advertisement
Jost Jonas (54) and his group have prospectively studied a large cohort of patients with glaucoma and suspect glaucoma (the Erlangen Glaucoma Register) with repeated standard automated perimetry) plus normal controls (administrative university staff). In the tradition of Jonas the number of subjects was large. The 333 patients were a mixed group including patients with ocular hypertension, so-called preperimetric glaucoma and manifest glaucoma. The composition of the patient material was a little unusual for a clinic-based study, with a rather small percentage of patients with POAG (40 or 12%), and a higher number of NTG patients (73 or 22%). Mean age was remarkably low for a glaucoma cohort - 46.8 years. The paper addresses the relationship between central corneal thickness and glaucoma damage at the time of referral and with perimetric progression. The authors find that low CCT was significantly associated with larger damage at baseline (first finding). They also find that there was no association between CCT and the risk for progression (second finding). An extensive discussion is provided by the authors. The first finding is in agreement with observations made by several other groups. I agree with the authors that the most plausible explanation of the first finding is 'a selection artifact' by referring ophthalmologists. Glaucoma patients with thinner corneas have lower pressure readings on Goldmann tonometry, and we and many others have observed how patients with very clear manifest normal tension glaucoma are missed in ophthalmic practice - probably just because they fail to raise a suspicion of glaucoma in the examining ophthalmologist unless the discs are very abnormal. The normal tension glaucoma patient has a good chance of (or a high risk of) being classified as normal after a comprehensive eye examination - even if the reason for the visit is a positive family history of glaucoma.
There was no association between CCT and the risk for progressionThe second finding might be unexpected in the light of the results from OHTS, and the authors discuss this apparent discrepancy. CCT has been measured quite differently in OHTS and in the current study, and it may well be quite important that in OHTS CCT was measured long after randomization and well into the study. I have greater difficulties in understanding the concerns expressed by Jonas and co-workers "how the OHTS corrected the intraocular pressure measurement values for their dependence on central corneal thickness". The OHTS authors performed a proper multivariate analysis including Goldmann applanation IOP and CCT in the same analysis, and in that analysis CCT came out as important. We do not (yet) use corrected IOP values in clinical management; instead we are rely on applanation IOP values and we can measure CCT. If then CCT is important it remains important as long as we cannot correct IOP values for CCT. I find that under these conditions OHTS' conclusions of thin CCTs being a risk factor (or at least a risk indicator) for glaucoma damage to be a good conclusion (and most convincing if the CCT values had been obtained at baseline in stead of well into the study). To me it then does not really matter whether the increased risk is due to false low IOP readings in eyes with thin corneas or whether thin corneas are associated with some other feature, e.g., a thin lamina, that may make the eye more vulnerable. This question is interesting but not crucial for clinical management. Our results in EMGT agree with the second finding of Jonas et al. in the current paper - we did not find CCT to be associated with risk. This is a little surprising with the large evidence that higher IOP is a risk factor for progression, and it may be even somewhat more surprising in the current study that included a lot of patients with ocular hypertension. It may be that the current study was underpowered to let a truly increased risk in ocular hypertension be reflected in a significant association between thin corneas and progression.