Prenatal and postnatal inflammation-related risk factors for retinopathy of prematurity.
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ABSTRACT:
SUBMITTER: Goldstein GP
PROVIDER: S-EPMC6592770 | biostudies-literature | 2019 Jul
REPOSITORIES: biostudies-literature
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Project description:At preterm birth, the retina is incompletely vascularized. Retinopathy of prematurity (ROP) is initiated by the postnatal suppression of physiological retinal vascular development that would normally occur in utero. As the neural retina slowly matures, increasing metabolic demand including in the peripheral avascular retina, leads to signals for compensatory but pathological neovascularization. Currently, only late neovascular ROP is treated. ROP could be prevented by promoting normal vascular growth. Early perinatal metabolic dysregulation is a strong but understudied risk factor for ROP and other long-term sequelae of preterm birth. We will discuss the metabolic and oxygen needs of retina, current treatments, and potential interventions to promote normal vessel growth including control of postnatal hyperglycemia, dyslipidemia and hyperoxia-induced retinal metabolic alterations. Early supplementation of missing nutrients and growth factors and control of supplemental oxygen promotes physiological retinal development. We will discuss the current knowledge gap in retinal metabolism after preterm birth.
| S-EPMC9691009 | biostudies-literature
Project description:Retinopathy of prematurity (ROP), a blinding condition affecting preterm infants, accounts for up to 40% of all childhood blindness worldwide. ROP is an interruption of retinal vascular maturation, which is physiologically complete at full term and thus ongoing at the time of preterm birth. Although ROP demonstrates delayed onset following preterm birth, representing a window for therapeutic intervention, we cannot cure or prevent this disease. The in-utero environment, including placental function, is increasingly recognized for contributions to preterm infant disease risk. Herein, we examine the clinical associations between presence and severity of acute placental inflammation to ROP risk. Using logistic regression, we find a protective relationship between presence and severity of acute placental inflammation and preterm infant development of ROP. This is most significant for infants born in the absence of maternal preeclampsia. Further, we examine the underlying molecular mediators that may inform this protective paradigm. Adopting a candidate approach analyzing proteins with described ROP risk associations, we find that placental HTRA1 and FABP4 protein expression is significantly decreased within placental tissues characterized by acute inflammation. Additionally, HTRA1 and VEGFA demonstrate inverse longitudinal trends within the peripheral circulation for infants born in the presence compared to absence of acute placental inflammation. An agnostic approach, including whole transcriptome and differential methylation placental analysis, identifies novel mediators and pathways that may underly protection. Taken together, these data build on emerging literature showing disparate associations between acute placental inflammation and ROP development within preeclamptic or non-preeclamptic preterm infant populations and identifies novel placental mechanisms that may inform postnatal risk associations in preterm infants.
2023-01-01 | GSE218039 | GEO
Project description:Several studies propose that Retinopathy of Prematurity (ROP) is a multifactorial disorder implicating many prenatal and postnatal factors. The objective of our study was to determine the incidence and the risk factors that influenced ROP development and progression. We retrospectively compiled data of preterms with birth weight (BW) ≤ 1.500 g and/or gestational age (GA) < 32 weeks, or BW between 1.501 and 2.000 g and/or GA ≥ 32 weeks with oxygen supply > 72 h or unstable clinical course screened for ROP in Regional University Hospital of Málaga from 2015 to 2018. 202 infants (44.7%) developed ROP and 66 exhibited progression (32.7% of ROP infants). In the univariate analysis, many risk factors were associated with ROP. In the subsequent multivariate analysis, GA, oxygen therapy and weight at 28 days of life, mechanical ventilation duration, non-invasive ventilation, surfactant administration and late-onset sepsis were independently associated with the development. However, oxygen therapy duration, late-onset sepsis and weight at 28 days were associated with the progression. The ROP development and progression risk factors were different. Our results are important to facilitate screening, early diagnosis and ROP treatment while reducing unneeded examinations.
| S-EPMC9767907 | biostudies-literature
Project description:Retinopathy of prematurity (ROP) is a retinal vasoproliferative disease that affects premature infants. Despite improvements in neonatal care and management guidelines, ROP remains a leading cause of childhood blindness worldwide. Current screening guidelines are primarily based on two risk factors: birth weight and gestational age; however, many investigators have suggested other risk factors, including maternal factors, prenatal and perinatal factors, demographics, medical interventions, comorbidities of prematurity, nutrition, and genetic factors. We review the existing literature addressing various possible ROP risk factors. Although there have been contradictory reports, and the risk may vary between different populations, understanding ROP risk factors is essential to develop predictive models, to gain insights into pathophysiology of retinal vascular diseases and diseases of prematurity, and to determine future directions in management of and research in ROP.
| S-EPMC6089661 | biostudies-literature
Project description:ImportanceThe current guidelines for retinopathy of prematurity (ROP) detection programs in the United States include a range of birth weights (BWs) and gestational ages and likely require examinations of many premature infants who are at low risk for developing serious retinopathy.ObjectiveTo determine the incidence, onset, and early course of ROP in what to our knowledge is the largest cohort to date that is representative of infants who are undergoing ROP screening.Design, setting, and participantsThis secondary analysis of data from the Postnatal Growth and Retinopathy of Prematurity (G-ROP) retrospective cohort study was conducted in 29 hospitals in the United States and Canada between January 2006 and December 2011 and included 7483 infants who underwent serial ROP examinations.Main outcomes and measuresMost severe ROP in either eye, classified as no ROP, mild ROP, type 2 ROP, or type 1 ROP (per Early Treatment for ROP Study criteria). Onset at postmenstrual age for zone I disease and stage of ROP, plus disease, and treatment.ResultsThis study included 7483 infants with a mean (SD) BW of 1099 (259) g and a mean (SD) gestational age of 28 (3) weeks who underwent ROP examinations. Of these, 3224 infants (43.1%) developed ROP, 459 (6.1%) developed type 1 and 472 (6.3%) type 2 ROP, 514 (6.9%) underwent treatment in 1 or both eyes, and 147 (2%) had zone I disease. Additionally, 98.1% of type 1 or 2 ROP cases occurred in infants with a BW of less than 1251 g. Only about half of the eyes (49.4%) were vascularized into zone III by 37 weeks postmenstrual age.Conclusions and relevanceThese findings add to our knowledge of ROP screening as they include all eligible infants, not just high-risk infants as in previous studies. More than 40% of at-risk premature infants develop some stage of ROP, and most retinopathy regresses without treatment. However, approximately 12.5% develop severe ROP, which occurs almost exclusively among infants with a BW of less than 1251 g.
| S-EPMC6583045 | biostudies-literature
Project description:ImportanceMost premature infants will not develop retinopathy of prematurity (ROP) of clinical relevance, yet screening evaluations often continue beyond hospital discharge, even for those infants without ROP.ObjectivesTo identify the characteristics of infants at low risk for ROP, for whom further postdischarge screening may be of limited value.Design, setting, and participantsThis study took place in North American neonatal intensive care units where clinicians had expertise in ROP. Infants with birth weight less than 1251 g who were born at or transferred into an Telemedicine Approaches to Evaluating Acute-Phase ROP (e-ROP) study center were enrolled. The study included post hoc analysis of prospectively collected in-hospital ROP examination results among infants enrolled in the e-ROP study. We characterized infants without ROP and performed logistic regression on the subset of infants who were 27 to 33 weeks' gestational age to determine characteristics associated with the absence of ROP during all in-hospital examinations.Main outcomes and measuresThe main measure was the absence of ROP prior to hospital discharge; the main outcome was treatment for ROP.ResultsA total of 1257 infants born at 22 to 35 weeks' gestation (median [interquartile range (IQR)], 26 [25-28] weeks) with birth weights less than 1251 g (median [IQR], 860 [690-1040] g) underwent 4113 ROP examinations between 31 and 47 weeks' postmenstrual age. Overall, 1153 examinations (38%) showed no ROP, and 456 infants (36%) did not have ROP prior to study center discharge or study end point. Among infants without ROP during examinations at 32 and 33 weeks' postmenstrual age, 16 (9.4%) and 14 (5.3%) subsequently underwent ROP treatment, respectively. At hospital discharge, there was no ROP in 59% of infants of 27 to 33 weeks' gestational age, compared with 15% of those who were less than 27 weeks' gestational age (difference, 44% [95% CI, 38.5%-48.1%]; P ≤ .001). With more than 85% follow-up among infants without ROP by 37 weeks' postmenstrual age, none (95% CI, 0%-0.98%) were treated for ROP. In multivariate analysis of infants born at 27 to 33 weeks' gestation, larger birth weight (OR, 4.1 [95% CI, 1.6-10.3]) and higher gestational age (OR, 4.0 [95% CI, 1.5-10.8]) were significantly associated with absence of ROP.Conclusions and relevanceThese findings suggest that, for infants of 27 weeks' gestational age or greater and birth weights larger than 750 g, if no ROP has been detected by discharge at near-term postmenstrual age, then further ROP surveillance has limited value. Studies of all infants at risk are needed to develop more specific, objective criteria for termination of ROP surveillance and focus resources on infants at higher risk of ROP.Trial registrationClinicalTrials.gov Identifier: NCT01264276.
| S-EPMC6439829 | biostudies-literature
Project description:BackgroundPreterm infants with anaemia are treated with recombinant human erythropoietin (rhEPO). It is debated whether rhEPO treatment is a risk factor for retinopathy of prematurity (ROP). We evaluated longitudinal EPO and haemoglobin levels, blood transfusions and neonatal morbidities as risk factors for severe ROP.MethodThis prospective study included 78 Swedish infants, born <28 weeks gestational age (GA), screened for ROP. We tested serum EPO levels on postnatal days 1, 7, 14 and 28 and at postmenstrual ages 32, 36 and 40 weeks. Haemoglobin levels and blood transfusions were recorded during postnatal weeks 1-4. Anaemia was defined as haemoglobin ≤110 g/L.ResultsDuring postnatal week 1, infants with severe ROP requiring treatment (28%) more frequently developed anaemia (42.9% versus 8.0%, P = 0.003) and had higher mean EPO levels (postnatal day 7: 14.2 versus 10.8 mIU/mL, P = 0.003) compared to infants with no or less severe ROP not requiring treatment. In multivariable analyses, GA and anaemia during week 1 remained significant risk factors, but elevated EPO level postnatal day 7 was no longer significant.ConclusionsAmong infants born <28 weeks GA, anaemia during week 1 was a significant risk factor for severe ROP requiring treatment but not elevated EPO levels.
| S-EPMC6422731 | biostudies-literature
Project description:Retinopathy of prematurity (ROP) is an important cause of childhood blindness globally, and the incidence is rising. The disease is characterized by initial arrested retinal vascularization followed by neovascularization and ensuing retinal detachment causing permanent visual loss. Although neovascularization can be effectively treated via retinal laser ablation, it is unknown which children are at risk of entering this vision-threatening phase of the disease. Laser ablation may itself induce visual field deficits, and there is therefore a need to identify targets for novel and less destructive treatments of ROP. Inflammation is considered a key contributor to the pathogenesis of ROP. A large proportion of preterm infants with ROP will have residual visual loss linked to loss of photoreceptor (PR) and the integrity of the retinal pigment epithelium (RPE) in the macular region. Recent studies using animal models of ROP suggest that choroidal degeneration may be associated with a loss of integrity of the outer retina, a phenomenon so far largely undescribed in ROP pathogenesis. In this review, we highlight inflammatory and neuron-derived factors related to ROP progression, as well, potential targets for new treatment strategies. We also introduce choroidal degeneration as a significant cause of residual visual loss following ROP. We propose that ROP should no longer be considered an inner retinal vasculopathy only, but also a disease of choroidal degeneration affecting both retinal pigment epithelium and photoreceptor integrity.
| S-EPMC5567917 | biostudies-literature
Project description:The immature retinas of preterm neonates are susceptible to insults that disrupt neurovascular growth, leading to retinopathy of prematurity. Suppression of growth factors due to hyperoxia and loss of the maternal-fetal interaction result in an arrest of retinal vascularisation (phase 1). Subsequently, the increasingly metabolically active, yet poorly vascularised, retina becomes hypoxic, stimulating growth factor-induced vasoproliferation (phase 2), which can cause retinal detachment. In very premature infants, controlled oxygen administration reduces but does not eliminate retinopathy of prematurity. Identification and control of factors that contribute to development of retinopathy of prematurity is essential to prevent progression to severe sight-threatening disease and to limit comorbidities with which the disease shares modifiable risk factors. Strategies to prevent retinopathy of prematurity will depend on optimisation of oxygen saturation, nutrition, and normalisation of concentrations of essential factors such as insulin-like growth factor 1 and ω-3 polyunsaturated fatty acids, as well as curbing of the effects of infection and inflammation to promote normal growth and limit suppression of neurovascular development.
| S-EPMC4389630 | biostudies-literature
Project description: Not available
| S-EPMC4020289 | biostudies-literature