Anemia, thrombocytopenia and neutropenia in perinatal period may result from placentally transferred maternal IgG allo or autoantibodies against RBC, Plt and PMN antigens (Ags). Alloantibodies (alloAbs) against RBC Ags most commonly cause of severe fetoneonatal anemia are anti-D and other alloAbs of the Rh system (anti-c, anti-c plus anti-E) as well as anti-Kell. Although maternal anti-D immunoprophylaxis has dramatically reduced the prevalence of feto-neonatal Rh hemolytic disease, during the last decade in our Neonatal Unit 60 affected infants have been observed. More than 70% of them showed early plus late or late severe anemia which had often required prenatal and/or postnatal RBC transfusions (Ts).

Perinatal anemia due to IgG autoAbs seems to be rare also because AIHA in pregnancy has been seldom reported.

During the last 15 yrs two mothers with chronic warm-type AIHA, observed by us, have delivered neonates without anemia.

Neonatal alloimmune thrombocytopenia (NAIT), induced by maternal Abs to fetal Plt-specific Ags, occurs in about 1/1000 pregnancies in Caucasian population. Plt reduction is usually severe and purpura is present at or shortly after birth. Much feared is intracranial hemorrhage (ICH), which may occur early in utero, causing neurological damage and even death. Some affected infants may also go unrecognized because asymptomatic. AlloAb most frequently involved is anti-HPA-1a. Due to the high recurrence rate of NAIT in subsequent pregnancies, the determination of paternal HPA-1 genotype is necessary to address the management of pregnancies following an index case.

During the last few yrs we have diagnosed three mothers with anti-HPA-1a alloimmunization. One woman was examined only after four unlucky pregnancies; two interrupted by spontaneous abortion and the others ended preterm with fetal and neonatal death respectively, both due to ICH. The father was HPA-1a homozygous. In the other two mothers diagnosis was made soon after delivering of infants who showed early purpura, severe thrombocytopenia, and fully recovered after treatment.

From 1987 to 1996 among 81 infants of mothers with chronic AITP, only 8(<10%) showed Plt n ° <50 × 109 /L and purpura. High-dose IVIG and/or steroids, associated in two cases to ExT plus random donor Plt Ts were used. All the infants recovered without complications.

Neonatal alloimmune neutropenia (NAIN), in Caucasian population, occurs in 0,5-2 per 1000 live births. AlloAbs against fetal PMN-specific Ags are involved, mainly anti-NA1. Neonates may show infections specially of the skin but may also go asymptomatic. Two infants with severe NAIN due to anti-NA1 Abs have been diagnosed by us during the last four yrs. Both showed cutaneous infections cured by antibiotics. Asymptomatic neutropenia has lasted for 8 wks in the first and for 8 mths in the other infant, also treated with high-dose IVIG. Maybe the use of G-CSF can reverse neutropenia more rapidly

A transient neonatal neutropenia, defined “isoimmune”, is due to maternal immunization against a non polymorphic epitope of the FcRIIIb(CD16) on PMNs of their child. The mothers lack NA1 and NA2 Ags (NA-null) and CD16 on PMNs. The risk of immunization of pregnant women lacking FcRIIIb is not known and transfusion induced immunization has not been reported.

Newborns of mothers with autoimmune neutropenia may also show neutropenia but it has never been clearly reported.