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Long-term follow-up of herpetic non-necrotizing retinopathy with occlusive retinal vasculitis and neovascularization.

Albert K, Masset M, Bonnet S, Willermain F, Caspers L - J Ophthalmic Inflamm Infect (2015)

Bottom Line: Acyclovir was then added and immunosuppressive tapered and eventually stopped resulting in a resolution of vasculitis.Therapeutic and diagnostic vitrectomy was performed, and PCR was found to be positive for varicella zoster virus (VZV) in a vitreous specimen.A good response was obtained on oral antiviral therapy.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Centre Hospitalier Universitaire Saint-Pierre, Rue Haute 322, 1000 Brussels, Belgium ; Centre Hospitalier Universitaire Brugmann, Place Arthur Van Gehuchten 4, 1020 Brussels, Belgium.

ABSTRACT

Background: Herpetic necrotizing retinitis is a well-recognized entity. A few cases of herpetic non-necrotizing retinitis were previously reported.

Findings: We retrospectively report two cases of herpetic non-necrotizing retinopathy with a long follow-up. A 19-year-old woman presented with a bilateral diffuse occlusive retinal vasculitis, peripheral neovascularization, and no signs of retinal necrosis. Long-lasting immunosuppressive treatment failed to control the vasculitis until herpes simplex virus type 1 (HSV1) was demonstrated by polymerase chain reaction (PCR) in the aqueous. Acyclovir was then added and immunosuppressive tapered and eventually stopped resulting in a resolution of vasculitis. Only two relapses occurred during the next 6 years and responded rapidly to oral acyclovir. An 11-year-old boy presented with unilateral scar of stromal keratitis, severe vitritis, and optic disc neovascularization, followed 6 weeks later by peripheral occlusive retinal vasculitis. Therapeutic and diagnostic vitrectomy was performed, and PCR was found to be positive for varicella zoster virus (VZV) in a vitreous specimen. The inflammation responded to oral acyclovir therapy. Recurrence of anterior uveitis with iris depigmentation occurred 4 months after treatment was arrested. After 4 years, he presented again with a recurrence of anterior inflammation and cystoid macular edema (CME). No sign of inflammation was seen for the next 10 years.

Conclusions: These rare cases support the possible role of herpes viruses (HSV or VZV) in occlusive vasculitis without retinal necrosis. PCR was useful to raise the diagnosis and to adapt the treatment. A good response was obtained on oral antiviral therapy.

No MeSH data available.


Related in: MedlinePlus

Patient 1: fluorescein angiography during immunosuppressive treatment. Retinal photocoagulation was performed in both eyes. Despite immunosuppressive treatment, vasculitis remained active in both eyes.
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Fig3: Patient 1: fluorescein angiography during immunosuppressive treatment. Retinal photocoagulation was performed in both eyes. Despite immunosuppressive treatment, vasculitis remained active in both eyes.

Mentions: All known causes of ocular vasculitis as sarcoidosis, presumed tuberculosis-related vasculopathy, systemic lupus erythematosus, antiphospholipid syndrome, Wegener’s granulomatosis, Susac’s syndrome, multiple sclerosis, Behçet’s disease, and syphilis were excluded by an extensive workup. An extensive blood analysis, chest x-ray, tuberculin skin test, bronchoalveolar lavage, and gallium scan were performed, but all results returned negative. A diagnosis of bilateral idiopathic occlusive vasculitis was raised. Oral corticosteroid therapy was administered, and laser photocoagulation of the ischemic zones was performed. Therapeutic response remained poor. Therefore, immunosuppressive agents were added. However, despite a strong immunosuppressive treatment, multiple recurrences of occlusive vasculitis occurred with recurrent hemorrhages in the posterior pole, mild vitritis, and rare episodes of anterior chamber inflammation. New ischemic areas were treated with additional laser photocoagulation. After 3 years follow-up, she developed a cystoid macular edema (CME) in the right eye with VA of 20/25; vision of the left eye remained 20/20. A therapeutic vitrectomy was performed in 1996. Despite this treatment, she continued to develop vasculitis, progressing towards the posterior pole (Figure 3). In 1998, at recurrence of vasculitis associated with anterior cells, an anterior chamber paracentesis was performed, demonstrating HSV 1 by PCR in two aqueous specimens.Figure 3


Long-term follow-up of herpetic non-necrotizing retinopathy with occlusive retinal vasculitis and neovascularization.

Albert K, Masset M, Bonnet S, Willermain F, Caspers L - J Ophthalmic Inflamm Infect (2015)

Patient 1: fluorescein angiography during immunosuppressive treatment. Retinal photocoagulation was performed in both eyes. Despite immunosuppressive treatment, vasculitis remained active in both eyes.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4385048&req=5

Fig3: Patient 1: fluorescein angiography during immunosuppressive treatment. Retinal photocoagulation was performed in both eyes. Despite immunosuppressive treatment, vasculitis remained active in both eyes.
Mentions: All known causes of ocular vasculitis as sarcoidosis, presumed tuberculosis-related vasculopathy, systemic lupus erythematosus, antiphospholipid syndrome, Wegener’s granulomatosis, Susac’s syndrome, multiple sclerosis, Behçet’s disease, and syphilis were excluded by an extensive workup. An extensive blood analysis, chest x-ray, tuberculin skin test, bronchoalveolar lavage, and gallium scan were performed, but all results returned negative. A diagnosis of bilateral idiopathic occlusive vasculitis was raised. Oral corticosteroid therapy was administered, and laser photocoagulation of the ischemic zones was performed. Therapeutic response remained poor. Therefore, immunosuppressive agents were added. However, despite a strong immunosuppressive treatment, multiple recurrences of occlusive vasculitis occurred with recurrent hemorrhages in the posterior pole, mild vitritis, and rare episodes of anterior chamber inflammation. New ischemic areas were treated with additional laser photocoagulation. After 3 years follow-up, she developed a cystoid macular edema (CME) in the right eye with VA of 20/25; vision of the left eye remained 20/20. A therapeutic vitrectomy was performed in 1996. Despite this treatment, she continued to develop vasculitis, progressing towards the posterior pole (Figure 3). In 1998, at recurrence of vasculitis associated with anterior cells, an anterior chamber paracentesis was performed, demonstrating HSV 1 by PCR in two aqueous specimens.Figure 3

Bottom Line: Acyclovir was then added and immunosuppressive tapered and eventually stopped resulting in a resolution of vasculitis.Therapeutic and diagnostic vitrectomy was performed, and PCR was found to be positive for varicella zoster virus (VZV) in a vitreous specimen.A good response was obtained on oral antiviral therapy.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Centre Hospitalier Universitaire Saint-Pierre, Rue Haute 322, 1000 Brussels, Belgium ; Centre Hospitalier Universitaire Brugmann, Place Arthur Van Gehuchten 4, 1020 Brussels, Belgium.

ABSTRACT

Background: Herpetic necrotizing retinitis is a well-recognized entity. A few cases of herpetic non-necrotizing retinitis were previously reported.

Findings: We retrospectively report two cases of herpetic non-necrotizing retinopathy with a long follow-up. A 19-year-old woman presented with a bilateral diffuse occlusive retinal vasculitis, peripheral neovascularization, and no signs of retinal necrosis. Long-lasting immunosuppressive treatment failed to control the vasculitis until herpes simplex virus type 1 (HSV1) was demonstrated by polymerase chain reaction (PCR) in the aqueous. Acyclovir was then added and immunosuppressive tapered and eventually stopped resulting in a resolution of vasculitis. Only two relapses occurred during the next 6 years and responded rapidly to oral acyclovir. An 11-year-old boy presented with unilateral scar of stromal keratitis, severe vitritis, and optic disc neovascularization, followed 6 weeks later by peripheral occlusive retinal vasculitis. Therapeutic and diagnostic vitrectomy was performed, and PCR was found to be positive for varicella zoster virus (VZV) in a vitreous specimen. The inflammation responded to oral acyclovir therapy. Recurrence of anterior uveitis with iris depigmentation occurred 4 months after treatment was arrested. After 4 years, he presented again with a recurrence of anterior inflammation and cystoid macular edema (CME). No sign of inflammation was seen for the next 10 years.

Conclusions: These rare cases support the possible role of herpes viruses (HSV or VZV) in occlusive vasculitis without retinal necrosis. PCR was useful to raise the diagnosis and to adapt the treatment. A good response was obtained on oral antiviral therapy.

No MeSH data available.


Related in: MedlinePlus