Does Vascular Endothelial Growth Factor (VEGF) or Complement Factor H Gene Polymorphism Play a Role in the Treatment Success With VEGF Inhibitors in Patients With Choroidal NeoVascularization (CNV)?

This study is not yet open for participant recruitment.

Verified by Medical University of Vienna, December 2008

First Received: December 22, 2008 No Changes Posted

Sponsored by:	Medical University of Vienna
Information provided by:	Medical University of Vienna
ClinicalTrials.gov Identifier:	NCT00813514

Purpose

Age related macular degeneration (AMD) is a multifactorial disease with a strong genetic component. Most importantly a genetic polymorphism in the gene encoding for the complement factor H (CFH) has been recently identified which is highly associated with an increased risk of developing AMD. This Tyr402His polymorphism located on chromosome 1q31 has been implicated to play a role in the development of the disease.

For this purpose a total of 200 patients with wet AMD will be included in the study. As described in detail below, the current study aims to identify potentially non-responders to anti-VEGF therapy based on genetic analysis of VEGF polymorphism and complement factor H polymorphism.

Condition	Intervention
Choroidal Neovascularization Age-Related Macular Degeneration	Genetic: VEGF genotyping

Study Type:	Interventional
Study Design:	Diagnostic, Open Label, Uncontrolled, Single Group Assignment, Safety Study
Official Title:	Does VEGF or Complement Factor H Gene Polymorphism Play a Role in the Treatment Success With VEGF Inhibitors in Patients With CNV?

Resource links provided by NLM:

Genetics Home Reference related topics: X-linked juvenile retinoschisis

MedlinePlus related topics: Macular Degeneration

U.S. FDA Resources

Further study details as provided by Medical University of Vienna:

Primary Outcome Measures:

Visual acuity using ETDRS charts [ Time Frame: 2 x 5 minutes ] [ Designated as safety issue: No ]
Central retinal thickness (Optical coherence tomography) [ Time Frame: 2 x 20 minutes ] [ Designated as safety issue: No ]
VEGF genotyping [ Time Frame: 1 week ] [ Designated as safety issue: No ]

Estimated Enrollment:	200
Study Start Date:	January 2009
Estimated Study Completion Date:	January 2010
Estimated Primary Completion Date:	December 2009 (Final data collection date for primary outcome measure)

Arms	Assigned Interventions
1: No Intervention Open longitudinal study with observer masked analysis	Genetic: VEGF genotyping blood sample for gene analysis

Eligibility

Ages Eligible for Study:	50 Years to 90 Years
Genders Eligible for Study:	Both
Accepts Healthy Volunteers:	No

Criteria

Inclusion Criteria:

Men and women aged over 50 years
Angiographically verified neovascular AMD
Active primary or recurrent subfoveal lesion with CNV secondary to AMD
Activity to be proven by fluorescein angiography
Best corrected visual acuity assessed using ETDRS charts of 20/40 to 20/320 in the study eye
CNV to be treated with intravitreal ranibizumab
Signed informed consent

Exclusion Criteria:

Prior treatment with any intravitreal drug in the study eye
Prior treatment with verteporfin photodynamic therapy in the study eye
Prior treatment with systemic bevacizumab
Prior treatment with any intravitreal drug or verteporfin photodynamic therapy in the non-study eye within the 3 moths before the study entry
Laser photocoagulation within 1 month before study entry in the study eye
Previous participation in any clinical trial within 1 month before the entry of the study
Subfoveal fibrosis or atrophy in the study eye
CNV in either of the two eye due to causes other than AMD such as histoplasmosis or pathological myopia
Retinal pigment epithelial tear involving the macula in the study eye
Any concurrent intraocular condition in the study eye that could either require medical or surgical intervention during the 12 month study period or that could contribute to a loss of best corrected visual acuity over the 12 months study period (e.g. diabetic retinopathy, cataract, uncontrolled glaucoma). The decision on exclusion is to be based on the opinion of the local principal investigator.
Active intraocular inflammation
Acute angle-closure glaucoma or narrow angle glaucoma due to the risk of IOP elevation caused by the administration of tropicamide

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00813514

Contacts

Contact: Gerhard Garhöfer, MD

+431404002981

Locations

Austria
Department of Clinical Pharmacology, Medical University of Vienna
Vienna, Austria

Sponsors and Collaborators

Medical University of Vienna

Investigators

Principal Investigator:

Leopold Schmetterer, Prof. Dr.

Department of Clinical Pharmacology

More Information

No publications provided

Responsible Party:	Department of Clinical Pharmacology, Medical University Vienna, Austria ( Dr. Fuchsjäger- Mayrl )
Study ID Numbers:	OPHT-270907
Study First Received:	December 22, 2008
Last Updated:	December 22, 2008
ClinicalTrials.gov Identifier:	NCT00813514 History of Changes
Health Authority:	Austria: Agency for Health and Food Safety

Keywords provided by Medical University of Vienna:

AMD
VEGF genotyping
complement H gene polymorphism
Vascular Endothelial Growth Factor A

Study placed in the following topic categories:

Uveal Diseases
Immunologic Factors
Eye Diseases
Choroid Diseases
Macular Degeneration
Retinal Degeneration
Complement Factor H

Endothelial Growth Factors
Immunosuppressive Agents
Choroidal Neovascularization
Metaplasia
Mitogens
Neovascularization, Pathologic
Retinal Diseases

Additional relevant MeSH terms:

Uveal Diseases
Immunologic Factors
Growth Substances
Eye Diseases
Physiological Effects of Drugs
Choroid Diseases
Macular Degeneration
Retinal Degeneration
Complement Factor H

Endothelial Growth Factors
Immunosuppressive Agents
Pharmacologic Actions
Choroidal Neovascularization
Pathologic Processes
Metaplasia
Neovascularization, Pathologic
Complement Inactivating Agents
Retinal Diseases

ClinicalTrials.gov processed this record on August 28, 2009