We used for comparative analyses BlastP (available at: https://blast.ncbi.nlm.nih.gov/Blast.cgi?PAGE=Proteins) and the whole virus proteome (available at: https://www.ncbi.nlm.nih.gov/nuccore/MN908947).
Abstract:Background: The objective was to evaluate the diagnostic value of RHD fetal genotyping from the plasma of D-mothers as soon as 10 weeks' gestation in a routine clinical practice in Belgium. Study design and methods: A prospective study was conducted between November 2002 and December 2006. DNA extraction was performed in an automated closed tube system. Fetal RHD/SRY genotypes were detected in the plasma of 563 pregnant mothers by real-time polymerase chain reaction (PCR) targeting multiple exons 4, 5, and 10 of the RHD gene and targeting an SRY gene sequence. These were compared to the D phenotypes determined in the 581 babies they delivered. Results: By combining amplification of three exons, the concordance rate of fetal RHD genotypes in maternal plasma and newborn D phenotypes at delivery was 100 percent (99.8% including one unusual false-positive). The presence of nonfunctional RHD genes and the absence of a universal fetal marker, irrespective of fetal sex, did not influence the accuracy of fetal RhD status prediction. The RHD genotyping from 18 twin pregnancies was also assessed. Five weak D women were excluded from the RHD fetal genotyping prediction. Three discrepant results (0.5%) between predicted fetal genotype and cord blood phenotype were not confirmed by the baby phenotypes from venipuncture blood. Conclusion: Prenatal prediction of fetal RHD by targeting multiple exons from the maternal plasma with realtime PCR is highly sensitive and accurate. Over 4 years, this experience has highly modified our management of D-pregnant women.
BACKGROUND: Bone marrow transplantation with minor ABO incompatibility may be followed by moderate delayed hemolysis of the recipient's red cells by donor‐derived ABO antibodies. This reaction may be more severe after transplantation of peripheral blood progenitor cells (PBPCs). CASE REPORT: A 16‐year‐old boy underwent an allogeneic PBPC transplant from his HLA‐mismatched mother as treatment for acute myeloblastic leukemia that had proved resistant to induction chemotherapy. Transfusion of the unmanipulated PBPCs proceeded without any complication, despite the difference in ABO blood group (donor, O Rh‐positive; recipient, A Rh‐positive). On Day 7, a rapid drop in hemoglobin to 4 g per dL was observed, which was attributed to a massive hemolysis. All the recipient's group A red cells were destroyed within 36 hours. This delayed and rapidly progressive hemolytic anemia was not associated with the transfusion of the donor's plasma. Rather, the anti‐A titer increased in parallel with marrow recovery, which suggested an active synthesis of these antibodies by immunocompetent cells from the donor against the recipient's red cells. The mother's anti‐A titer was retrospectively found to be 2048. Her unusually high titer is probably due to prior sensitization during pregnancies. On Day 12, the patient developed grade IV graft‐versus‐host disease, which proved resistant to all treatments instituted and led to his death on Day 35. CONCLUSION: PBPC transplantation with minor ABO incompatibility may be associated with significant risk of massive delayed hemolysis.
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