Neonatal Neutropenia

Data on the use of Granulocyte colony-stimulating factor (G-CSF) in pregnant cancer patients are scarce. The International Network of Cancer, Infertility and Pregnancy (INCIP) reviewed data of pregnant patients treated with chemotherapy and G-CSF, and their offspring. Among 2083 registered patients, 42 pregnant patients received G-CSF for the following indications: recent chemotherapy induced febrile neutropenia (5; 12%), dose dense chemotherapy (28, 67%), poly chemotherapy (7, 17%), or prevention of neutropenia at delivery (2; 5%). Among 24 women receiving dose dense chemotherapy, three (13%) patients recovered from asymptomatic neutropenia within 5 days. One patient developed pancytopenia following polychemotherapy after which the pregnancy was complicated by chorioamnionitis and intrauterine death. Nineteen singleton livebirths (49%) were born preterm. Sixteen neonates (41%) were admitted to the Neonatal Intensive care Unit (NICU). No neonatal neutropenia occurred. Two neonates had congenital malformations. Out of 21 children in follow-up, there were four children with a motor development delay and two premature infants had a delay in cognitive development. In conclusion, the rate of maternal and neonatal complications are similar to those described in (pregnant) women treated with chemotherapy. Due to small numbers and limited follow-up, rare or delayed effects among offspring exposed to G-CSF in utero cannot be ruled out yet.

Download Full-text

Intravenous gammaglobulin in treatment of isoimmune neonatal neutropenia

European Journal of Pediatrics ◽

10.1007/bf00441407 ◽

1988 ◽

Vol 148 (3) ◽

pp. 218-219 ◽

Cited By ~ 9

Author(s):

T. Hanada ◽

R. Shin ◽

M. Hosoi ◽

K. Saito ◽

H. Takita

Keyword(s):

Intravenous Gammaglobulin ◽

Neonatal Neutropenia

Download Full-text

Effect of Recombinant Granulocyte Colony-Stimulating Factor on Blood Neutrophil Concentrations among Patients with “Idiopathic Neonatal Neutropenia”: A Randomized, Placebo-controlled Trial

Journal of Perinatology ◽

10.1038/sj.jp.7210961 ◽

2003 ◽

Vol 23 (6) ◽

pp. 493-497 ◽

Cited By ~ 15

Author(s):

Sandra E Juul ◽

Robert D Christensen

Keyword(s):

Controlled Trial ◽

Blood Neutrophil ◽

Granulocyte Colony Stimulating Factor ◽

Colony Stimulating Factor ◽

Neonatal Neutropenia ◽

Stimulating Factor

Download Full-text

Alloimmune neonatal neutropenia due to an antibody to the neutrophil Fc- gamma receptor III with maternal deficiency of CD16 antigen

Blood ◽

10.1182/blood.v77.7.1572.1572 ◽

1991 ◽

Vol 77 (7) ◽

pp. 1572-1580 ◽

Cited By ~ 38

Author(s):

DF Stroncek ◽

KM Skubitz ◽

LB Plachta ◽

RA Shankar ◽

ME Clay ◽

...

Keyword(s):

Healthy Person ◽

Maternal Serum ◽

Maternal Antibody ◽

Fc Gamma Receptor ◽

Glycosyl Phosphatidylinositol ◽

Gamma Receptor ◽

Rabbit Polyclonal Antibody ◽

Specific Antigens ◽

Neonatal Neutropenia ◽

Cd16 Antigen

Abstract Antibodies to the neutrophil-specific antigens NA1 and NA2 are associated with alloimmune neonatal neutropenia (ANN), autoimmune neutropenia of childhood, and acute pulmonary transfusion reactions. These antigens have been found to be located on the neutrophil Fc-gamma receptor III (FcRIII). The mother of a child with ANN was found to lack both NA antigens and to produce an antibody that reacted with all normal neutrophils tested. We used maternal antibody and a CD16 monoclonal antibody (MoAb) that has specificity for FcRIII to immunoblot and immunoprecipitate neutrophil membranes of various NA phenotypes. Both antibodies immunoblotted an approximately 40- to 70-Kd glycoprotein (GP) on NA1, NA2-positive membrane, an approximately 40- to 55-Kd GP on NA1-homozygous membranes, and an approximately 55- to 70- Kd GP on NA2-homozygous membranes. Both antibodies also immunoprecipitated a 50- to 80-Kd GP from NA1, NA2-positive cells, a 50- to 60-Kd GP from NA1-homozygous cells, and a 55- to 80-Kd GP from NA2- homozygous cells. To further examine the specificity of the maternal antibody, sequential immunoprecipitation studies were performed using maternal antisera and a CD16 MoAb. After extracts of 125I surface- labeled neutrophils were precleared with maternal serum, CD16 MoAbs no longer immunoprecipitated any GP. Neither the CD16 MoAb nor a rabbit polyclonal antibody specific for FcRIII detected any GP in maternal neutrophil membranes by immunoblotting. Neutrophil FcRIII is a glycosyl- phosphatidylinositol anchored membrane GP as is decay accelerating factor and both are absent from neutrophils of patients with paroxysmal nocturnal hemoglobinuria (PNH). Maternal neutrophil membranes were probed with antibody specific for DAF and an 80-Kd GP was detected. This woman also has had no clinical evidence of PNH. These studies provide further evidence that the NA1 and NA2 antigens are on FcRIII and identify a healthy person whose neutrophils lack not only the neutrophil specific antigens NA1 and NA2 but multiple other epitopes of FcRIII and, therefore, likely lack FcRIII entirely.

Download Full-text

Characterization of a New Alloantigen (SH) on the Human Neutrophil Fcγreceptor IIIb

Blood ◽

10.1182/blood.v89.3.1027 ◽

1997 ◽

Vol 89 (3) ◽

pp. 1027-1034 ◽

Cited By ~ 137

Author(s):

Juergen Bux ◽

Ernst-Ludwig Stein ◽

Philippe Bierling ◽

Patricia Fromont ◽

Mary Clay ◽

...

Keyword(s):

Nucleotide Sequence Analysis ◽

Polymorphism Analysis ◽

Mutational Event ◽

Coding Region ◽

Specific Pcr ◽

Pcr Products ◽

Polymerase Chain ◽

Antigen Frequency ◽

Neonatal Neutropenia

Abstract Polymorphic structures of the neutrophil Fcγreceptor IIIb (FcγRIIIb) result in alloantibody formation that causes alloimmune neonatal neutropenia and transfusion reactions. Alloantigens located on FcγRIIIb include the antigens NA1 and NA2. In four cases of alloimmune neonatal neutropenia, granulocyte-specific alloantibodies directed against a thus far unknown antigen were detected by granulocyte agglutination and immunofluorescence tests in the maternal sera. By the use of the monoclonal antibody–specific immobilization of granulocyte antigens (MAIGA) assay, the new antigen, termed SH, was located on the FcγRIIIb. Nucleotide sequence analysis of the FcγRIIIb coding region from a SH(+) individual showed a single-base C→A mutation at position 266, which results in an Ala78Asp amino acid substitution. A family study confirmed that this nucleotide difference is inherited, and corresponds to the SH phenotype. Serologic typing of 309 randomly selected individuals showed an antigen frequency of 5% in the white population. The same frequency was found by genotyping, for which a technique based on polymerase chain reaction (PCR) using sequence-specific primers (PCR-SSP) was developed. Typing of all SH(+) individuals for NA1 and NA2, and PCR-restriction fragment length polymorphism analysis of the NA-specific PCR products from five SH(+) individuals using the SH-specific endonuclease SfaN I showed that SH antigen is very probably the result of an additional mutational event in the NA2 form of the FcγRIIIB gene. Immunochemical studies also demonstrated that the SH determinants reside on the 65- to 80-kD NA2 isoform of the FcγRIIIb. Our findings show the existence of an additional polymorphism of the FcγRIIIb, which can result in alloantibody formation causing alloimmune neonatal neutropenia.

Download Full-text