Abstract
Purpose :
To investigate the role of Val66Met Single Nucleotide Polymorphism (SNP) in symptom change of dry eye disease (DED) patients following treatment.
Methods :
Thirty-six patients were followed-up for a minimum of 6 months for treatment efficacy and symptom response. Saliva for SNP analysis was collected at baseline. Patients were asked to rate their symptoms on a scale of 0 to 4. Additionally, during each follow-up, patients were asked about their symptom experience as follows: no change; 25% better; 50% better; 75% better; or worse. Prescribed DED treatments for each patient were also collected, and scored as either 1 point or 2 points based on aggressiveness. The last follow-up time for each patient was selected for analysis. Mean and median baseline scores and follow-up scores were generated and compared for each patient using a paired t-test. DED treatment and change in symptom score were stratified by genotype.
Results :
Mean age was 53 years + 15.7. Forty-two percent were clinically diagnosed with depression. The genotype distribution for Val66Met was 0.1% for AA, 30.6% for GA, and 63.9% for GG. The average mean follow-up of those patients was 15.52 + 8.4 months and the median follow-up was 20.3 months. Patients with GG genotype showed significant decreases in dryness and pain symptoms between baseline and the last follow-up time point (dryness: 3.0 to 1.7, P=0.005; pain: 2.2 to 0.5, P=0.002) whereas patients with the GA genotype did not exhibit significant decreases in the dryness and pain symptoms (2.5 till 2.0 P=0.4 for dryness; 1.5 to 0.4 P=0.1 for pain). Thirty one percent of patients with the GG genotype said that their symptoms improved by 25%, 46.2% reported no change in symptoms, and 23.1% reported that their symptoms became worse. As for patients with the GA genotype, 25.0% said that their symptoms improved by 25%, 62.5% reported no change in symptoms, and 12.5% reported that their symptoms became worse (P=0.90). Additionally, 62.5% of DED patients with the GA genotype were clinically diagnosed with depression, compared to 30.8% of DED patients with the GG genotype. As for prescribed treatments, the mean level of aggressiveness between GG and GA genotype did not differ clinically nor statistically (2.7 and 2.8, respectively, P=0.8).
Conclusions :
This study suggests that Val66Met SNP in the BDNF gene may regulate the efficacy of DED treatment.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.