Evaluation of Angle Closure as a Risk Factor for Reduced Corneal Endothelial Cell Density: Comment
Corneal endothelial cell loss in patients with angle closure disease is a subclinical finding and is attributed to intermittent/chronic rise in intraocular pressure (IOP) in primary angle closure (PAC)/primary angle closure glaucoma (PACG), acute angle closure crisis, postlaser iridotomy, the presence of coexisting endothelial dystrophies, and following intraocular cataract or glaucoma surgeries.1,2
The article by Vardraj et al3 was a remarkable read considering the fact that endothelial health was being assessed for the first time across all stages of angle closure disease (primary angle closure suspect (PACS), PAC, and PACG) in eyes that were completely naïve to any intervention. There are, however, certain points we would like to discuss further.
First, the prevalence of angle closure disease is less common in age below 50 years.4 The endothelial health is presumably better in younger age and loses count as age progresses. So including subjects, below 40 years may probably confound the results obtained in the study.
Second, the power of the study has not been mentioned by the authors. As multiple groups were compared, we believe that the power of the study would have determined the probability of finding a difference between study groups if a true difference existed. Also, there was an asymmetric distribution of patients in each group [PAC/PACG (127 eyes, 15.6%), PACS (466, 57.3%), and open angle (221, 27.1%)] which can cause bias in the result interpretation.
Third, PAC and PACG are 2 different entities. In PACG, the duration and magnitude of IOP rise are much more compared with PAC sufficient to cause optic disc and field damage. The number of PAC and PACG patients was not clearly mentioned. Eight participants in the study who were previously on medications were included in the PAC/PACG group but no further information has been given about them. So we assume that these 8 patients were of PACG. Clubbing the 2 groups together is not desirable.
Fourth, severe IOP elevation is one of the exclusion criteria for the subjects. However, the magnitude of IOP rise that defines severe IOP elevation has not been mentioned. Also the number of medications used in the PACG group has not been mentioned, as a higher number of medications would suggest a greater degree of IOP elevation.
Regarding methodology, authors have mentioned about the unreliability of visual fields in their population. But in clinically uncertain cases visual fields may be necessary to make a diagnosis and not including them in the methodology may cause result misinterpretation. In some cases of PAC with high pressures without obvious disc changes, sometimes the optic disc cupping may not be evident until a later stage, and visual fields are required because the damage more than is clinically visible especially in angle closure glaucoma.
The results obtained in the study are confusing as PACS was found to have significant reduction of the endothelial count when compared with controls although the observed group differences were minor and likely of limited clinical significance as pointed out by the authors. The results obtained could have been due to the grossly unequal distribution of subjects among the 3 groups. One other limitation as mentioned by the authors is the cross-sectional design of the study. A prospective study with long duration follow-up is needed for a reliable outcome and correct interpretation of results.