期刊
LANCET
卷 382, 期 9902, 页码 1445-1457出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0140-6736(13)60178-6
关键词
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资金
- Swedish Medical Research Council [2011-2432]
- Swedish Government [ALFGB-137491]
- VINNOVA [2009-00221]
- Research to Prevent Blindness Senior Investigator Award
- US National Institutes of Health [NEI EY017017, NEI EY022275, NIH P01 HD18655]
- Lowy Medical Foundation
- US National Eye Institute [EY021820]
- US National Institute of Neurological Disorders and Stroke (ELGAN) [NS040069]
- European Union [NEUROBID 241778, NEO-CIRC 282533]
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 omega-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.
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