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Aim: The aim of this study was to evaluate and compare the 24-month follow-up results of intravitreal conbercept with ranibizumab in the treatment of choroidal neovascularization (CNV), secondary to pathological myopia (PM). Methods: Fifty-nine patients' 64 eyes with pathological myopic CNV were retrospectively reviewed. Thirty-one eyes underwent conbercept treatment (group C) and 33 eyes underwent ranibizumab treatment (group R), respectively. No patients have received any treatment before. The main outcome of the best-corrected visual acuity (BCVA) uses an international standard visual acuity chart and is converted to the minimum resolution logarithm (LogMAR) visual acuity. Results: There were no significant differences between the two groups at the baseline statisticlly. At 24 months, the mean logMAR BCVA of group C increased from 0.95 ± 0.54 to 0.58 ± 0.39 (P <.001) and the mean central macular thickness (CMT) decreased from 280.97 ± 62.69 μm to 242.35 ± 90.39 μm (P =.033). The mean logMAR BCVA of group R increased from 0.86 ± 0.40 to 0.54 ± 0.28 (P <.001) and the mean CMT was reduced from 303.58 ± 61.95 μm to 251.82 ± 84.74 μm (P =.005). There was no significant difference in logMAR BCVA and CMT between the two groups (P =.962, P =.667, respectively). The mean number of injections was 3.94 ± 1.88 in group C and 4.06 ± 1.82 in group R (P =.788). During the follow-up period, no ocular complications and systemic adverse reactions were observed. Conclusion: Similar visual acuity and improved morphology were achieved in both groups. The two drugs were also found to be safe and effective in the treatment of pathological myopic CNV. [ABSTRACT FROM AUTHOR]

Purpose: Dickkopf 1 (DKK1) functions as a natural antagonist of the canonical Wnt/β-catenin pathway. The purpose of this study was to examine the expression of DKK1 in vitreous samples of patients with pathological myopia, in order to search for possible correlations between DKK1 and axial length. Materials and Methods: The expression of DKK1 and other cytokines in vitreous samples of 44 non-myopic eyes, 42 eyes with low-to-moderate myopia, and 51 eyes with pathological myopia were examined using multiplex cytokine detection technology. Ophthalmologic characteristics, including axial length and subfoveal choroidal thickness, were clinically measured for further analysis. Results: The intravitreous levels of DKK1 (P <.0001) were markedly higher in the pathological myopia group than in the control group. There were no differences of DKK1 levels in different vitreoretinal conditions. Additionally, we found that the DKK1 levels were positively correlated with HGF (β = 0.268, P =.032), and TIMP-3 (β = 0.209, P =.047) levels, as well as with axial length (β = 0.714, P <.0001) in the pathological myopia group. Conclusions: Elevated levels of DKK1 were found in the eyes with elongated axial length. [ABSTRACT FROM AUTHOR]

Purpose: To determine the prevalence of posterior segment manifestations among consecutive patients with pathological myopia attending our University Hospital general ophthalmology clinic and their association with age, refractive error, axial length and each other. Methods: Patients diagnosed with pathological myopia underwent full ophthalmological examination, optical coherence tomography, fluorescein angiography, and ocular ultrasonography. Manifestations detected were recorded for each eye and their prevalence and association with age, refractive error, axial length and each other was determined. Results: A total of 127 eyes of 77 patients with pathological myopia were examined. The most prevalent manifestation was peripheral retinal lesions, found in 63.8% of examined eyes, followed by tigroid fundus, found in 59.1%. Peripheral lesions were significantly associated with more myopia (P =.02) and longer axial length (P =.046). The commonest peripheral lesion was white without pressure, found in 37.8% of eyes. Lattice degeneration was found in 11.8% and snail track degeneration in 4.7% and was not associated with degree of myopia or axial length. Diffuse chorioretinal atrophy was present in 40.9% of eyes, while patchy atrophy was present in 18.9%. Macular holes were present in 4.7% of eyes and were significantly associated with foveoschisis (P =.035) and retinal detachment (P =.003), while foveoschisis was present in 5.5% and was significantly associated with older age (P =.012), longer axial length (P =.010) and patchy chorioretinal atrophy (P =.024). Retinal detachment was found in 6.3% of eyes and retinal breaks in 4.7%. Posterior staphyloma was detected in 33.1% and lacquer cracks and choroidal neovascular membranes in 6.3% of eyes. Conclusions: The prevalence of pathological myopia manifestations may differ between different populations. This may be due to the multiple genetic and environmental factors involved which may result in a variable natural history of the condition among different populations. [ABSTRACT FROM AUTHOR]

Purpose: To elucidate the role of the protein coding laminin α1 (LAMA1) gene in pathological myopia (PM) at the transcriptional level. To achieve this, the binding affinity of single nucleotide polymorphism (SNP) rs2089760—located on the LAMA1 promoter gene—to human fetal scleral fibroblast (HFSF) nucleoprotein was investigated and its effect on LAMA1 transcriptional initiation activity was analyzed. Methods: Binding interactions of the HFSF nucleoprotein and biotin-labeled SNP rs2089760 probe were investigated by amplifying the LAMA1 promoter gene and performing overlap extension polymerase chain reaction (PCR) to obtain the G/A mutation of LAMA1 SNP rs2089760. Recombinant adenovirus vectors, Ad5f11p-pLAMA1SNPa-Luc2, Ad5f11p-pLAMA1SNPg-Luc2, and Ad5f11p-CMV-RLuc, were constructed. Fluorescence intensity ratios of firefly luciferase (FLuc) and renilla luciferase (RLuc) vectors were measured 48 h after HFSF infection.Results: Both specific and mutant probes banded precisely with HFSF nucleoprotein. The intensity value of the mutant probe was significantly lower than that of the specific probe (p< 0.05). HFSFs were successfully infected by the recombinant adenoviruses. The FLuc/RLuc fluorescence intensity ratio of Ad5f11p-pLAMA1SNPa-Luc2 (0.0238 ± 0.0009) was significantly lower than that of Ad5f11p-pLAMA1SNPg-Luc2 (0.0281 ± 0.0015) (p< 0.05).Conclusions: It is highly likely that SNP rs2089760 in the LAMA1 promoter region is located at the transcription factor binding site. The SNP rs2089760 G > A mutation reduces transcription factor binding ability and transcriptional initiation activity, and negatively regulates gene transcription of LAMA1. We suggest that LAMA1 SNP rs2089760 plays an important role in the development of PM. [ABSTRACT FROM PUBLISHER]