| Project/Area Number |
06672298
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory medicine
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| Research Institution | Fukushima Medical College |
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Principal Investigator |
OHTA Hitoshi Fukushima Medical College, Blood Transfusion Service Associate Professor, 医学部, 助教授 (20150279)
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| Co-Investigator(Kenkyū-buntansha) |
UJIIE Niro Fukushima Medical College, Neonatology Assistant Professor, 医学部, 講師 (10168685)
ENDO Chikara Fukushima Medical College, Gynecology Assistant Professor, 医学部, 講師 (50168829)
OKUBO Mituo Fukushima Medical College, Internal Medicine Assistant, 医学部, 助手 (40260781)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Neonatal alloimmune thrombocytopenia / Anti-platelet antibody / PCR-SSP / Amniotic fluid cells / HPA-4 / Genotype / Prenatal diagnosis / fetus / Platelet / Alloimmunization / DNA診断 / 遺伝子増幅 / 血小板型 / プライマー |
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| Research Abstract |
To reveal the prevalence of maternal alloimmunization to platelet antigens (HPA) and the incidence of neonatal alloimmune thrombocytopenia (NAT), 10,000 maternal sera were tested for the presence of anti-HPA antibodies using the Mixed Passive Haemagglutination. Ninety-six anti-HPA were found ; anti-HPA-4b, -5a, -5b and anti-Nak^a in 23,2,70 and one pregnant women, respectively.
Optimal management of NAT requires the determination of fetal HPA status as early as possible. We explored the feasibility of fetal HPA-4 genotyping by amplification of DNA from amniotic cells using sequence specific primers-polymerase chain reaction (PCR-SSP). Three babies in which fetal HPA-4 type from amniotic fluid cells was completely concordant with type using the blood of these infants studied. Two fetuses were shown to be homozygous PHA-4a/a, and had normal platelet counts. The third fetus was heterozygous HPA-4a/b incompatible with maternal antibody, and developed thrombocytopenia. These findings suggest that HPA-4 genotyping can be reliable determinied from amniotic fluid by DNA amplification.
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