Rxe9;sumxe9;
U
ne thrombop
xe9;nie n
xe9;onatale peut r
xe9;v
xe9;ler plusieurs causes. Un nouveau-n
xe9;
xe9;tait hospitalis
xe9; au 3
e jour de vie pour u
ne thrombop
xe9;nie initialement li
xe9;e
xe0; u
ne thrombop
xe9;nie mater
nelle auto-immu
ne. Deux jours plus tard, il pr
xe9;sentait u
ne infection materno-fœtale due au virus chikungunya (CHIKV) dans le cadre de l’
xe9;pid
xe9;mie qui s
xe9;vissait
xe0; l’
xee;le de la R
xe9;union. Le typage des groupes plaquettaires des parents montrait u
ne incompatibilit
xe9; plaquettaire dans le syst
xe8;me human platelet antigen (HPA)-3 avec absence d’alloanticorps dans le sang mater
nel. Devant la persistance d’u
ne thrombop
xe9;nie mod
xe9;r
xe9;e, le diagnostic de syndrome de Bernard-Soulier (BSS)
xe9;tait port
xe9; un an plus tard sur l’absence de glycoprot
xe9;i
ne Ib et IX
xe0; la cytom
xe9;trie en flux. Cette observation montre la difficult
xe9;
xe0; caract
xe9;riser u
ne thrombop
xe9;nie et rappelle qu’u
ne pathologie acquise peut s’associer
xe0; u
ne pathologie constitution
nelle.
Summary
Neonatal thrombocytopenia may stem from several origins. A newborn was hospitalized on the 3rd day of life with thrombocytopenia likely due to maternofetal autoimmune thrombocytopenia. Two days later, he displayed a chikungunya virus infection, during a severe epidemic on Reunion Island. The characterization of human platelet antigen (HPA) in the parents showed incompatibility in the HPA-3 system; however, no detectable antiHPA-3a antibody was found in the mother's serum. The persistence of moderate thrombocytopenia led to the diagnosis, using flow cytometry, of Bernard-Soulier syndrome (BSS), with no detectable GPIbIX. This case shows that neonatal inherited thrombocytopenia may be difficult to characterize, especially when it is associated with an acquired cause.