Morphological justifi cation of the pathogenesis of angleclosure glaucoma

Objective . To prove the role of interrelated autoimmune, hemostatic and infl ammatory mechanisms in the pathogenesis of angleclosure glaucoma on the basis of experimental morphological research. Material and methods. The work was performed on 3 denucleated eyes of patients with terminal “creeping” angle-closure glaucoma (ACG) and 2 eyes with terminal ACG during an intractable acute exacerbation. Sagittal sections through the area of Schlemm’s canal, as well as serial cross sections, were examined by the method of paraffi n sections stained with hematoxylin-eosin (HE). To assess the degree of the infl ammatory response in the eye tissues, the density of infl ammatory cells was calculated within the standard eyepiece micrometer grid at a magnifi cation of × 20. Results . The formation of peripheral anterior synechiae between the periphery of the iris and the trabecular meshwork in the iridocorneal angle is the main etiological factor in chronic angle closure. Several mechanisms contribute to the formation of anterior synechiae. First of all, in our opinion, it is autoimmune infl ammation. Edema and hyperemia of the ciliary processes pushes the iris anteriad, collagen fi bers of the trabecular meshwork are damaged; delayed endothelialization of the trabecular plate occurs, and the angle of the anterior chamber narrows and closes as a result. The resistance to the outfl ow of intraocular fl uid increases. Ischemia, due to increased intraocular pressure (IOP), causes the formation of new vessels in the iris, where aggregates of blood cells are observed. The walls of the newly formed vessels are defective, which contributes to hemorrhages. Thus, in addition to autoimmune infl ammation, we observe signs of endothelial dysfunction syndrome associated with infl ammatory processes with ACG. Conclusions . 1. The pathogenesis of chronic angleclosure glaucoma is based on autoimmune processes, as proved by lymphocytoplasmocytic infl ammatory infi ltration with an addition of pigment-containing macrophages and fi broblasts at the junction of the iris with the cornea. 2. The detection of intravascular aggregates is a proof of impaired hemostasis in angle-closure glaucoma. 3. Parietal thrombus formation in the newly formed vessels of the iris, fi brin in the tissues are evidence of chronic endothelial dysfunction in ACG. 4. The capillaries of the ciliary processes surrounded by a fi brin ring indicate an acute vasomotor disorder and the release of plasma containing fi brinogen into the surrounding tissue. This is indirect evidence of emotional and vasomotor instability in patients with this form of glaucoma. 5. Disturbances in the systems of immunity and hemostasis are interrelated processes. 6. Increased iris stiff ness is ACG biomarker and may serve as a further target for therapeutic intervention.