Abstract:Background Cigarette smoking has been regarded as a risk factor for the incidence of a wide variety of chronic illness; however, its effect on thickness of the retina or choroid is still unknown. Methods A consummate literature search was conducted in PubMed and Embase up to January, 2018. The quantitative synthesis was conducted by Stata 12.0. Results A total of 13 observational studies were included in this meta-analysis. In this meta-analysis of all available observational studies, no significant effect of … Show more
“…Some have suggested that these differences were driven by thicker inner and outer nuclear layers in males 49 . While smoking has been identified as a modifiable risk factor for AMD 5 , 50 – 53 , we did not find any association between macular retinal thickness and smoking at baseline, which is also consistent with previous reports 54 , 55 . Once adjusted for age, baseline differences in retinal thickness among eyes with a grade 0 were driven by patients from the Chr1-prot-del group.…”
The two most common genetic contributors to age-related macular degeneration (AMD), a leading cause of irreversible vision loss worldwide, are variants associated with CFH-CFHR5 on chromosome 1 (Chr1) and ARMS2/HTRA1 on chromosome 10 (Chr10). We sought to determine if risk and protective variants associated with these two loci drive differences in macular retinal thickness prior and subsequent to the onset of clinically observable signs of AMD. We considered 299 individuals (547 eyes) homozygous for risk variants or haplotypes on Chr1 or Chr10 exclusively (Chr1-risk and Chr10-risk, respectively) or homozygous for a neutral haplotype (Chr1-neu), for the protective I62 tagged haplotype (Chr1-prot-I62) or for the protection conferring CFHR1/3 deletion haplotype (Chr1-prot-del) on Chr1 without any risk alleles on Chr10. Among eyes with no clinically observable signs of AMD, the deletion of CFHR1/3, which is strongly protective against this disease, is associated with significantly thicker retinas in the perifovea. When controlling for age, Chr10-risk eyes with early or intermediate AMD have thinner retinas as compared to eyes from the Chr1-risk group with similar disease severity. Our analysis indicates that this difference likely results from distinct biological and disease initiation and progression events associated with Chr1- and Chr10-directed AMD.
“…Some have suggested that these differences were driven by thicker inner and outer nuclear layers in males 49 . While smoking has been identified as a modifiable risk factor for AMD 5 , 50 – 53 , we did not find any association between macular retinal thickness and smoking at baseline, which is also consistent with previous reports 54 , 55 . Once adjusted for age, baseline differences in retinal thickness among eyes with a grade 0 were driven by patients from the Chr1-prot-del group.…”
The two most common genetic contributors to age-related macular degeneration (AMD), a leading cause of irreversible vision loss worldwide, are variants associated with CFH-CFHR5 on chromosome 1 (Chr1) and ARMS2/HTRA1 on chromosome 10 (Chr10). We sought to determine if risk and protective variants associated with these two loci drive differences in macular retinal thickness prior and subsequent to the onset of clinically observable signs of AMD. We considered 299 individuals (547 eyes) homozygous for risk variants or haplotypes on Chr1 or Chr10 exclusively (Chr1-risk and Chr10-risk, respectively) or homozygous for a neutral haplotype (Chr1-neu), for the protective I62 tagged haplotype (Chr1-prot-I62) or for the protection conferring CFHR1/3 deletion haplotype (Chr1-prot-del) on Chr1 without any risk alleles on Chr10. Among eyes with no clinically observable signs of AMD, the deletion of CFHR1/3, which is strongly protective against this disease, is associated with significantly thicker retinas in the perifovea. When controlling for age, Chr10-risk eyes with early or intermediate AMD have thinner retinas as compared to eyes from the Chr1-risk group with similar disease severity. Our analysis indicates that this difference likely results from distinct biological and disease initiation and progression events associated with Chr1- and Chr10-directed AMD.
“…A consistent trend was observed in each analysis; however, P -values were not consistently significant probably due to the large variation within groups. Previously, tobacco-associated retinal changes were also observed in otherwise healthy subjects ( Yang et al , 2019 ). However, the change was observed as thinning of retinal nerve fibre layer and ganglion cell layer.…”
Retinitis pigmentosa is an inherited neurodegenerative disease of the retina. We investigated smoking as a modifiable environmental factor for the progression of this currently untreatable disease. Clinical data, smoking history, macular function, and morphology including visual acuity, visual field sensitivity, ellipsoid zone width, and central retinal thickness were investigated. Association between pack × years and these parameters were evaluated using generalized estimating equation models to adjust confounding factors such as age and sex. 410 patients with retinitis pigmentosa (≥20 years old; 209 female) were included, 164 had a smoking history. Patients without smoking history revealed a better visual acuity than non-smokers (0.39 vs 0.57, P = 0.001). The pack × years index was associated with worse visual acuity and thinner central retinal thickness after adjusting for age and sex (P = 0.0047 and 0.0099, respectively). Visual field and ellipsoid zone width showed a non-significant decline with increasing pack × years. This study indicates an association of smoking with worse macular function and structural integrity in retinitis pigmentosa patients, and hence a potential detrimental effect of smoking on the disease course.
“…Smoking was considered to be a possible factor that affects choroidal thickness. However, a meta-analysis showed that no significant effect of tobacco smoking on choroidal thickness change was detected (Yang et al, 2019 ). Furthermore, it was noted in this study that no significant difference exists in SFChT between smokers and nonsmokers.…”
Background: This study aims to evaluate ocular changes in patients with ischemic stroke using multimodal imaging and explore the predictive value of ocular abnormalities for ischemic stroke.Methods: A total of 203 patients (ischemic stroke group, 62; control group, 141) were enrolled in this study. Basic data from patients, including age; gender; height; weight; history of hypertension, hyperlipidemia, diabetes, alcohol use, and coronary heart disease; and smoking status, were collected. Consequently, Doppler color ultrasound, color fundus photography, and optical coherence tomography (OCT) examinations were conducted. Differences in traditional risk factors and ocular parameters between the two groups were compared, and binary logistic regression was used for multivariate analysis.Results: The central retinal artery equivalent (CRAE) in the ischemic stroke group was 150.72 ± 20.15 μm and that in the control group was 159.68 ± 20.05 μm. The difference was statistically significant (P = 0.004). Moreover, the subfoveal choroidal thickness (SFChT) in the ischemic stroke group was 199.90 ± 69.27 μm and that in the control group was 227.40 ± 62.20 μm. The difference was statistically significant (P = 0.006). Logistic regression results showed that smoking [odds ratio (OR) = 2.823; 95% confidence interval (95% CI) = 1.477–5.395], CRAE (OR = 0.980; 95% CI = 0.965–0.996), and SFChT (OR = 0.994; 95% CI = 0.989–0.999) are associated with increased risk of ischemic stroke when ocular parameters were combined with traditional risk factors. The area under the receiver operating characteristic (ROC) curve was 0.726, which shows good diagnostic accuracy.Conclusion: SFChT may be a diagnostic marker for early detection and monitoring of ischemic stroke. Combined with traditional risks, retinal artery diameter, and choroidal thickness, the prediction model can improve ischemic stroke prediction.
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