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10.1155/2015/392983

http://scihub22266oqcxt.onion/10.1155/2015/392983
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C4573635!4573635!26425349
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suck abstract from ncbi

pmid26425349      J+Ophthalmol 2015 ; 2015 (ä): ä
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  • The Vitreomacular Interface in Diabetic Retinopathy #MMPMID26425349
  • Agarwal D; Gelman R; Prospero Ponce C; Stevenson W; Christoforidis JB
  • J Ophthalmol 2015[]; 2015 (ä): ä PMID26425349show ga
  • Diabetic retinopathy (DR) is a leading health concern and a major cause of blindness. DR can be complicated by scar tissue formation, macular edema, and tractional retinal detachment. Optical coherence tomography has found that patients with DR often have diffuse retinal thickening, cystoid macular edema, posterior hyaloid traction, and tractional retinal detachment. Newer imaging techniques can even detect fine tangential folds and serous macular detachment. The interplay of the vitreous and the retina in the progression of DR involves multiple chemokine and other regulatory factors including VEGF. Understanding the cells infiltrating pathologic membranes at the vitreomacular interface has opened up the possibility of new targets for pharmacotherapy. Vitrectomies for DR remain a vital tool to help relieve tension on the macula by removing membranes, improving edema absorption, and eliminating the scaffold for new membrane formation. Newer treatments such as triamcinolone acetonide and VEGF inhibitors have become essential as a rapid way to control DR at the vitreomacular interface, improve macular edema, and reduce retinal neovascularization. These treatments alone, and in conjunction with PRP, help to prevent worsening of the VMI in patients with DR.
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