Given such differences between DME intravitreal therapies, several studies have investigated how these drugs change the intraocular milieu of inflammatory and pro-permeability mediators. Previous reports have claimed that intravitreal bevacizumab (IVB) decreases AH VEGF levels with no effect on IL-6, IL-8, IP-10, and MCP-1.
14,19 Moreover, intravitreal ranibizumab (IVR) (Lucentis; Genentech, Inc., San Francisco, CA, USA) has also been shown not to affect AH levels of different molecules such as IL-1Ra, IL-5, IL-6, IL-8, IP-10, MCP-1, and TNF-α.
20 On the other hand, steroid agents have proven to have an impact on the distribution of several mediators. For example, intravitreal triamcinolone acetonide has been reported to differentially decrease intraocular IL-6, IP-10, MCP-1, and platelet-derived growth factor (PDGF)-AA when compared to IVB in DME.
19 Similarly, significant associations have also been described between the DEX effect on DME thickening and several AH levels of inflammatory mediators such as insulin-like growth factor binding protein (IGFBP)-1, IGFBP-3, prolactin, matrix metalloproteinase (MMP)-9, endocrine-gland VEGF (EG-VEGF), endostatin, angiopoietin-2, persephin, MIP-1, thrombospondin (THSP)-2, hepatocyte growth factor (HGF), IL-8, and C-X-C motif ligand (CXCL)-16.
21 Finally, recent studies have even described an association between baseline levels of some AH agents such as ICAM-1 and eotaxin-1 with DME response to IVR objectively measured by OCT.
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