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Editors Selection IGR 23-1

Laser Treatment: Post-iridotomy Cataract

Comment by Sirisha Senthil on:

100468 Cataract progression after Nd:YAG laser iridotomy in primary angle-closure suspect eyes, Chang DS; Jiang Y; Kim JA et al., British Journal of Ophthalmology, 2023; 107: 1264-1268

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Chang et al., in a prospective Zhongshan Angle Closure Prevention Trial, evaluated the rate and type of cataract progression following laser peripheral iridotomy (LPI). Among 889 participants with bilateral primary angle-closure suspect (PACS), one randomly selected eye underwent LPI and the contralateral eye of the participant served as untreated control. Post LPI, they were followed up for 72 months and progression in cataract was compared between the LPI and controls using LOCS III grading system. Progression was defined as increase in grade of cataract by at least two units or cataract surgery.

LPI does not increase the risk for cataract formation

The study conclusion that LPI does not increase the risk for cataract formation is sound and is supported by a prospective study design with long follow-up and ideal (fellow eye) comparative group. The following is an important clinically relevant result of the study. Nine eyes in each group received cataract surgery with five participants receiving surgery in both eyes. The total cumulative probability of reaching pre-defined cataract progression was 21.2% in LPI-treated eyes and 19.4% in control eyes (p = 0.401). The differences in the average nuclear grades and cortical grades were not clinically significant, although there was statistically significant difference. The average nuclear grades were slightly higher at 72 months among LPI-treated eyes (both NO and NC: 2.9 vs 2.8, p < 0.001, table 2). However, the average cortical grades were lower in LPI-treated eyes (0.76 vs 0.82, p = 0.030, table 2). This significant difference in p-value is possibly due to large sample size.

The authors also mentioned that the total energy used for LPI was not associated with greater risk of cataract progression in a multivariate analysis among treated eyes (p = 0.072). This possibly suggests that there is no biological causal relationship between LPI and cataract progression.

The following two results of 10% for overall cataract and 50% for NC progression risk are 'relative risk' and need to be interpreted along with the absolute risk of 21.2% vs 19.4% for overall cataract and 4.61% vs 3.04%) for NS. The overall risk of cataract progression in LPI-treated eyes appeared 10% higher compared with controls (HR = 1.10 (95% CI 0.88 to 1.36) (table 3, figure 1), this was not statistically significant. The risk of cortical and PSC progression remained unchanged between eyes, and while the risk of nuclear sclerosis progression was approximately 50% higher in LPI-treated eyes, this was not statistically significant (HR = 1.49 (95% CI 0.91 to 2.42).

The incidence rate of cataract progression was 3.7 per 100 eye-years in LPI-treated eyes and 3.4 per 100 eye-years in control eyes. This considers the follow-up period of individual participants during the study period. While interpreting this result, one also needs to consider the fact that the number of events were small and about 30% participants dropped out by the end of the study, that possibly has resulted in wide confidence interval of Hazard ratios.

The studies by Lim¹ and Vijaya² show increased risk of cataract with LPI.

The main issue with these studies is no control group in the Lim et al. study and an inappropriate control group in the Vijaya et al. study.

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