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[Corneal endothelial cells in cicatricial retinopathy of prematurity]
Y Kagotani1, K Nomura, M Yamamoto
1Ophthalmic Division, Kobe Children's Hospital, Hyogo-ken, Japan.
Insights
This study found that lower birth weight in premature infants with cicatricial retinopathy of prematurity may impair corneal endothelial cell development. Xenon photocoagulation showed minimal long-term impact on corneal endothelium morphology.
Area of Science:
- Ophthalmology
- Neonatal Medicine
- Cell Biology
Background:
- Cicatricial retinopathy of prematurity (ROP) is a leading cause of blindness in premature infants.
- The long-term effects of ROP treatment on corneal endothelial cells are not fully understood.
- Specular microscopy is a non-invasive technique to assess corneal endothelial cell morphology.
Purpose of the Study:
- To investigate the impact of birth weight and xenon photocoagulation therapy on corneal endothelial cell morphology in children with cicatricial retinopathy of prematurity.
- To compare corneal endothelial cell parameters (mean cell area, cell density, coefficient of variation, hexagonality) between different birth weight and treatment groups.
- To evaluate the potential influence of xenon photocoagulation on corneal endothelial cell development and integrity.
Main Methods:
- Specular microscopy was used to examine corneal endothelial cells in 40 children with cicatricial ROP.
- Seventy-seven eyes were categorized into four groups based on birth weight (<1,000 g vs. ≥1,000 g) and treatment (xenon photocoagulation vs. no treatment).
- Statistical analysis (Student's t-test) was performed to compare morphological parameters between groups.
Main Results:
- A significantly smaller mean cell area was observed in infants with birth weight <1,000 g who received xenon photocoagulation compared to other groups, suggesting impaired corneal endothelial development in low birth weight infants.
- No significant differences in corneal endothelial cell parameters were found between groups with birth weight ≥1,000 g, regardless of treatment.
- Xenon photocoagulation showed no significant impact on coefficient of variation or hexagonality in most comparisons, indicating minimal long-term endothelial cell damage.
- However, four eyes in the low birth weight, xenon-treated group exhibited higher coefficient of variation and lower hexagonality, suggesting potential corneal damage from xenon absorption.
Conclusions:
- Lower birth weight appears to be associated with poorer corneal endothelial cell development in infants with cicatricial ROP.
- Xenon photocoagulation therapy for cicatricial ROP has a limited long-term influence on corneal endothelial morphology.
- Extremely low birth weight infants may be susceptible to corneal endothelial cell damage from xenon absorption during photocoagulation treatment.
Abstract:
We investigated corneal endothelial cells with specular microscopy in 40 children with cicatricial retinopathy of prematurity. Seventy-seven eyes were divided into 4 groups based on birth weight (< 1,000 g: group 1; > or = 1,000 g: group 2) and therapy at acute proliferative phase (xenon photocoagulation: group A; none: group B). Each morphological parameter, mean cell area, cell density, coefficient of variation (CV) and hexagonality, was compared between the two groups statistically according to Student's t-test. The mean cell area in group 1-A (233.3 +/- 17.2 microns 2) was significantly smaller than in groups 1-B (255.9 +/- 21.0 microns 2) and 2-A (250.5 +/- 23.5 microns 2) (p < 0.01). It seemed that corneal endothelial development is poor at lower birth weight. No significant difference was found between the parameters of groups 2-A and 2-B. Moreover, CV and hexagonality showed no significant difference in all comparisons. These results strongly suggested that xenon photocoagulation in the active phase of retinopathy of prematurity had little influence on endothelial morphology, at least after a long interval. Four eyes in group 1-A, however, had larger CV (0.3-0.4) and smaller hexagonality (< 60%), suggesting that the cell damage might be caused by xenon absorption by the cornea of extremely low-birth-weight infants.