Pregnancy Disorders Appear to Modify the Risk for Retinopathy of Prematurity Associated With Neonatal Hyperoxemia and Bacteremia.
Abstract Objective: To explore (1) whether extremely low gestational age newborns exposed to inflammation-associated pregnancy disorders differ in retinopathy of prematurity (ROP) risk from infants exposed to placenta dysfunction-associated disorders, and (2) whether ROP risk associated with postnatal hyperoxemia and bacteremia differs among infants exposed to these disorders. Methods: Pregnancy disorders resulting in preterm birth include inflammation-associated: preterm labor, prelabor premature rupture of membranes (pPROM), cervical insufficiency, and abruption and placenta dysfunction-associated: preeclampsia and fetal indication. The risk of severe ROP associated with pregnancy disorders was evaluated by multivariable analyses in strata defined by potential effect modifiers, postnatal hyperoxemia and bacteremia. Results: Compared to preterm labor, infants delivered after pPROM were at reduced risk of plus disease (Odds ratio = 0.4, 95% confidence interval: 0.2-0.8) and prethreshold/threshold ROP (0.5, 0.3-0.8). Infants delivered after abruption had reduced risk of zone I ROP (0.2, 0.1-0.8) and prethreshold/threshold ROP (0.3, 0.1-0.7). In stratified analyses, infants born after placenta dysfunction had higher risks of severe ROP associated with subsequent postnatal hyperoxemia and bacteremia than infants born after inflammation-associated pregnancy disorders. Conclusion: Infants exposed to placenta dysfunction have an increased risk of severe ROP following postnatal hyperoxemia and bacteremia compared to infants exposed to inflammation-associated pregnancy disorders.
Available from: Thomas Schmitz
- "It is a stage of development when the WM displays enhanced vulnerability to such insults as hypoxia–ischemia, chronic hypoxia, inflammation, and excitotoxicity (Back, 2006; Khwaja and Volpe, 2008; Scafidi et al., 2009; Volpe, 2009). Recent evidence indicates an additional, poorly understood threat of hyperoxia, which may potentially arise from premature delivery (Sorensen and Greisen, 2009) and/or placental dysfunction (Lee et al., 2013), suggesting an association of blood gas abnormalities with neurodevelopmental disability (Leviton et al., 2010). This has prompted investigation into the specific effects of high normobaric oxygen using rodent models. "
[Show abstract] [Hide abstract]
ABSTRACT: The pathological mechanisms underlying neurological deficits observed in individuals born prematurely are not completely understood. A common form of injury in the preterm population is periventricular white matter injury (PWMI), a pathology associated with impaired brain development. To mitigate or eliminate PWMI, there is an urgent need to understand the pathological mechanism(s) involved on a neurobiological, structural, and functional level. Recent clinical data suggest that a percentage of premature infants experience relative hyperoxia. Using a hyperoxic model of premature brain injury, we have previously demonstrated that neonatal hyperoxia exposure in the mouse disrupts development of the white matter (WM) by delaying the maturation of the oligodendroglial lineage. In the present study, we address the question of how hyperoxia-induced alterations in WM development affect overall WM integrity and axonal function. We show that neonatal hyperoxia causes ultrastructural changes, including: myelination abnormalities (i.e., reduced myelin thickness and abnormal extramyelin loops) and axonopathy (i.e., altered neurofilament phosphorylation, paranodal defects, and changes in node of Ranvier number and structure). This disruption of axon-oligodendrocyte integrity results in the lasting impairment of conduction properties in the adult WM. Understanding the pathology of premature PWMI injury will allow for the development of interventional strategies to preserve WM integrity and function.
[Show abstract] [Hide abstract]
ABSTRACT: Abstract To determine that slower weight premature twins have more risk to develop severe retinopathy of prematurity (ROP) than the higher weight twins. We know that the lower weight twins had less optimal intra-uterine environments than their higher weight twins. We screened ninety-four consecutive premature twins for ROP. We compared the lower weight twins (n=47) against their higher weight twins (n=47). The risk of severe ROP (ROP stage 3 o greater) was significantly higher in the lower weight twin group (p < 0.006). In the same way, in the lower weight twin group the non perfused area of the temporal retinal artery was higher than that of the other group (an average of 1.2 diameters of the optic nerve head), in the 4-6 postnatal weeks (p < 0.004). The lower weight twin group have an increased risk of severe ROP associated with bacteremia (p = 0.045), or a weight gain less than 7 grams per day in the 4-6 postnatal weeks (p = 0.013) or a supplementary postnatal oxygen > 4 days (p = 0.007) compared to the higher weight twin group. We confirm Dr. Lee´s work that less optimal prenatal factors, in preterm twins, increase the risk of severe ROP.
Available from: Hye Kyoung Hong
[Show abstract] [Hide abstract]
Alteration of retinal angiogenesis during development leads to retinopathy of prematurity (ROP) in preterm infants, which is a leading cause of visual impairment in children. A number of clinical studies have reported higher rates of ROP in infants who had perinatal infections or inflammation, suggesting that exposure of the developing retina to inflammation may disturb retinal vessel development. Thus, we investigated the effects of systemic inflammation on retinal vessel development and retinal inflammation in neonatal rats.
To induce systemic inflammation, we intraperitoneally injected 100 μl lipopolysaccharide (LPS, 0.25 mg/ml) or the same volume of normal saline in rat pups on postnatal days 1, 3, and 5. The retinas were extracted on postnatal days 7 and 14, and subjected to assays for retinal vessels, inflammatory cells and molecules, and apoptosis.
We found that intraperitoneal injection of LPS impaired retinal vessel development by decreasing vessel extension, reducing capillary density, and inducing localized overgrowth of abnormal retinal vessels and dilated peripheral vascular ridge, all of which are characteristic findings of ROP. Also, a large number of CD11c+ inflammatory cells and astrocytes were localized in the lesion of abnormal vessels. Further analysis revealed that the number of major histocompatibility complex (MHC) class IIloCD68loCD11bloCD11chi cells in the retina was higher in LPS-treated rats compared to controls. Similarly, the levels of TNF-α, IL-1β, and IL-12a were increased in LPS-treated retina. Also, apoptosis was increased in the inner retinal layer where retinal vessels are located.
Our data demonstrate that systemic LPS-induced inflammation elicits retinal inflammation and impairs retinal angiogenesis in neonatal rats, implicating perinatal inflammation in the pathogenesis of ROP.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.