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Possible association with obesity‐related loci and outcome of wet AMD
Author(s) -
Kaarniranta K.,
Helisalmi S.,
Birling A.,
Saavalainen L.,
Tolppola O.,
Vajanto V.,
Uusitupa M.,
Paterno J.J.
Publication year - 2016
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2016.0666
Subject(s) - medicine , dyslipidemia , body mass index , obesity , visual acuity , diabetes mellitus , diabetic retinopathy , ophthalmology , macular degeneration , medical record , prospective cohort study , endocrinology
Purpose To investigate whether obesity‐related genes affect a visual outcome of anti‐VEGF‐treatment in wet AMD. Methods Thirty‐seven patients with wet AMD (mean age: 77.0 years) in Kuopio University Hospital, Finland, solely treated with anti‐VEGF as needed, were genotyped for 40 recently associated obesity‐related loci using the Sequenom iPlex platform. Diabetes and other causes of macular oedema diagnosed by ophthalmologist were exclusion criteria. Obesity‐loci were examined with respect to retrospective clinical monitoring data, including also visual acuity (VA) measured by Snellen decimals. Results Visual outcome was associated with rs10938397 (GNPDA2), rs1555543 (PTBP2), and rs7359397 (SH2B1). Mean differences in VA between the two homotsygotes were 0.25 (p = 0.03), 0.25 (p = 0.002), and 0.26 (p = 0.003), respectively. Genotypes did not differ by age, baseline VA, body mass index (BMI), gender, the number of anti‐VEGF injections, smoking, or the use of dyslipidemia medication, expect for rs10938397 (mean BMI difference 3.2 kg/m 2 , p = 0.38) and rs7359397 (mean age difference 8.5 years, p = 0.14). Conclusions Our data suggest, that at least rs1555543 (PTBP2) might have some effect on the visual outcome of anti‐VEGF‐treatment in wet AMD. The present study may be affected by the small sample, and it need to be replicated in a larger prospective setup. Diseases associated with PTBP2 include cancer‐associated retinopathy. Nevertheless, the potential role of the abundant genetic variation in modifiying drug responses in wet AMD should be further investigated.