Retinopathy of prematurity.
Retinopathy of prematurity.
复制标题
DOI：
10.1016/s0140-6736(13)60178-6
复制
发表时间：
2013-10-26
期刊：
影响因子：
168.9
通讯作者：
Dammann, Olaf
中科院分区：
文献类型：
--
作者：
Hellstrom, Ann;Smith, Lois E. H.;Dammann, Olaf
早产儿的未成熟视网膜易受损伤，破坏神经血管生长，导致早产儿视网膜病变。由于高氧和母胎相互作用的丧失导致生长因子的抑制导致视网膜血管形成的停滞（阶段1）。随后，代谢活性增加，但血管化不良，视网膜变得缺氧，刺激生长因子诱导的血管增生（第2阶段），这可能导致视网膜脱离。在极早产儿中，控制给氧可减少但不能消除早产儿视网膜病变。识别和控制导致早产儿视网膜病变发展的因素对于预防进展为严重的视力威胁疾病和限制疾病与可改变的风险因素共享的合并症至关重要。预防早产儿视网膜病变的策略将取决于氧饱和度、营养的优化和必需因子（如胰岛素样生长因子1和ω-3多不饱和脂肪酸）浓度的正常化，以及抑制感染和炎症的影响，以促进正常生长并限制对神经血管发育的抑制。
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.