RESUMO
BACKGROUND: Transient donor hydrops (TDH) is defined as donor hydrops developed within days after laser therapy for twin-twin transfusion syndrome (TTTS) followed by resolution later. The purpose of this study was to evaluate the incidence, neonatal outcomes and predisposing factors of post laser therapy TDH in severe TTTS. METHODS: A total of 142 patients with severe TTTS who received laser therapy were included into this study. The pre-operative characteristics and neonatal outcomes were compared between TTTS with and without post laser therapy TDH. All live neonates received cranial ultrasound examination after delivery, mild cerebral injury was defined as exhibiting at least one of the following: intraventricular hemorrhage (IVH) grade I and II, lenticulostriate vasculopathy and subependymal pseudocysts; severe cerebral injury comprised at least one among the following: IVH grade III or grade IV, cystic periventriculoleukomalacia (PVL) grade II or more, porencephalic cysts, and ventricular dilatation. Fetal survival was defined as living more than 30 days after delivery.
Assuntos
Transfusão Feto-Fetal/cirurgia , Fetoscopia/efeitos adversos , Hidropisia Fetal/epidemiologia , Doenças do Recém-Nascido/epidemiologia , Fotocoagulação a Laser/efeitos adversos , Adulto , Doença Cerebrovascular dos Gânglios da Base/epidemiologia , Doença Cerebrovascular dos Gânglios da Base/etiologia , Lesões Encefálicas/epidemiologia , Lesões Encefálicas/etiologia , Estudos de Casos e Controles , Hemorragia Cerebral Intraventricular/epidemiologia , Hemorragia Cerebral Intraventricular/etiologia , Feminino , Transfusão Feto-Fetal/complicações , Transfusão Feto-Fetal/embriologia , Fetoscopia/métodos , Glioma Subependimal/epidemiologia , Glioma Subependimal/etiologia , Humanos , Hidropisia Fetal/etiologia , Incidência , Recém-Nascido , Doenças do Recém-Nascido/etiologia , Fotocoagulação a Laser/métodos , Gravidez , Resultado da Gravidez , Gravidez de GêmeosRESUMO
Hydrocephalus formation is a frequent complication of neuropathological insults associated with neuroinflammation. However, the mechanistic role of neuroinflammation in hydrocephalus development is unclear. We have investigated the function of the proinflammatory acting inhibitor of κB kinase (IKK)/nuclear factor κB (NF-κB) signaling system in neuroinflammatory processes and generated a novel mouse model that allows conditional activation of the IKK/NF-κB system in astrocytes. Remarkably, NF-κB activation in astrocytes during early postnatal life results in hydrocephalus formation and additional defects in brain development. NF-κB activation causes global neuroinflammation characterized by a strong, astrocyte-specific expression of proinflammatory NF-κB target genes as well as a massive infiltration and activation of macrophages. In this animal model, hydrocephalus formation is specifically induced during a critical time period of early postnatal development, in which IKK/NF-κB-induced neuroinflammation interferes with ependymal ciliogenesis. Our findings demonstrate for the first time that IKK/NF-κB activation is sufficient to induce hydrocephalus formation and provides a potential mechanistic explanation for the frequent association of neuroinflammation and hydrocephalus formation during brain development, namely impairment of ependymal cilia formation. Therefore, our study might open up new perspectives for the treatment of certain types of neonatal and childhood hydrocephalus associated with hemorrhages and infections.