Recent Advances In Diagnosis And Management Of Posterior Uveitis

Abstract

Uveitis is inflammation of the uvea. There are many Uveitis entities; several classification schemes are clinically useful. According to standardization of uveitis nomenclature working group (SUN) the four commonly used classifications for describing Uveitis entities are temporal, morphological, anatomical, and etiological. The anatomical classification uses the terms iritis, iridocyclitis, vitritis, retinochoroiditis, choroiditis, and panuveitis. The etiological classification is either infectious or noninfectious. Investigations of a case of posterior uveitis are multiple and include laboratory as ESR, skin biopsy for leprosy, tuberculin skin tests, PCR, ELISA, IFA, Imaging studies as chest X ray, FA,ICG and OCT. In non-infectious causes, therapy is usually aimed at dampening down the immune response with corticosteroids being the first line treatment. In sight threatening disease immunosuppressive agents as methotrexate, cyclosporine and cyclophosphamide may need to be added to improve or preserve sight. Another new treatment modality is the use of intraocular pharmacotherapy via intravitreal injection and surgically placed implants as (Retisert) that shows a significant reduction in recurrence rate and improvement in visual acuity for approximately 3 years after implant Autoimmune posterior uveitis is a treatable condition that may require the use of systemic immunomodulatory medications to halt its progression. Although corticosteroids remain the primary initial treatment for patients with uveitis, use of non-corticosteroid immunomodulatory agents in selected patients with uveitis allows for improved control and decreased risk of corticosteroid-induced side effects. Based on the increasing knowledge of the immune mechanisms that underlie autoimmune diseases, a new group of “biologicals” has been generated. These are immunologically active proteins focussing on specific cells, receptors or ligands. They target those immune responses that are involved in uveitis, either by blocking inflammatory cytokines (anti-TNF therapies such as etanercept, infliximab or adalimumab), by affecting T-helper cells (anti-IL2 receptor such as daclizumab) or suppressing the autoantigen-specific immune response by induction of mucosal tolerance (oral tolerance). The impressive efficacy of TNFα-targeted therapies in sight-threatening, otherwise treatment-refractory uveitis is an argument in favor of expanding the role of these agents in non-infectious ocular inflammation. Introduction of these agents earlier in the course of the disease may prevent the structural damage that results in permanent visual impairment. The rapid action of anti-TNFα agents could also be utilized as a rescue therapy in acute severe relapse, particularly in patients who have contraindications to high dose corticosteroids. Infectious posterior uveitis is a big entity of uveitis, it may be caused by bacteria such as tuberculosis and syphilis which were thought to be the cause of the majority of cases of uveitis, viruses such as herpes virus. protozoa such as toxoplasmosis which are a principle cause of uveitis and fungi, can also produce a variety of uveitis syndromes. Because specific antimicrobial therapy can be curative and prevent long term visual sequelae, early diagnosis of infectious causes of uveitis should be a priority to ensure good prognostic outcome. Management of a case of uveitis depends on the diagnosis of the cause followed by the proper therapy, the outcome however depends on the stage of the disease and the promptness of diagnosis with therapy.