In the JournalsPerspective

Intravitreal ranibizumab associated with subfoveal choroidal thinning in idiopathic disease

Intravitreal ranibizumab therapy was associated with thinning of the subfoveal choroid in patients treated for unilateral idiopathic subfoveal choroidal neovascularization, a study found.

The prospective study included 16 patients with unilateral idiopathic subfoveal choroidal neovascularization who underwent a single intravitreal injection of 0.5 mg ranibizumab and subsequent injections as needed.

Investigators used enhanced depth imaging optical coherence tomography to measure subfoveal choroidal thickness (SFCT). Mean patient age was 31.9 years. Visual acuity was also evaluated.

Patients received a mean 1.25 intravitreal ranibizumab injections. Mean total follow-up was 4.9 months. Mean follow-up after the final ranibizumab injection was 4.4 months.

Best corrected visual acuity improved significantly, from 0.50 to 0.23 1 month after the initial injection (P < .001).

SFCT decreased from 354 μm at baseline to 328 μm in treated eyes at 1 month (P < .001). However, SFCT increased significantly, to 342 μm, at the final visit.

SFCT changed insignificantly in untreated contralateral eyes.

“It remained elusive whether the choroidal thinning was due to a direct pharmacological effect of ranibizumab or whether it was secondary due to the foveal retinal thinning,” the authors said.

Central retinal thickness decreased significantly in treated eyes, from 400 μm at baseline to 221 μm at 1 month (P < .001) and 214 μm at the final visit (P = . 02).

Disclosure: See the study for a full list of all authors’ relevant financial disclosures.

Intravitreal ranibizumab therapy was associated with thinning of the subfoveal choroid in patients treated for unilateral idiopathic subfoveal choroidal neovascularization, a study found.

The prospective study included 16 patients with unilateral idiopathic subfoveal choroidal neovascularization who underwent a single intravitreal injection of 0.5 mg ranibizumab and subsequent injections as needed.

Investigators used enhanced depth imaging optical coherence tomography to measure subfoveal choroidal thickness (SFCT). Mean patient age was 31.9 years. Visual acuity was also evaluated.

Patients received a mean 1.25 intravitreal ranibizumab injections. Mean total follow-up was 4.9 months. Mean follow-up after the final ranibizumab injection was 4.4 months.

Best corrected visual acuity improved significantly, from 0.50 to 0.23 1 month after the initial injection (P < .001).

SFCT decreased from 354 μm at baseline to 328 μm in treated eyes at 1 month (P < .001). However, SFCT increased significantly, to 342 μm, at the final visit.

SFCT changed insignificantly in untreated contralateral eyes.

“It remained elusive whether the choroidal thinning was due to a direct pharmacological effect of ranibizumab or whether it was secondary due to the foveal retinal thinning,” the authors said.

Central retinal thickness decreased significantly in treated eyes, from 400 μm at baseline to 221 μm at 1 month (P < .001) and 214 μm at the final visit (P = . 02).

Disclosure: See the study for a full list of all authors’ relevant financial disclosures.

    Perspective

    The study demonstrates that an increase in choroidal thickness is seen in eyes with idiopathic choroidal neovascularization. This finding has been reported in patients with central serous and polypoidal disease. The authors found a reduction in choroidal thickness after intravitreous ranibizumab administration at 1 month. The measurements of choroidal thickness vary greatly.

    Articles have shown discrepancies in being able to obtain accurate reproducible measurements, and the changes in thickness that occur at different times of the day, and after drinking coffee. The choroidal thickness seemed to return to baseline when the disease recurs. The cause of the increase in thickness is not known. When swept source OCT becomes available, we should be able to see if the decrease in thickness is related to constriction of the choroidal vessels (Haller and Sattler layer) or to edema in the choroid. It will also be interesting to see if the thickening of the choroid predisposes one to develop idiopathic choroidal neovascularization, central serous, or polypoidal disease, or is a consequence of developing a neovascular membrane, central serous or polypoidal disease.

    • David Boyer, MD
    • Retina-Vitreous Associates Medical Group Beverly Hills, Calif.

    Disclosures: Boyer is a consultant for Genentech, Novartis, Regeneron and Roche.