We read with great interest the article by Kolli and associates, which addressed an important and clinically relevant question regarding whether current follow-up schedules for patients with glaucoma could be optimized. By leveraging long-term real-world data, the study provides valuable evidence to inform follow-up strategies in glaucoma care. Nevertheless, beyond the limitations acknowledged by the authors, several methodological considerations may influence the interpretation of the findings and warrant further discussion.
First, the study may be susceptible to reverse causation. In routine clinical practice, follow-up intervals are not assigned randomly but are largely determined by clinicians’ assessments of disease severity, stability, and risk of progression. Patients perceived as stable are typically scheduled for longer follow-up intervals and may therefore accumulate greater delayed follow-up (DFU), whereas those considered at higher risk are monitored more closely. Consequently, DFU may partly reflect physician-driven risk stratification rather than an independent exposure. Although the analyses adjusted for several baseline clinical characteristics, the nuanced clinical judgment underlying follow-up recommendations is difficult to capture using routinely available covariates, leaving the possibility of residual confounding.
Second, DFU was characterized using summary measures, including mean delay duration, maximum delay duration, and the proportion of delayed visits. Although informative, these static metrics may not fully capture the temporal patterns of delayed care. For example, a single prolonged interruption in care may have different clinical implications than multiple intermittent short delays. Likewise, delays occurring immediately before disease progression may be more consequential than those occurring during periods of clinical stability. Time-dependent analytical approaches, such as time-varying exposure models or weighted cumulative exposure analyses, may better characterize the relationship between delayed follow-up patterns and glaucoma progression.
Third, treatment escalation was not considered as a potential mediator. Delayed follow-up may result in worsening intraocular pressure control or structural damage, which in turn may prompt clinicians to intensify treatment through additional medications, laser procedures, or surgery. Such interventions could mitigate subsequent visual field deterioration and thereby attenuate the observed association between DFU and progression. As a result, visual field progression alone may not fully capture the clinical consequences of delayed care. Evaluating the relationship between DFU and treatment modifications could provide a more comprehensive assessment of its impact.
Overall, we believe that this study represents an important contribution to the ongoing discussion regarding individualized follow-up strategies in glaucoma management. However, the observed null association between DFU and visual field progression may partially reflect methodological constraints, including reverse causation, limited characterization of temporal exposure patterns, and the potential influence of treatment escalation. Future prospective studies incorporating time-dependent analyses and treatment trajectories may help define safer and more personalized follow-up intervals for patients across different stages of glaucoma.
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