[The cellular aspects of amyloid angiopathies of the iris in open-angle glaucoma].
We studied cellular aspects of amyloid angiopathy of the iris upon decompensation of ocular pressure and the role of microcirculatory pathology in pathogenesis of the open angle glaucoma. A total of 115 iris biopsies were studied, which were taken during antiglaucoma operations and stained by Congo rot and thioflavine for amyloid and Toluidine blue for glycosaminoglycans. The biopsies from nine patients were studied at the ultrastructural level. Intravasal increase of the concentration of preamyloid proteins during spasms of the arterioles and capillaries should be considered as a provoking moment of the iris amyloidogenesis. Blockade of reticular structures of the microcirculatory basal membranes by preamyloid serum proteins, which provides for shedding of amyloid fibrils, dystrophic changes and detachment of the endothelial cells from the basal membrane, obliteration of lumens of the capillaries and arterioles, disturbed integrity of the microvascular barrier and accumulation of preamyloid and amyloid proteins in the extracellular matrix, ischemia and focal microinfarctions of the iris, and dystrophia of the melanocytes, are subsequent key factors. Amyloid angiopathy of the iris is a cause of ischemia of the anterior eye part, thus creating conditions for increased intraocular pressure and glaucoma.
Ziangirova
G G
GG
Antonova
O V
OV
D000682:Amyloid / Q000378:metabolism; D000686:Amyloidosis / Q000378:metabolism / Q000473:pathology*; D001706:Biopsy; D005902:Glaucoma, Open-Angle / Q000378:metabolism / Q000473:pathology*; D006651:Histocytochemistry; D006801:Humans; D007498:Iris / Q000098:blood supply / Q000378:metabolism / Q000648:ultrastructure; D007499:Iris Diseases / Q000378:metabolism / Q000473:pathology*; D008833:Microcirculation / Q000378:metabolism / Q000648:ultrastructure; D008854:Microscopy, Electron
D000682:Amyloid