Smoking and age-related macular degeneration: a review of association

Thornton, Judith; Edwards, Richard; Mitchell, Paul; Harrison, Roger; Buchan, Iain; Kelly, Simon P.

doi:10.1038/sj.eye.6701978

Cited by 458 publications

(323 citation statements)

References 45 publications

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“…37,38 There is, however, emerging evidence that responses to anti-VEGF therapy in n-AMD may be influenced by the genetic profile of the individual. 13,15,18 It is possible that other factors such as lifestyle may also affect the responsiveness to treatment and patients should be encouraged to quit smoking even if there is no evidence of reduced effectiveness of anti-VEGF agents in smokers 39,40 given the link between smoking and AMD and the risk to the fellow eye.…”

Section: Response Based On Change In Va In Terms Of Etdrs Lettersmentioning

confidence: 99%

Defining response to anti-VEGF therapies in neovascular AMD

Amoaku

Chakravarthy

Gale

et al. 2015

Eye

252

227

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Section: Response Based On Change In Va In Terms Of Etdrs Lettersmentioning

confidence: 99%

Defining response to anti-VEGF therapies in neovascular AMD

Amoaku

Chakravarthy

Gale

et al. 2015

Eye

252

227

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“…For each subject, we directly sequenced exon 12 of PLEKHA1, the entire putative coding region of LOC387715/ARMS2, and the promoter region and entire coding region of HTRA1 to identify the contribution that allelic risk factors such as those reported in the 10q26 region make independently and in combination with the factors most consistently associated with AMD susceptibility, CFH Y402H genotype [2][3][4][5][6]18 and smoking. 19 …”

mentioning

confidence: 99%

Alleles in the HtrA Serine Peptidase 1 Gene Alter the Risk of Neovascular Age-Related Macular Degeneration

DeAngelis

Adams

et al. 2008

Ophthalmology

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Objective-To examine if the genes encoding the pleckstrin homology domain-containing protein gene (PLEKHA1), hypothetical LOC387715/ARMS2 gene, and HtrA serine peptidase 1 gene (HTRA1) located on the long arm of chromosome 10 (10q26 region) confer risk for neovascular age-related macular degeneration (AMD) in an independent or interactive manner when controlling for complement factor H gene (CFH) genotype and smoking exposure.Design-Retrospective matched-pair case-control study.Participants-Hospital clinic-based sample of 134 unrelated patients with neovascular AMD who have a sibling with normal maculae (268 subjects).Methods-Disease status was ascertained by at least 2 investigators by review of fundus photographs and/or fluorescein angiography according to the Age-Related Eye Disease Study grading scale. If necessary, a home retinal examination was performed (n = 6). A combination of direct sequencing and analysis of 8 highly polymorphic microsatellite markers was used to genotype 33 megabases of the 10q26 region on leukocyte DNA. Smoking history was obtained via a standardized questionnaire and measured in pack-years. The family-based association test, haplotype analysis, multiple conditional logistic regression, and linkage analysis were used to determine significant associations. Main Outcome Measure-Neovascular AMD status.Results-Of the 23 variants we identified in the 10q26 region, 6 were significant. Four of the 6 were novel and included 2 genotypes that reduced risk of AMD. Many single-nucleotide polymorphisms (SNPs), including the previously reported variants rs10490924 (hypothetical NIH Public Access Author ManuscriptOphthalmology. Author manuscript; available in PMC 2014 November 24. Published in final edited form as:Ophthalmology. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptLOC387715/ARMS2) and rs11200638 (HTRA1), defined 2 significant haplotypes associated with increased risk of neovascular AMD. The coding HTRA1 SNP rs2293870, not part of the significant haplotypes containing rs10490924 and rs11200638, showed as strong an association with increased susceptibility to neovascular AMD. Linkage analysis supported our findings of SNP association (P<10 −15 ). No significant interactions were found between any of the SNPs in the 10q26 and smoking or between these SNPs and CFH genotype.Conclusions-Independent of CFH genotype or smoking history, an individual's risk of AMD could be increased or decreased, depending on their genotype or haplotype in the 10q26 region.Neovascular age-related macular degeneration (AMD) is characterized by the growth of abnormal new blood vessels beneath the retina that can cause severe and rapid vision loss due to hemorrhage and exudation. It is this more advanced form that is responsible for the majority of debilitating vision loss due to AMD. In the United States, it is predicted that about 3 million individuals over the age of 50 will have advanced AMD in at least one eye by 2020. 1Current diagnostic methods focus on the detection of ne...

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“…20,21 Analysis of pooled data from three population-based cohort studies showed that the relative risk of late AMD is 2.4 among current smokers as compared with those who never smoked, with an insignificant risk of 1.29 among former smokers. 22 However, current smokers who are homozygous for the complement factor H (CFH) Y402H polymorphism have a relative risk of 34.0 for late AMD as compared with non-smokers who do not have this polymorphism.…”

Section: Smokingmentioning

confidence: 99%

Looking beyond Lucentis on the management of macular degeneration

Fletcher

Chong

2008

Eye

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Purpose Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world. In the past decade, AMD research has improved our understanding of the pathogenesis of the condition. There is no doubt that anti-VEGF therapies will play a major role in the reduction of blindness, but it needs close monitoring and frequent treatments. In this review we summarise the key pathophysiology of the condition and some of the new treatment strategies under development. Methods Literature review. Results Oxidative stress, inflammation, hypoxia, and angiogenesis are key pathophysiological processes in AMD, this diversity has provided a variety of possible areas amenable to modification to enhance the treatment options for AMD.

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Smoking and age-related macular degeneration: a review of association

Cited by 458 publications

References 45 publications

Defining response to anti-VEGF therapies in neovascular AMD

Defining response to anti-VEGF therapies in neovascular AMD

Alleles in the HtrA Serine Peptidase 1 Gene Alter the Risk of Neovascular Age-Related Macular Degeneration

Looking beyond Lucentis on the management of macular degeneration

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