CD36 gene is associated with intraocular pressure elevation after intravitreal application of anti-VEGF agents in patients with age-related macular degeneration: Implications for the safety of the therapy
Language English Country Great Britain, England Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- Keywords
- Glaucoma, Schlemm´s canal, polymorphism, receptor, thrombospondin,
- MeSH
- CD36 Antigens genetics MeSH
- Angiogenesis Inhibitors therapeutic use MeSH
- Intravitreal Injections MeSH
- Polymorphism, Single Nucleotide * MeSH
- Humans MeSH
- Intraocular Pressure genetics MeSH
- Ocular Hypertension genetics MeSH
- Polymerase Chain Reaction MeSH
- Ranibizumab therapeutic use MeSH
- Aged MeSH
- Tonometry, Ocular MeSH
- Vascular Endothelial Growth Factor A antagonists & inhibitors MeSH
- Wet Macular Degeneration diagnosis drug therapy genetics MeSH
- Check Tag
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- CD36 Antigens MeSH
- Angiogenesis Inhibitors MeSH
- Ranibizumab MeSH
- Vascular Endothelial Growth Factor A MeSH
- VEGFA protein, human MeSH Browser
BACKGROUND: The wet form of age-related macular degeneration (AMD) is characterized by pathological vascularization of the outer retinal layers. The condition responds to treatment with antibodies against vascular endothelial growth factor (VEGF), but the patients receiving such anti-VEGF therapy sometimes show undesirable acute short-term increases in the intraocular pressure (IOP). The cause of this adverse effect is unknown, and here, we are testing a hypothesis that it is related to CD36 gene polymorphisms. MATERIALS AND METHODS: A group of 134 patients with AMD were given three therapeutic doses of anti-VEGF antibody (ranibizumab) at monthly intervals. Their IOP was measured immediately before and 30 min after each injection. Patients' DNA was analyzed, and the changes in IOP were matched against seven polymorphisms of the CD36 gene. RESULTS: Three polymorphisms were found to be associated with increases in IOP: rs1049673 (p = 0.006), rs3211931 (p = 0.01), and rs1761667 (p = 0.043) at the time of the third injection only. Pronounced elevations (IOP > 25 mmHg) were associated with rs1049673 polymorphism: GC genotype (p < 0.01) and CC genotype (p < 0.05); both increasing the risk 2.6-fold, the presence of C-allele conferring a 1.5-fold greater risk and with rs3211931 polymorphism: AG genotype (p < 0.01) and GG genotype (p < 0.05); increasing the risk 2.6-fold (AG) and 2.7-fold (GG). CONCLUSIONS: CD36 receptor may be involved in mediating the effects of VEGF on IOP. The findings will help to identify the patients at risk of acutely elevated IOP following the anti-VEGF therapy.
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