Alan Nurden: FNAIT Remains an Important Clinical Challenge in Inherited Bleeding Disorders
Alan Nurden, Emeritus Research Director at CNRS, Co-Founder of the French National Reference Centre for Inherited Platelet Disorders (CRPP), shared a post on LinkedIn about a recent article by Huiying Zhi et al. published in Blood, adding:
“Fetal/neonatal alloimmune thrombocytopenia is an important medical issue.
The HPA-1a/b alloantigen system is located on the beta3 subunit of the platelet alphaIIbbeta3 integrin and antibodies can form in HPA-1b homozygous mothers when the fetus has inherited the paternal HPA-1a antigen.
But why does it appear in only about 30 percent of potential cases?
Here Debra and Peter Newman and their colleagues use a mouse model to show how fetal maternal hemorrhage is a determining factor in antibody production and that elimination of alloantigen incompatible fetal platelets from the mother’s circulation using an HPA-1a-specific monoclonal antibody prophylactically effectively decreases maternal alloantibody production.
While reading this impressive study, I thought of patients with the inherited bleeding disorder, Glanzmann thrombasthenia (GT), where the platelet alphaIIbbeta3 integrin is absent and where for mothers the likelihood of fetal maternal hemorrhage is much greater.
For mothers with beta3 gene mutations, the HPA-1 antigens will be lost when the beta3 integrins fail to form, but for patients with alphaIIb gene mutations, beta3 will be present within the alphavbeta3 integrin (in small amounts in platelets but also in endothelial and other cells including bone and the reproductive system).
It is therefore to be hoped that when such patients are genotyped that this includes the integrin carrying HPA systems.
For example, my group showed many years ago that most of the French Manouche GT patients are HPA-1b+/+.
As currently investigated prophylactic treatments targeting an increased fibrin generation at bleeding sites improve the quality of life of patients with GT then the number of pregnancies may increase.
Likewise, if as I hope gene therapy becomes available it may be advisable that the replaced alphaIIb or beta3 genes have compatible alloantigen systems.
Patients with GT benefit considerably from personalized medicine of which genotyping is an essential part.”
Title: Transfusing HPA-mismatched platelets to mimic fetomaternal hemorrhage elicits fetal/neonatal alloimmune thrombocytopenia
Authors: Huiying Zhi, Douglas Sheridan, Peter J Newman, Debra K Newman
Read the Full Article on Blood
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