Alterations of Retinal Pigment Epithelium–Photoreceptor Complex in Patients with Type 2 Diabetes Mellitus without Diabetic Retinopathy: A Cross-Sectional Study

Abstract

Aim. A cross-sectional study was performed to examine the alterations of the retinal pigment epithelium– (RPE–) photoreceptor complex layer in type 2 diabetes mellitus (DM) without diabetic retinopathy (DR), using spectral-domain optical coherence tomography (SD-OCT). Methods. Patients with type 2 DM without DR and healthy controls without DM were recruited. All participants underwent examinations including SD-OCT. The thickness measurements of the retinal neural layers were calculated after automatic segmentation. An independent-sample t-test was used to compare the means of the thickness of retinal neural layers in patients with DM and healthy controls. Results. Sixty-seven eyes from 67 patients with DM and 30 eyes from 30 healthy controls were included in this study. No significant differences were found in age (P = 0.601), gender (P = 0.560), axial length (P = 0.414), best-corrected visual acuity (P = 0.963), or intraocular pressure (P = 0.112) between the two groups. There were significant increases in the hemoglobin A1c value (P < 0.001) and mean thicknesses of the RPE–photoreceptor complex layer in the foveal area (P = 0.027) and paracentral area (P = 0.001) in the DM group compared to the control group, whereas the thickness of the retinal nerve fiber and ganglion cell layers in the foveal and paracentral areas between the two groups showed no significant differences. Conclusion. Lesions in the RPE–photoreceptor complex are present without vascular abnormalities, which may precede the alterations of ganglion cells in patients with type 2 DM.

Analysis of the Choroid and Its Relationship with the Outer Retina in Patients with Diabetes Mellitus Using Binarization Techniques Based on Spectral-Domain Optical Coherence Tomography

“…Knowing that the number of photoreceptors per RPE cell in the macula is increased and adding that phagocytosis is disturbed by hypoxia, we explain the accumulation of shed OS that is not readily engulfed. Thus, the increase in RPE thickness points to the compromised function of the outer retina [ 44 ]. We used multiple photoreceptor-related layers, such as: ONL, IS + OS and an estimated PR entire thickness to detect even smaller changes or to check if they are simultaneously affected by the choroidal damage.…”

Vitamin D Protects against Oxidative Stress and Inflammation in Human Retinal Cells

“…A mixture of IFN-γ, TNF-α, and IL-1β has been shown to decrease the expression of specific genes that play an important role in processes, such as visual cycle, epithelial morphology, melanogenesis, and phagocytosis, in cultured ARPE-19 cells [74]. Therefore, downregulation of those levels by VITD may potentially contribute to restore the RPE dysfunction implicated in retinal diseases, including DR [75,76]. It has been demonstrated that a higher secretion of IL-10 would be a protective factor against the development of proliferative DR (PDR) when proinflammatory cytokines, such as IL-1β, are elevated, as shown in vitreous of PDR patients [77].…”

Optical Coherence Tomography Biomarkers of the Outer Blood—Retina Barrier in Patients with Diabetic Macular Oedema

“…One possible explanation is that over the RPE cells, new cells grow in order to compensate and to minimise the fluid leakage within the retina [ 5 ]. Another hypothesis is that the disturbance of the RPE cells' phagocytosis induces the accumulation of shed outer segments that are not timely engulfed in the RPE-photoreceptors' complex [ 19 ].…”

“…RPE and photoreceptor layers are regarded as a functional unit due to their interdependence. Structural and functional changes of this complex were found also in patients with DR without DMO [ 19 ]. When analysing the total thickness of the photoreceptors (inner and outer segment plus ONL), the decreased values we found in the PDR-DMO group and in the NPDR-DMO group could be attributed to a thinner PROS (photoreceptor outer segment) length in the context of a relative outer retinal hypoperfusion induced by hypoxia, as shown by Verma et al [ 30 ].…”

“…As Nesper et al [ 31 ] and Muir et al [ 32 ] pointed out, the decrease of choroidal blood flow creates a hypoxic environment for the RPE and photoreceptor cells with subsequent disruption of phagocytosis and increased fragility of the RPE cells. In a feedback loop, more superoxide and soluble inflammatory factors are produced that aggravate the condition [ 19 ].…”