Genetic Biomarkers for the Response to Anti-VEGF (Vascular Endothelial Growth Factor).Treatment in Wet Age-related Macular Degeneration (Wet ARMD)
1 other identifier
interventional
501
1 country
1
Brief Summary
Age-Related Macular Degeneration (ARMD) is the most common cause of blindness in the adult population of the Western World. It affects the macula - the region of the retina most rich in photoreceptors and responsible for central vision. The ethiology of ARMD remains poorly understood. Population-based studies have demonstrated a complex ethiology, with contributions from a combination of genetic and environmental factors. Two major forms of ARMD are clinically distinguishable: the dry and wet form. The latter represents the more aggressive clinical subgroup, and is characterized by the abnormal growth of new blood vessels (neovascularization) under the macula, thus leading to the accumulation of fluid under the retina, bleeding, progression to fibrosis, and finally loss of central vision. The pathogenesis of this neovascularization is not fully understood, although the VEGF pathway is well known to be involved in angiogenesis and was implicated in the development of the new vessels under the macula. The VEGFs are the most specific and potent stimulators of the angiogenesis. Molecules that bind and inactivate the VEGF have been developed for the treatment of ARMD and they are applied in ARMD clinic through intra vitreal injections.The difference seen in response to anti VEGF treatment for ARMD between the patients is suggestive for the presence of factors influencing the effect of the drug. Some of these could be genetic variants within genes involved in ARMD pathogenesis or VEGF pathway. Few associations with markers within genes previously found to be related with the pathogenesis of ARMD have been found. It remains unknown whether variants involved in the anti VEGF treatment response could influence the therapeutic outcome. The purpose of this trial is to evaluate the association between a panel of selected polymorphic markers in the VEGF pathway and the response to therapy with anti VEGF antibody for ARMD. The hypothesis is that the individual genotype influences the response to the anti VEGF. This can lead to identification of genetic biomarkers allowing treatment individualization and optimization of the visual outcomes.
Trial Health
Trial Health Score
Automated assessment based on enrollment pace, timeline, and geographic reach
participants targeted
Target at P75+ for not_applicable
Started Aug 2013
Longer than P75 for not_applicable
1 active site
Health score is calculated from publicly available data and should be used for screening purposes only.
Trial Relationships
Click on a node to explore related trials.
Study Timeline
Key milestones and dates
Study Start
First participant enrolled
August 1, 2013
CompletedFirst Submitted
Initial submission to the registry
April 25, 2016
CompletedFirst Posted
Study publicly available on registry
May 4, 2016
CompletedPrimary Completion
Last participant's last visit for primary outcome
January 18, 2018
CompletedStudy Completion
Last participant's last visit for all outcomes
January 18, 2018
CompletedJanuary 23, 2018
January 1, 2018
4.5 years
April 25, 2016
January 18, 2018
Conditions
Keywords
Outcome Measures
Primary Outcomes (18)
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
Baseline
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
3 months after treatment
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
6 months after treatment
Snellen visual acuity test result
The visual acuity test is used to determine the smallest letters you can read on a standardized chart (Snellen chart).
12 months after treatment
Number of injections received per year
1 year
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
Baseline
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
3 months after treatment
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
6 months after treatment
Central foveal thickness (µm)
Measured by optical coherence tomography (Heidelberg \& Zeiss)
12 months after treatment
Presence of Intra Retinal Cysts (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Baseline
Presence of Intra Retinal Cysts (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
3 months after treatment
Presence of Intra Retinal Cysts (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
4 months after treatment
Presence of Subretinal Fluid (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Baseline
Presence of Subretinal Fluid (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
3 months after treatment
Presence of Subretinal Fluid (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
4 months after treatment
Presence of Pigment Epithelial Detachment (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
Baseline
Presence of Pigment Epithelial Detachment (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
3 months after treatment
Presence of Pigment Epithelial Detachment (yes/no)
Tested by optical coherence tomography (Heidelberg \& Zeiss)
4 months after treatment
Study Arms (1)
wet ARMD patients
EXPERIMENTALPatients with the wet form of ARMD who receive or have received in the past anti VEGF intra vitreal injections. Diagnosis of wet ARMD is made based on clinical data-visual acuity, fundus presence of subretinal fluid and/or haemorrhage and/or hard exudates, fundus photographs -color and red free, optical coherence tomography (SD-OCT), fluorescein angiography and indocyanine green angiography showing the presence and activity of subretinal neovascularisation.
Interventions
After signing informed consent, a blood sample is taken and DNA extracted according to standard procedures. The samples are genotyped with the Mass Array iPlex Gold. Processing of the data is done using the previously described protocol by Lambrechts and co. Statistical analysis will be done to evaluate the association between the different genetic variants and the clinical outcomes collected during the standard of care follow-up for ARMD.
Eligibility Criteria
You may qualify if:
- Patients with the wet form of ARMD who receive or have received in the past anti VEGF intra vitreal injections
You may not qualify if:
- Patients whi had received treatments other than anti VEGF, before the use of anti-VEGF
- Patients without follow-up
- Patients receiving anti-VEGF because of another pathology than ARMD
Contact the study team to confirm eligibility.
Sponsors & Collaborators
Study Sites (1)
CHU Brugmann
Brussels, 1020, Belgium
MeSH Terms
Conditions
Interventions
Condition Hierarchy (Ancestors)
Intervention Hierarchy (Ancestors)
Study Officials
- PRINCIPAL INVESTIGATOR
Laurence Postelmans, MD
CHU Brugmann
Study Design
- Study Type
- interventional
- Phase
- not applicable
- Allocation
- NA
- Masking
- NONE
- Purpose
- BASIC SCIENCE
- Intervention Model
- SINGLE GROUP
- Sponsor Type
- OTHER
- Responsible Party
- PRINCIPAL INVESTIGATOR
- PI Title
- Head of clinic
Study Record Dates
First Submitted
April 25, 2016
First Posted
May 4, 2016
Study Start
August 1, 2013
Primary Completion
January 18, 2018
Study Completion
January 18, 2018
Last Updated
January 23, 2018
Record last verified: 2018-01
Data Sharing
- IPD Sharing
- Will not share