title: Changes in aqueous concentrations of various cytokines after intravitreal triamcinolone versus bevacizumab for diabetic macular edema.
abstract: OBJECTIVE
  To investigate the changes in aqueous inflammatory and angiogenic cytokine levels after intravitreal injection of triamcinolone or bevacizumab for reducing foveal thickness in diabetic macular edema (DME).
  
  
  METHODS
  Prospective, interventional case series.
  
  
  METHODS
  Twenty-two eyes of 11 patients with bilateral DME and 6 eyes of 6 patients undergoing cataract surgery participated in this study. In each DME patient, 1 eye received an intravitreal injection of 4 mg triamcinolone acetonide and the other eye received 1.25 mg bevacizumab. Aqueous humor samples were obtained before and 4 weeks after the intravitreal injection in the DME group and before the surgery in the control group. Aqueous concentrations of interleukin (IL)-6, IL-8, interferon-induced protein (IP)-10, monocyte chemotactic protein (MCP)-1, platelet-derived growth factor (PDGF)-AA, and vascular endothelial growth factor (VEGF) were measured by multiplex bead assay.
  
  
  RESULTS
  Before the administration of the drugs, aqueous levels of IL-8, IP-10, MCP-1, and VEGF were significantly higher in the DME group than in the control group. After intravitreal injection, foveal thickness was more decreased in the triamcinolone acetonide (IVTA) group compared with the bevacizumab (IVBe) group. IL-6, IP-10, MCP-1, PDGF-AA, and VEGF were significantly decreased in the IVTA group, but only VEGF in the IVBe group. Aqueous levels of VEGF were more decreased in the IVBe group than in the IVTA group.
  
  
  CONCLUSIONS
  These findings suggest that the pathogenesis of DME is not only related to VEGF dependency, but also to other mechanisms suppressed by corticosteroids. We suppose that these cytokines would have an important role in both the pathogenesis of DME and the underlying mechanism of intravitreal injections.
authors.affiliation: Department of Ophthalmology, Hongik Hospital, Seoul, Korea.
authors.forename: Hee Jin
authors.initials: HJ
authors.lastname: Sohn
authors.forename: Dae Heon
authors.initials: DH
authors.lastname: Han
authors.forename: Im Tae
authors.initials: IT
authors.lastname: Kim
authors.forename: In Kyung
authors.initials: IK
authors.lastname: Oh
authors.forename: Kyun Hyung
authors.initials: KH
authors.lastname: Kim
authors.forename: Dae Yeong
authors.initials: DY
authors.lastname: Lee
authors.forename: Dong Heun
authors.initials: DH
authors.lastname: Nam
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D001082:Aqueous Humor / Q000378:metabolism*; D000068258:Bevacizumab; D016207:Cytokines / Q000378:metabolism*; D003930:Diabetic Retinopathy / Q000188:drug therapy* / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007429:Intraocular Pressure; D058449:Intravitreal Injections; D008269:Macular Edema / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D014222:Triamcinolone Acetonide / Q000627:therapeutic use*; D014792:Visual Acuity
chemical_list: D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D016207:Cytokines; D005938:Glucocorticoids; D000068258:Bevacizumab; D014222:Triamcinolone Acetonide