Journal of Clinical and Experimental Ophthalmology

Journal of Clinical and Experimental Ophthalmology
Open Access

ISSN: 2155-9570

Short Communication - (2015) Volume 6, Issue 4

Anti-vascular Endothelial Growth Factor for Choroidal Neovascularization Associated with Toxoplasmosis: A Case Series

Farzan Kianersi1, Zahra Naderi Beni2, Afsaneh Naderi Beni2*, Heshmatollah Ghanbari1 and Mostafa Ahmadi2
1Department of Ophthalmology, Isfahan University of Medical Sciences, Isfahan, Iran
2Shahrekord University of Medical Sciences, Shahrekord, Iran
*Corresponding Author: Afsaneh Naderi Beni, Shahrekord University of Medical Sciences, Shahrekord, Iran, Tel: +98-381-2224400 Email:

Abstract

The purpose of the study was to evaluate the efficacy and safety of intravitreal anti-vascular endothelial growth factor (anti-VEGF) in treatment of choroidal neovascularization (CNV) secondary to toxoplasmic retinochoroiditis in five patients. After six months the CNV resolved as confirmed by fluorescein angiography and optical coherence tomography (OCT) in all patients. The visual acuity improved from mean 20/400 to 20/80 and Central Macular Thickness (CMT) decreased from 390 μm to 253 μm, which was maintained till the last follow-up visit

Introduction

Treatment modalities for choroidal neovascularization (CNV) due to ocular toxoplasmosis include laser photocoagulation, surgery, corticosteroids, and verteporfin therapy. Intravitreal injection of Anti-vascular endothelial growth factor (anti-VEGF ) in the treatment of CNV due to other conditions appears to be an effective and safe therapeutic option. We report 5 cases of successful treatment with anti-VEGF for symptomatic CNV due ocular toxoplasmosis.

Methods

The Isfahan University Medical Center approved this study. Our study population consisted of 5 patients with CNV due to ocular toxoplasmosis (3 women, 2 men) with a mean (SD) age of 27.2 (7.1) years, all with documented notes suggested of clinical and serological diagnosis of toxoplasmosis retinichoriditis and had been treated with oral sulfadiazine and pyrimethamine, along with systemic steroids at least 6 months before referral to our clinic.

All patients received a complete ophthalmologic evaluation. The anterior chamber and vitreous cavity were quiet in all patients. No signs suggestive of age-related macular degeneration were found. Fluorescein (FA) criteria included evidence of leakage caused by CNV (100% classic without an occult component) secondary to ocular toxoplasmosis and presence of intraretinal or subretinal fluid documented by optical coherence tomography (OCT). Intravitreal anti-VEGF treatment was recommended for all patients (bevacizumab, 1.25 mg for 4 eyes and ranibizumab 0.5 mg for one eye).

Results

CNV was inactive in all eyes after Intravitreal anti-VEGF treatments with an absence of leakage demonstrated by fluorescein angiography, complete disappearance of exudative signs and reduction of retinal thickness shown by OCT (Figure 1).

clinical-experimental-ophthalmology-Fluorescein-angiography

Figure 1: Fluorescein angiography (FA) and OCT before and after treatment in 5 cases with choroidal neovascularization associated with toxoplasmosis.

The mean follow-up was 14.4 months (range 6–24 months). Pre-injection visual acuity measured 20/250 or worse in all eyes. According to the last follow-up examination, visual acuity measured 20/30, 20/200, 20/200, 20/100 and 20/100 in eyes (Table 1). Mean Central macular thickness (CMT) at baseline was 399 μm (380-410 μm). At the last check, mean CMT reduction was 149 μm (65-175 μm), with a mean thickness of 253 μm (range, 215-300 μm) (p=0.0002).

Patient sex Age  Initial VA(Before treatment) Final VA eye Follow-up(mo) Injection MT Pretreatment MT Posttreatment Investigation(s) Serology status
1 F 27 0.08 20/30  OD 24 m Avastin 395 300 FA, OCT IgG, positive; IgM, negative
2 F 32 0.07 20/200 OS 6 m Avastin 410 250 FA, OCT IgG, positive; IgM, negative
3 M 24 0.06 20/200 OD 12 m Avastin 380 215 FA, OCT IgG, positive; IgM, negative
4 M 16 0.05 20/100 OS 15 m Avastin 400 250 FA, OCT IgG, positive; IgM, negative
5 F 37 0.07 20/100 OS 15 m ranibizumab 410 235 FA,OCT IgG, positive; IgM, negative

Table 1: Demographic and clinical characteristics of the patients in the study.

No injection or drug-related complications, including endophthalmitis, cataract, retinal detachment, glaucoma, or uveitis, were observed.

Discussion

CNV formation secondary to toxoplasmosis retinochoroiditis is a rare event with a poor visual prognosis. Treatment modalities for CNV secondary to toxoplasma retinochoroiditis include laser photocoagulation, submacular surgery, PDT, and anti-VEGF agents [1].

Because of the young age of our patients and occurrence of permanent scotoma or a blind spot in the central visual field with laser photocoagulation, this technique is not suitable for treatment. Surgery can have its own complications and does not prevent recurrences.

Photodynamic therapy appears to be effective. Although, an early recovery of visual acuity has been observed with PDT, multiple treatments have been required [2].

In our small series of patients at 6- to 25-month follow up, leakage diminished in all patients. A reduction of CMT was recorded in all subjects. This change of retinal morphology is likely to be the result of a combined antiexudative effect due to the decrease of vessel permeability and the antiproliferative effect due to the inhibition of further CNV growth following the VEGF blockage [1]. These anatomical improvements were associated with concomitant increases in VA. The mechanism of this outcome remains uncertain.

A previous case reports of CNV due to toxoplasmosis treated with IVB show an improvement of the patient’s BCVA [3-5]. In our patients, VA increased to normal levels and was preserved until the end of follow-up. Unlike the repeated injections generally needed in patients of CNV secondary to age-related macular degeneration [1] in our study only one injection was required to achieve a good visual outcome.

Our data seem to confirm the efficacy and safety of anti-VEGF therapy in eyes with CNV secondary to ocular toxoplasmosis, although we realize that the present study has some limitations, including the limited number of patients and the absence of a standard protocol for follow-up and treatment.

References

  1. Kianersi F, NaderiBeni A, NaderiBeni Z, Ghanbari H (2015) Intravitrealbevacizumab for treatment of choroidal neovascularization secondary to toxoplasmicretinochoroiditis: a case series. SeminOphthalmol 30:181-187.
  2. Oliveira LB, Reis PA (2004) Photodynamic therapy-treated choroidalneovascular membrane secondary to toxoplasmicretinochoroiditis. Graefes Arch ClinExpOphthalmol242:1028-1030.
  3. Guthoff R, Goebel W (2009)Intravitrealbevacizumab for choroidal neovascularization in toxoplasmosis. ActaOphthalmol 87:688-690.
  4. Ben Yahia S, Herbort CP, Jenzeri S, Hmidi K, Attia S, et al. (2008) Intravitrealbevacizumab (Avastin) as primary and rescue treatment for choroidal neovascularization secondary to ocular toxoplasmosis. International Ophthalmol28:311-316.
  5. Lin CJ, Chen SN, Hwang JF, Hu PS (2011) Successful treatment of toxoplasmosis-associated choroidalneovascular lesions with bevacizumab and antiparasitic therapy. Retin Cases Brief Rep 5:348-351.
Citation: Kianersi F, Beni ZN, Beni AN, Ghanbari H, Ahmadi M (2015) Anti-vascular Endothelial Growth Factor for Choroidal Neovascularization Associated with Toxoplasmosis: A Case Series. J Clin Exp Ophthalmol 6:463.

Copyright: © 2015 Kianersi F, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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