AIM: To systematically review whether the increased fluctuation of intraocular pressure(IOP) is a risk factor for open angle glaucoma(OAG) progression. METHODS: Scientific studies relevant to IOP fluctuation and glaucoma progression were retrieved from MEDLINE,EMBASE and CENTRAL databases, and were listed as references in this paper. The hazard ratio(HR) was calculated by using fixed or random-effects models according to the heterogeneity of included studies. RESULTS: Individual data for 2211 eyes of 2637 OAG patients in fourteen prospective studies were included in this Meta-analysis. All studies were longitudinal clinical studies with follow-up period ranging from 3 to 8.5 y. The combined HR was 1.23(95%CI 1.04-1.46, P=0.02) for the association between IOP fluctuation and glaucoma onset or progression with the evidence of heterogeneity(P<0.1).Subgroup analyses with different types of IOP fluctuation were also evaluated. Results indicated that the summary HR was 0.98(95%CI 0.78-1.24) in short-term IOP fluctuation group, which showed no statistical significance with heterogeneity, whereas, the combined HR was 1.43(95%CI1.13-1.82, P=0.003) in long-term IOP fluctuation group without homogeneity. Sensitivity analysis further showed that the pooled HR was 1.10(95%CI 1.03-1.18, P=0.004) for long-term IOP fluctuation and visual function progression with homogeneity among studies(P=0.3). CONCLUSION: Long-term IOP fluctuation can be a risk factor for glaucoma progression based on the presentedevidence. Thus, controlling the swing of IOP is crucial for glaucoma or glaucoma suspecting patients.
·AIM: To evaluate the reliability of β-III-Tubulin protein as a retinal ganglion cell(RGC) marker in the experimental glaucoma model.·METHODS: Glaucoma mouse models were established by injecting polystyrene microbeads into the anterior chamber of C57BL/6J mice, then their retinas were obtained 14 d and 28 d after the intraocular pressure(IOP)was elevated. Retinal flat mounts and sections were double-labeled by fluorogold(FG) and β-III-Tubulin antibody or single-labeled by β-III-Tubulin antibody,then RGCs were counted and compared respectively.· RESULTS: IOP of the injected eyes were elevated significantly and reached the peak at 22.8 ±0.7 mm Hg by day 14 after injection, then dropped to 11.3 ±0.7 mm Hg by day 28. RGC numbers counted by FG labeling and β-III- Tubulin antibody labeling were 64 807 ± 4930 and64 614 ±5054 respectively in the control group, with no significant difference. By day 14, RGCs in the experimental group decreased significantly compared to the control group, but there was no significant difference between the FG labeling counting and the β-III-Tubulin antibody labeling counting either in the experimental group or in the control group. The result was similar by day 28, with further RGC loss.·CONCLUSION: Our result suggested that the β-III-Tubulin protein was not affected by IOP elevation and can be used as a reliable marker for RGC in experimental models of glaucoma.
Sleep accounts for a third of one's lifetime, partial or complete deprivation of sleep could elicit sever disorders of body function. Previous studies have reported the higher prevalence of sleep disorders in glaucoma patients, but the definite mechanism for this phenomenon is unknown. On the other hand, it is well known by us that the intrinsically photosensitive retinal ganglion cells(ip RGCs) serve additional ocular functions, called non-image-forming(NIF) functions, in the regulation of circadian rhythm, melatonin secretion, sleep, mood and others. Specifically, ip RGCs can directly or indirectly innervate the central areas such as suprachiasmatic nucleus(SCN), downstream pineal gland(the origin of melatonin), sleep and wake-inducing centers and mood regulation areas, making NIF functions of ip RGCs relate to sleep. The more interesting thing is that previous research showed glaucoma not only affected visual functions such as the degeneration of classical retinal ganglion cells(RGCs), but also affected ip RGCs. Therefore, we hypothesize that higher prevalence of sleep disorders in glaucoma patients maybe result from the underlying glaucomatous injuries of ip RGCs leading to the abnormalities of diverse NIF functions corresponding to sleep.
