జర్నల్ ఆఫ్ క్లినికల్ అండ్ ఎక్స్పెరిమెంటల్ ఆప్తాల్మాలజీ
అందరికి ప్రవేశం

నైరూప్య

Retinal Fiber Layer and Macular Ganglion Cell Layer Thickness in Diabetic Patients

Maalej Afef, Khallouli Asma, Bouguerra Chaker, Ajili Faida and Rannen Riadh

Background: To compare the ganglion cell-inner plexiform layer (GCIPL) thickness and the retinal nerve fibre layer (RNFL) thickness between type 2 diabetic patient's eyes with and without diabetic retinopathy (DR) and normal eyes.

Methods: In this comparative case-control study two groups of 58 eyes were examined by SD-OCT with peripapillary RNFL, and macular GCIPL assessment. The first group includes 58 eyes of type 2 diabetic patients (33 eyes without DR, 25 eyes with moderate DR, without diabetic macular edema), the second group included 58 eyes of non-diabetic, non-glaucomatous patients. We compared RNFL and GCIPL thicknesses among different groups. We evaluated the potential systemic risk factors for RNFL and GCIPL loss (HBA1C, the presence of DR, other vascular diseases).

Results: The two groups were matched concerning the age, gender and the intra-ocular pressure (IOP) level. A significant differences between the two groups was found for the average, superior and inferior RNFL thickness (p<0.001, p=0.005 and p=0.01 respectively). Concerning the GCIPL thickness, it was significantly less in the diabetic eyes (p<0.001), but no significant difference was noted between the diabetic patient's eyes without DR and the healthy controls in all quadrants for the RNFL and the GCIPL. Multivariate linear regression analysis concluded that the diabetic duration, the HbA1c were correlated to RNFL and GCIPL loss in diabetic patient's eyes and the presence of arterial hypertension as well as lipid disorders were found as risk factors in the non-diabetic group.

Conclusion: RNFL and GCIPL loss seems to be the earliest retinal changes in diabetic patients, and associated with diabetic duration and poor control. These results can explain the higher risk of primitive angle closure glaucoma in diabetic patients and confirm the neurodegeneration theory in DR's physiopathology.