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The interest in the role of CCT in glaucoma continues, but quality in experimental design has not characterized the area. Some prospective studies find CCT to be a risk factor for progression in those with established field loss, while others find no such association. To elucidate this area, we need longitudinal studies of the full spectrum of glaucoma patients. Choi et al. (298) limit their cross-sectional study to newly diagnosed cases exhibiting relatively focal nerve fiber layer damage with IOP below the magic number (21). The rationale for such selectivity is not apparent, and there was no explicit definition of what constituted 'glaucomatous' disc or field change. Ascertainment bias is very likely to confound any meaningful conclusion from this design. The authors agree that persons with normal IOP are less likely to be identified as having glaucoma than those with higher IOP, tending to give this group a different damage profile from all those with glaucoma. Thus, thinner CCT probably results in a delay in diagnosis as the explanation for this study's findings. We should study all those defined as OAG (by specific disc and field criteria), analyzing IOP as a parametric variable to prevent the loss of significance if the IOP effect (when present) is not fortuitously different on each side of a dichotomous magic number.
Finally, in this report, peak IOP and CCT were associated with damage level as univariates, but in multivariate analysis, IOP lost significance, probably due to interactive correlation between CCT and IOP, which should be accounted for, lest inappropriate conclusions be reached.