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Introduction Ocular involvement due to varicella-zoster virus (VZV) infection includes conjunctivitis, scleritis, keratitis, uveitis, and necrotizing retinitis. Non-necrotizing chorioretinopathy as a late manifestation has been described. Case report A 50-year-old immunocompetent man developed herpes zoster ophthalmicus (HZO) in the right V1 dermatome with acute anterior uveitis (AAU) treated with oral valaciclovir and topical steroid and a chalazion in the upper eyelid with associated madarosis. Four months later, he presented recurrence of the AAU and multiple areas of chorioretinal atrophy on fundoscopy. Biopsy of the upper eyelid lesion revealed granulomatous inflammation of the eyelid margin and polymerase chain reaction study (PCR) tested positive for VZV-specific DNA. The iridocyclitis was resolved with oral valaciclovir at maximum doses with minimal choroidal pigmentary changes. Discussion VZV ophthalmic infection starts by reactivation from the trigeminal ganglion, and it spreads to the isthmus of the pilosebaceous follicles and the epidermis, which can cause involvement of follicle and sebaceous glands. Chorioretinopathy is a rare form of late-onset non-necrotizing herpetic uveitis characterized by atrophic-appearing hypopigmented lesions, the pathogenesis of which is unknown. A direct viral infection or secondary to occlusive choroidal vasculitis is postulated at the level of the choriocapillaris and more recently it has been referred to as “choroidal vitiligo” due to possible involvement of choroidal melanocytes, as occurs in cases of cutaneous vitiligo due to VZV infection. |
