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The prenatal phase of retinopathy of prematurity
Olaf Dammann1,2,3, José Carlos Rivera4,5, Sylvain Chemtob4,5,6
1Deptartments of Public Health & Community Medicine, Pediatrics, and Ophthalmology, Tufts University School of Medicine, Boston, USA.
Insights
Prenatal inflammation, often from intrauterine infection, may initiate retinopathy of prematurity (ROP). This suggests a critical in-utero phase influencing ROP development and outcomes.
Area of Science:
- Neonatal ophthalmology
- Perinatal medicine
- Developmental biology
Background:
- Retinopathy of prematurity (ROP) is a significant cause of visual impairment in premature infants.
- Current models often focus on postnatal factors, but a prenatal component is increasingly suspected.
Purpose of the Study:
- To review and synthesize existing literature on prenatal risk factors for retinopathy of prematurity.
- To evaluate the hypothesis that ROP's etiology commences before birth.
Main Methods:
- A subjective summary and synthesis of selected experimental and epidemiological studies.
- Focus on publications supporting the prenatal origin of ROP.
Main Results:
- Evidence suggests a pre-in-utero phase in ROP development, challenging existing etiological models.
- Intrauterine infection-associated inflammatory responses are implicated as initiators of this prenatal phase.
Conclusions:
- A novel aetio-pathogenetic model for ROP is proposed, emphasizing a critical prenatal phase.
- Prenatal factors may modify the impact of postnatal stressors (infection, hyperoxia) on ROP pathogenesis.
Aim:
To explore the current literature on prenatal inflammation-associated risk factors for retinopathy of prematurity (ROP).
Methods:
Subjective summary of selected experimental and epidemiological publications that support the authors' central hypothesis that the aetiology of ROP begins before birth.
Results:
Based on current evidence we suggest that, contrary to current aetiological models, the process of ROP development begins with a prephase in utero. This beginning is likely initiated by inflammatory responses that are associated with intrauterine infection.
Conclusion:
We propose a novel aetio-pathogenetic model of ROP and suggest that the effects of postnatal exposure to inflammatory stressors (resulting from infection or hyperoxia or both) as well as those of other pre- and postnatal contributors to the complex pathogenesis of ROP might be modified by the prenatal phase of the disease.
