July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
The Effect of alcohol after intravitreal anti-VEGF treatment in AMD - in a cellular level
Author Affiliations & Notes
  • Soyeon Jung
    Ophthalmology and Inha Vision Science Laboratory, Inha University School of Medicine, Incheon, Korea (the Republic of)
  • Hee Seung Chin
    Ophthalmology and Inha Vision Science Laboratory, Inha University School of Medicine, Incheon, Korea (the Republic of)
  • Footnotes
    Commercial Relationships   Soyeon Jung, None; Hee Seung Chin, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 1451. doi:
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      Soyeon Jung, Hee Seung Chin; The Effect of alcohol after intravitreal anti-VEGF treatment in AMD - in a cellular level. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1451.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Intravitreal anti-VEGF injection is a current standard treatment for suppression of neovascularization in patients with age-related macular degeneration (AMD). Even though the relationship between AMD and alcohol consumption is not clearly demonstrated, in a clinical situation, it is seen that the response of intravitreal anti-VEGF injection has relevance to alcohol consumption. Thus, in this study, we try to evaluate the effect of alcohol after anti-VEGF treatment in cellular level.

Methods : We grouped human RPE cells (ARPE-19) into four groups - control group, a group with Avastin 0.5mg/ml, a group with ethanol 600mM, and a group with Avastin 0.5mg/ml and ethanol 600mM. The fourth group was treated Avastin 0.5mg/ml first, and after 6hours later, ethanol 600mM was treated. After 24hours, the cell culture supernates were collected and the amount of VEGF was measured. Also, HUVEC (human umbilical vein endothelial cell) capillary tube formation assay was executed to evaluate the neovascular effect of the four groups. For comparison, a group with human VEGF (rhVEGF) 5ng/ml and a group with Avastin 0.5mg/ml and rhVEGF 5ng/ml were included in tube formation assay.

Results : The VEGF amount measured in control group was 368.14pg/ml and group with ethanol 600mM was 382.70pg/ml. There is no VEGF expression in the group of Avastin 0.5mg/ml and the group of Avastin and ethanol. In tube formation assay, we analyzed the number and total length per micrometer squre of extremities, nodes, junctions, segments, branches in tube formation. The number of branches per micrometer square in control group was 1.45±0.16, Avastin group was 1.64±0.30, ethanol group was 2.14±0.21, Avastin and ethanol group was 2.21±0.11, rhVEGF group was 1.70±0.18, and Avastin and rhVEGF group was 1.61±0.04. In one-way analysis of variance with Scheffe post hoc test, the number of branches per micrometer square of ethanol group and Avastin and ethanol group show statistical significance(p=0.032, 0.017, each).

Conclusions : In a cellular level, the VEGF expression was not reported, but tube formation increased in a group with Avastin and alcohol. Through these results, we can assume that alcohol can affect the anti-VEGF treatment response in cellular level and the alcohol effect is related to neovascularization. However, the neovascularization is not directly related to expression of VEGF itself.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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