Thank you for the article, Khaled. But in this case, the stroke was in the first hour of life, and the possibility of infection causing a false-positive of anti-beta2-glycoprotein-I was ruled out, since the baby has the antibody reagent until nowadays, in elevated titers, and there was no site of infection detectable. The mother does not have the antibody, ruling out a placental transmission.
All the other possible (known) common causes are roled out by great services of Pediatric Neurology, Rheumatology and Hematology. Now we are investing if there was placentary transmission of this antibody, however its IgG level remain elevated (> percentile 99).
Not a case report, but in the series of the neonatal thrombo-embolism
"N. DEMIREL, M. AYDIN, A. ZENCIROGLU, A. Y. BAS, N. YARALI*, N. OKUMUS, G. CINAR & M. S. IPEK. Neonatal thrombo-embolism: risk factors, clinical features and outcome. Annals of Tropical Paediatrics (2009) 29, 271–279"
Although I haven't seen a case like this, this syndrome is a posible cause through tromboembolism and the risk will be present until the elimination of the immuneglobulins IgG that have crossed the placenta
Although I didn't see a case of antiphospholipid syndrome presented with stroke in the neonatal period, I know a case of antiphospholipid syndrome presented with neonatal aortic thrombosis that mimicing aortic coartation in the neonatal period.
A mãe não apresenta nenhum dos anticorpos positivos, dosados em mais de uma ocasião, sugerindo uma SAF primária, o que torna o caso ainda mais instigante..
There are many instances where APLA may be positive and neonate may not exhibit thrombotic features. There is also a hypothesis that pathological antibodies in APLA are mainly IgG2 which are transferred less through placenta. Having said that, there are many reports where APLA was found as a trigerring factor (even bystander) for the underlying prothrombotic state in neonatal age group. I have attached an article which reiterates the same. Thank you.