Blood group A mothers are more likely to develop anemia during antenatal intravenous immunoglobulin treatment of fetal and neonatal alloimmune thrombocytopenia.
BACKGROUND
Incompatibility between parental platelet (PLT) antigens may lead to sensitization of mother and development of fetal and neonatal alloimmune thrombocytopenia (FNAIT) resulting in fetal thrombocytopenia. Intravenous immunoglobulin (IVIG) with or without prednisone is the most effective, evidence-based antenatal treatment for subsequent FNAIT-affected pregnancies. IVIG infusion causes hemolysis in other settings, the degree depending upon patient blood groups (BGs).


METHODS
In ClinicalTrials.gov NCT00194987, 102 pregnant women received randomized antenatal treatment: Arm A received 2 g/kg/week IVIG; Arm B received 1 g/kg/week IVIG + 0.5 mg/kg/day prednisone. This post hoc analysis explored BG and anemia in 69 FNAIT mothers treated with Arm A or Arm B without salvage treatment to explore the effects of IVIG and steroid treatment on development of anemia in these women. Mothers whose treatment changed, for example, those with insufficient or unknown fetal PLT response who received salvage therapy, were excluded.


RESULTS
For Arm A, 17 of 21 (hemoglobin [Hb] < 10 g/dL) mothers with anemia but only three of 15 mothers without anemia had BG-A and/or BG-B (p = 0.0005). BG was unrelated to anemia in Arm B; only nine of 33 Arm B mothers became anemic during treatment. The mean decrease in Hb level in women with BG-non-O was 1.9 g/dL and in women with BG-O was 1.1 g/dL (p = 0.004). Anemia was not caused by iron deficiency; the lowest mean corpuscular volume was 79.


CONCLUSIONS
FNAIT women with BG-non-O more frequently develop anemia secondary to high-dose IVIG infusion (2 g/kg/week), quite possibly from isohemagglutinin-mediated hemolysis; maternal Hb requires monitoring. IVIG at 1 g/kg/week did not cause anemia in women with BG-non-O; concomitant prednisone likely alleviated the IVIG effect. Maternal BG could influence selection of antenatal treatment for FNAIT.
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University.
Madhavi
M
Lakkaraja
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University.
Jenny C
JC
Jin
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University.
Karen C
KC
Manotas
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University.
Cheryl A
CA
Vinograd
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University.
Polina
P
Ferd
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University.
Julia
J
Gabor
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University.
Megan
M
Wissert
Department of Obstetrics and Gynecology, Columbia University Medical Center, New York, New York.
Richard L
RL
Berkowitz
Platelet and Neutrophil Immunology Laboratory, Blood Center of Wisconsin, Milwaukee, Wisconsin.|Department of Medicine, Division of Hematology-Oncology, Medical College of Wisconsin, Wauwatosa, Wisconsin.
Janice G
JG
McFarland
Department of Pediatrics, Division of Hematology, Weill Medical College of Cornell University. jbussel@med.cornell.edu.
James B
JB
Bussel
D000740:Anemia / Q000139:chemically induced / Q000209:etiology* / Q000276:immunology; D001789:Blood Group Antigens; D005260:Female; D006454:Hemoglobins / Q000032:analysis; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage* / Q000009:adverse effects; D009035:Mothers; D011241:Prednisone / Q000494:pharmacology / Q000627:therapeutic use; D011247:Pregnancy; D013256:Steroids / Q000494:pharmacology / Q000627:therapeutic use; D054098:Thrombocytopenia, Neonatal Alloimmune / Q000188:drug therapy*; D016896:Treatment Outcome
D001789:Blood Group Antigens; D006454:Hemoglobins; D016756:Immunoglobulins, Intravenous; D013256:Steroids; D011241:Prednisone