Vascular endothelial growth factor gene polymorphism prevalence in patients with diabetic macular oedema and its correlation with anti-vascular endothelial growth factor treatment outcomes.
BACKGROUND
To study the possible association between vascular endothelial growth factor gene polymorphism and diabetic macular oedema, and its correlation to the outcomes of anti-vascular endothelial growth factor treatment.


METHODS
Prospective study.


METHODS
392 diabetic patients were included; 180 patients of them had no retinopathy, 212 patients had diabetic retinopathy. Diabetic retinopathy patients were classified into four groups as defined by the absence or presence of macular oedema or proliferative retinopathy.


METHODS
In all subjects, polymerase chain reaction-restriction fragment length polymorphism was conducted to detect the vascular endothelial growth factor gene C-634G polymorphism. Serum levels of vascular endothelial growth factor were estimated. Changes of visual acuity and central macular thickness after bevacizumab treatment in diabetic macular oedema patients of different genotypes were monitored for 9-12 months.


METHODS
Vascular endothelial growth factor C-634G genotypes distribution in different groups; correlation between genotypes, and changes in visual acuity and central macular thickness after intravitreal bevacizumab treatment.


RESULTS
CC genotype was significantly prevalent among diabetic macular oedema patients (P = 0.019). Significant higher serum levels of vascular endothelial growth factor were detected in diabetic retinopathy and diabetic macular oedema patients with CC genotype (P = 0.02, 0.016). After bevacizumab treatment, individuals with genotypes CG and GG have a decreased chance of positive treatment outcomes compared t with CC genotype (P < 0.001).


CONCLUSIONS
Vascular endothelial growth factor C-634G polymorphism (CC genotype) is a genetic risk factor for diabetic macular oedema, and its presence provides significantly better visual outcome following bevacizumab treatment.
Department of Clinical Pathology, Faculty of Medicine, Tanta University, Tanta, Egypt.
Sherien F
SF
El-Shazly
Mohamed H
MH
El-Bradey
Mohamed K
MK
Tameesh
D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D000068258:Bevacizumab; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000235:genetics; D003930:Diabetic Retinopathy / Q000097:blood / Q000188:drug therapy / Q000235:genetics*; D005260:Female; D005451:Fluorescein Angiography; D060005:Genotyping Techniques; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D008269:Macular Edema / Q000097:blood / Q000188:drug therapy / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D015995:Prevalence; D011446:Prospective Studies; D041623:Tomography, Optical Coherence; D016896:Treatment Outcome; D042461:Vascular Endothelial Growth Factor A / Q000097:blood / Q000235:genetics*; D014792:Visual Acuity
D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D000068258:Bevacizumab; D006442:Glycated Hemoglobin; D042461:Vascular Endothelial Growth Factor A; C467484:VEGFA protein, human; C517652:hemoglobin A1c protein, human
DMO; PCR-REFLP; VEGF; bevacizumab; polymorphism.