4. Etiology
• Macrophage :::: inflammatory response.
• Release cytokines (TNF –α & IL-2) infiltration of T-
helper lymphocytes release cytokines & recruit other
inflammatory cells to site of inflammation.
• In response, granulomas are formed &
immunoglobulin produced in large quantities by
stimulated B lymphocytes are sent into circulation.
• Sensitization & resultant immune response to
endogenous lung antigen or inhaled agents.
• Environmental factors : molds & insecticides.
5. Clinical features
• Asymptomatic.
• Respiratory symptoms, fever, fatigue or weight loss.
• Abnormal chest X-ray or laboratory tests.
• Biopsy : Non-caseating,granulomatous,non-infectious
inflammatory process.
• 2/3rd of case – remission with in a decade.
• 1/3rd of case - recurrent, progressive – significant organ
damage.
• Ocular involvement is about 26 % in chronic cases.
• B/L but may be U/L as well as markedly asymmetric.
8. Anterior Uveitis
• Most common
• 2/3rd ( 50-60%) will have
chronic granulomatous uveitis.
• Most have Mutton fat KPs,
large & dense, Iris nodules.
• Inflammatory vs Malignancy.
• Chronic form : 4th-6th decade &
causes cataract (8-17%) &
glaucoma (11-23%) with
increase in duration
• 15-45 % associated with acute
iridocyclitis .
• Mild vitritis ( occasional)
9. Posterior Segment
• Less common . 6-33%
• Clump of cells & proteinacous debris –
snowballs
• ‘Candle wax dripping’ (en taches de
bongie)
• Perivenous sheathing rarely
periarterioral.
• Deep yellow choroidal lesions
consistent with D-F nodules &
mottling of pigment epithelium (36%)
• Serous RD – large granuloma
• Chronic Cystoid Macular Oedema.
• Neovascularization of Optic Disc
(15%)
• Retinal & subretinal neovascularization
(R > SR)
• Peripapillary or macular subretinal
neovascular membrane.