Abstract
To compare the intravitreal concentrations of cellular mediators involved in neurodegeneration, inflammation, and angiogenesis in patients with proliferative diabetic retinopathy and other vitreoretinal diseases. A multiplex bead immunoassay was used to measure vitreous levels of pigment epithelium-derived factor, serum amyloid P, C-reactive protein, complement C4, alpha-1 antitrypsin, vascular endothelial growth factor, platelet-derived growth factor-AA, platelet-derived growth factor-BB, interleukin-6, interleukin-8, interleukin-10, tumor necrosis factor alpha and beta in patients undergoing 23-gauge vitrectomy for proliferative diabetic retinopathy and other diagnoses (control group). We evaluated 55 patients, of whom 24 had proliferative diabetic retinopathy and 31 had other diagnoses including vitreous hemorrhage, retinal detachment, macular hole, and epiretinal membrane. Patients with proliferative diabetic retinopathy demonstrated increased levels of serum amyloid P (85.49 vs. 31.38 ng/mL); C-reactive protein (59.89 vs. 41.75 ng/mL), vascular endothelial growth factor (2,330.11 vs. 554.25 pg/mL; p<0.001), platelet-derived growth factor A (127.32 vs. 39.11 pg/mL), platelet-derived growth factor B (29.37 vs. 7.12 pg/mL), interleukin-6 (69.37 vs. 33.58 pg/mL), interleukin-8 (175.25 vs. 59.71 pg/mL), and interleukin-10 (3.70 vs. 1.88 pg/mL); all p<0.004 when compared with the control group. Levels of pigment epithelium-derived factor (30.06 vs. 27.48 ng/mL; p=0.295), complement C4 (570.78 vs. 366.24 ng/mL; p=0.069), and alpha-1-antitrypsin (359.27 vs. 522.44 ng/mL; p=0.264) were not significantly different between the groups. Intravitreal levels of tumor necrosis factor-alpha and tumor necrosis factor-beta were undetectable. Serum Amyloid P, C-reactive protein, platelet-derived growth factor A, platelet-derived growth factor B, interleukin-6, and interleukin-8 were correlated positively with vascular endothelial growth factor. Cellular mediators involved in neurodegeneration and inflammation demonstrated increased levels in the vitreous humor of patients with proliferative diabetic retinopathy and may be part of the pathogenesis of diabetic retinopathy.
Highlights
Diabetic retinopathy is considered a microvascular complication of diabetes mellitus (DM), with diagnosis and classification based on visible vascular alterations detected on clinical examination
In the present study, we identified an increase in numerous factors involved in neurodegeneration and inflammation in patients with proliferative diabetic retinopathy (PDR)
Pentraxins (SAP and C-reactive protein (CRP)), platelet-derived growth factor (PDGF)-A and PDGF-B, and IL-6 and IL-8 were consistently increased in patients with PDR and correlated with vascular endothelial growth factor (VEGF), emphasizing their neuroinflammatory role in PDR
Summary
Diabetic retinopathy is considered a microvascular complication of diabetes mellitus (DM), with diagnosis and classification based on visible vascular alterations detected on clinical examination. The current clinical treatment aims to stabilize the vascular system, disregarding changes in the neurosensory retina[1,2]. Much evidence from experimental models and humans shows that DM involves a neurodegenerative process related to retinal vascular changes[1,2]. Human studies using optical coherence tomography and electrophysiology have confirmed this hypothesis, exhibiting significant anatomical changes and dysfunctions in the upper retinal layers even before vascular changes can be seen[1,2]. Growing evidence suggests that inflammatory mediators increase endothelial dysfunction and neurodegeneration in patients with diabetic retinopathy (DR), regardless of vascular endothelial growth factor (VEGF) levels[1,3,4]
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