Optic Disc and Retinal Structural Changes in Takayasu Arteritis: Implications for Normotensive Glaucoma.

Abstract

Objectives: Takayasu arteritis is a chronic large-vessel vasculitis that may lead to ocular hypoperfusion due to the involvement of major arteries. The ischemic hypothesis suggests that chronic reduction in ocular blood flow may predispose the optic nerve to structural damage, even when intraocular pressure is within normal limits. This study investigates whether Takayasu arteritis is associated with optic nerve head changes resembling early features of normotensive glaucoma.

Methods: The study included 62 patients with Takayasu arteritis (55 females, 7 males, mean age: 45.31 ± 13.42 years) and 51 healthy controls (48 females, 3 males, mean age: 45.53 ± 10.13 years). All participants underwent a comprehensive ophthalmological examination, including retinal nerve fiber layer (RNFL) thickness, ganglion cell layer thickness, Bruch's membrane opening-minimum rim width (BMO-MRW), subfoveal-peripapillary choroidal thickness, lamina cribrosa thickness, prelaminar tissue thickness, retinal vessel calibers, and 24-2 visual field testing.

Results: The most frequent ocular complication in patients was hypertensive retinopathy (73.4%), while Takayasu retinopathy was observed in 6.5% of patients. Lamina cribrosa thickness was significantly thinner in patients compared to controls (p < 0.001). Additionally, mean deviation values were lower (p = 0.03) and pattern standard deviation values were higher in patients (p = 0.01). A tendency for thinner average BMO-MRW thickness was noted in patients (p = 0.051). No significant differences were found in ganglion cell layer thickness, prelaminar tissue thickness, or RNFL analysis.

Conclusion: Optic nerve changes were observed in Takayasu arteritis patients under normotensive IOP conditions, particularly a significant reduction in lamina cribrosa thickness. However, no significant thinning was observed in RNFL or ganglion cell layer thickness, suggesting that these findings may reflect early or subclinical structural alterations rather than definitive glaucomatous damage. The lamina cribrosa thinning may serve as a potential biomarker of neurodegenerative effects in Takayasu arteritis, warranting long-term follow-up.