of Iraqui ancestry; over the first days of life he developed an increasing
level of jaundice; mom had not been helped starting adequately
breastfeeding at all; she had mixed-feeding the previous two sons and was
not very confident this time either (as expected). When d/c ed home, baby
was very sleepy (as expected) and, despite assisting/suggesting her to
wake him up, attach him frequently day and night, wear him STS and pumping
she did not manage doing much. All this not being enough, I learned his
father was G6PD deficient, but that they "had assured him it was not a
problem because the illness is transmitted through the female gender". On
day 7, after an office bilirubin level of 20 mg% (!) I decided to top the
baby up regularly with formula (mom had given him a bottle of formula on
and off) and to send him to hospital. Over there his bilirubin level was
17.2 mg% (phew)with no anemia. They put him under bili lights, drowned him
with formula, allowing mom to nurse occasionally with no encouragement
whatsoever to pump. Jaundice dropped down. Family was very happy with all
that. The blood chemistry revealed a low level of enzymatic activity
connected to glucose-6-phsophate-dehydrogenase,in face of *female
transmission* of the defect, which is the case most of the times but not
always, due to the differences in this particular gene expressivity and
penetration.
M.Ersilia Armeni
pediatrician, IBCLC, Rome (Italy)

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