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Published on: November 20, 2015
Immaturity, perinatal inflammation, and retinopathy of prematurity: a multi-hit hypothesis
Olaf Dammann1, Maria-Jantje Brinkhaus, Dorothee B Bartels
1Division of Newborn Medicine, Floating Hospital for Children at Tufts Medical Center, Boston, MA 02111, USA. odammann@tuftsmedicalcenter.org
Insights
Inflammation markers, both before and after birth, increase the risk of retinopathy of prematurity (ROP) in premature infants. This includes clinical signs of infection and inflammatory conditions like chorioamnionitis.
Area of Science:
- Neonatalogy
- Ophthalmology
- Genetics
Background:
- Retinopathy of prematurity (ROP) is a significant cause of visual impairment in preterm infants.
- Infection and inflammation are suspected contributors to ROP development and progression.
Purpose of the Study:
- To investigate the association between infection/inflammation markers and the risk of developing ROP.
- To determine if these markers influence the progression to severe stages of ROP.
Main Methods:
- A cohort of 73 preterm infants (gestational age <32 weeks) was studied.
- Clinical data and genetic polymorphisms in infection/inflammation-associated genes were analyzed.
- Statistical methods included descriptive and analytic approaches.
Main Results:
- Clinical markers of infection/inflammation were linked to a higher risk of ROP and progression to ROP grade 3.
- Genetic markers did not correlate with ROP occurrence but were associated with progression to high-grade disease.
- Low gestational age (<29 weeks) was the primary risk factor, with clinical chorioamnionitis and neonatal systemic inflammatory response syndrome further increasing ROP progression risk.
Conclusions:
- Both prenatal and postnatal exposure to inflammation contribute to ROP risk in preterm infants.
- Clinical signs of inflammation are key indicators for ROP risk and progression.
Objective:
To explore the relationship among markers of infection/inflammation in their association with retinopathy of prematurity (ROP).
Methods:
We studied clinical characteristics and 4 single nucleotide polymorphisms in infection/inflammation-associated genes in a group of 73 children with a gestational age<32 weeks. Forty-four children (60%) had ROP, of whom 13 (30% of those with ROP) progressed to stage 3 ROP. No child had grade 4 or 5 ROP. We employed both descriptive and analytic statistical methods.
Results:
Clinical variables of infection/inflammation were consistently associated with an increased risk of ROP. Among infants with ROP, they were also associated with progression to ROP grade 3. Genetic markers were not associated with ROP occurrence, but with progression to high grade disease. In tri-variable analyses exploring the effects of gestational age <29 weeks, clinical chorioamnionitis (CAM) and neonatal systemic inflammatory response syndrome (SIRS) on ROP occurrence, low gestational age was the most important antecedent, while additional individual or joint exposure to SIRS and CAM add appreciably to this risk of progression to high grade disease.
Conclusion:
Both antenatal and neonatal exposure to inflammation appear to contribute to the increased ROP risk in preterm infants.
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