Low-Dose Atropine Induces Changes in Ocular Biometrics in Myopic Children: Exploring Temporal Changes by Linear Mixed
Anders Hvid-Hansen1, Nina Jacobsen1,2, Jesper Hjortdal3
1Department of Ophthalmology, Copenhagen University Hospital-Rigshospitalet-Glostrup, DK-2600 Glostrup, Denmark.
Insights
Low-dose atropine eye drops, including a 0.1% loading dose, effectively slowed axial length elongation in children over six months. These changes in ocular biometrics, particularly axial length, contributed to reduced myopia progression.
Area of Science:
- Ophthalmology
- Pediatric Ophthalmology
- Myopia Control
Background:
- Myopia progression is a significant concern in pediatric populations.
- Low-dose atropine has shown promise in managing myopia, but its effects on ocular biometrics require further investigation.
- Understanding the mechanisms of atropine's efficacy is crucial for optimizing treatment strategies.
Purpose of the Study:
- To investigate changes in non-cycloplegic ocular biometrics during low-dose atropine treatment for myopia.
- To analyze the contribution of these biometric changes to the overall treatment effect on refractive error progression.
- To compare the effects of a 0.1% atropine loading dose and 0.01% atropine against a placebo.
Main Methods:
- A randomized, double-masked, placebo-controlled, multicenter trial was conducted.
- Participants received either 0.1% atropine loading dose, 0.01% atropine, or placebo for six months.
- Ocular biometrics including axial length (AL), anterior chamber depth (ACD), and lens thickness (LT) were measured; cycloplegic spherical equivalent (SE) was calculated.
Main Results:
- Axial length elongation was significantly reduced with both 0.1% atropine loading dose and 0.01% atropine compared to placebo after six months.
- Dose-dependent changes were observed in AL, ACD, LT, vitreous chamber depth (VCD), and choroidal thickness (ChT).
- Mediation analysis indicated that AL changes significantly contributed to the treatment effect on SE progression, with trends toward concentration dependency.
Conclusions:
- Low-dose atropine, particularly with a loading dose, effectively modifies ocular biometrics, leading to reduced myopia progression in children.
- Axial length elongation is a key mediator of atropine's effect on refractive error.
- The findings support a dose-dependent mechanism and highlight the importance of monitoring ocular biometrics during myopia management.
Abstract:
This study aimed to investigate changes in non-cycloplegic ocular biometrics during the initial six months of treatment with a 0.1% atropine loading dose and 0.01% atropine compared with a placebo and analyze their contribution to the treatment effect on cycloplegic spherical equivalent (SE) progression. The study was based on a randomized, double-masked, placebo-controlled, multicenter trial evaluating a 0.1% atropine six-month loading dose and 0.01% atropine in reducing myopic progression in Danish children. The treatment phase was 24 months, and the washout phase was 12 months. Parameters measured included changes in axial length (AL), anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and choroidal thickness (ChT), while cycloplegic SE and lens power were calculated. Longitudinal changes and contributions to treatment effects were analyzed using constrained linear mixed models and mediation analyses, respectively. After six months, AL was 0.13 mm shorter (95% confidence interval [CI], -0.18 to -0.07 [adjusted p < 0.001]) and 0.06 mm shorter (95% CI, -0.11 to -0.01 [adjusted p = 0.060]) with a 0.1% atropine loading dose and 0.01% atropine, respectively, compared to the placebo group. Similar concentration-dependent changes were found with ACD, LT, VCD, ChT, and cycloplegic SE. Although the treatment effects trended toward concentration-dependent responses, only the treatment effect mediated by AL at three months differed significantly between 0.01% atropine and a 0.1% atropine loading dose (adjusted p = 0.023). Several ocular biometrics, including AL, ACD, and LT, changed dose-dependently during low-dose atropine treatment. Moreover, the treatment effect of atropine on SE progression was mediated by a subset of ocular biometrics, mainly AL, with trends toward concentration dependency and distributional shifts over time.
