ABSTRACT
Aims: This study aims to investigate the effects of intravitreal octreotide on the growth factors, which have significant roles in the pathogenesis of proliferative vitreoretinopathy (PVR). Settings and Design: An experimental trial. Materials and Methods: 21 guinea pigs were randomly assigned to form 3 groups each including 7 animals. In group 1 (the control group), 0.2 ml saline solution was applied intravitreally in a location of 1.5 mm behind the limbus. In group 2 (the sham group), 0.07 IU dispase in 0.1 ml and 0.1 ml saline solution were applied via the same route. The guinea pigs in group 3 (the treatment group) were applied 0.07 IU dispase in 0.1 ml and 1 mg octreotide in 0.1 ml via the same route. Octreotide injection was applied twice during the period of 10 weeks of the experiment. At the end of the 10 weeks, eyes were enucleated and retinal homogenates were prepared. The platelet derivated growth factor (PDGF), insulin-like growth factor (IGF 1) and transforming growth factor (TGF ß) levels in homogenized retina tissue were measured by Enzyme Linked-Immuno-Sorbent Assay (ELISA) method. Statistical Analysis Used: Kruskal-Wallis variance analysis and Mann-Whitney U test. Results: In the treatment group, a significant decrease was observed in retinal PDGF levels (P < 0.01) while decreases in TGF ß and IGF 1 levels were not found to be significant (P > 0.05). Conclusions: Intravitreally applied octreotide at a dose of 1 mg has a highly strong effect on PDGF. This study suggests that intravitreal octreotide may suppress PVR development and that octreotide may merit investigation for PVR prophylaxis.
ABSTRACT
Aim: A clinical comparative trial was conducted to compare the levels of glycosylated hemoglobin (HbA1c) in patients with diabetic cystoid macular edema (CME) with and without serous macula detachment (SMD). Materials and Methods: Thirty patients (group 1) with diabetic CME in both eyes, but without SMD, and 30 patients (group 2) with diabetic CME and SMD in both eyes documented by optical coherence tomography (OCT) and fundus fluorescein angiography (FFA), were included in the study. In addition to the measurement of central macular thickness by OCT and visual acuity (VA) (as logMAR) using the the early treatment diabetic retinopathy study (ETDRS) chart, the concentrations of HbA1c were measured by high performance liquid chromatography (HPLC). Statistical analysis was done by independent samples t test. Results: The mean logMAR VA was 0.8 ± 0.22 (1.0–0.5) in group 1and 0.7 ± 0.16 (1.0–0.6) in group 2. The mean central macular thickness, as determined by OCT, was 468.70 ± 70.44 μm (344–602 μm) in group 1 and 477.80 ± 73.34 μm (354–612 μm) in group 2. The difference between the groups was not statistically significant (P = 0.626). The mean HbA1c levels were 8.16 ± 0.99% in group 1 and 10.05 ± 1.66% in group 2. The difference between the groups was statistically significant (P < 0.001). Conclusions: The presence of SMD and high HbA1c levels in the patients with diabetic CME may be indirectly suggestive of retinal pigment epithelium dysfunction.