Polymorphisms in the Human Matrix Metalloproteinase Genes MMP1, MMP3, and MMP9: Genetic Risk Factors of Primary Open Angle Glaucoma?

This study has been completed.
Sponsor:
Information provided by:
Medical University of Vienna
ClinicalTrials.gov Identifier:
NCT00312403
First received: April 6, 2006
Last updated: January 14, 2010
Last verified: January 2010

April 6, 2006
January 14, 2010
November 2005
November 2009   (final data collection date for primary outcome measure)
Genotyping results and putatively associated odds with occurence of primary open angle glaucoma. [ Time Frame: 15 minutes ] [ Designated as safety issue: No ]
Genotyping results and putatively associated odds with occurence of primary open angle glaucoma.
Complete list of historical versions of study NCT00312403 on ClinicalTrials.gov Archive Site
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Polymorphisms in the Human Matrix Metalloproteinase Genes MMP1, MMP3, and MMP9: Genetic Risk Factors of Primary Open Angle Glaucoma?
Polymorphisms in the Human Matrix Metalloproteinase Genes MMP1, MMP3, and MMP9: Genetic Risk Factors of Primary Open Angle Glaucoma?

Matrix metalloproteinases (MMPs) fulfill diverse important molecular functions and play pivotal roles in development, tissue morphogenesis, repair, aging, and inflammatory processes. MMPs are also important disease modulating factors, such as cancer, cardiovascular disease, rheumatoid arthritis or macular degeneration. Functional genetic variants have been described to fine-tune MMP activities at the gene transcriptional level and have been associated with increased genetic risk of e.g. arteriosclerosis or cancer. MMPs are also assumed to play a major role in the remodeling of the extracellular matrix (ECM) in the optic nerve head during glaucomatous optic neuropathy. MMP-1, MMP-3 and MMP-9 have been shown to be up-regulated in a variety of animal models of glaucoma. Here, we study three promoter SNPs within the genes encoding three members of the MMP family. By assessing the prevalence of genetic variants associated with either increased/decreased enzyme activity, we will (i) estimate their contribution to the genetic risk of developing primary open angle glaucoma (POAG) and (ii) investigate the potential role of MMPs in the functional pathology of POAG.

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Interventional
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Allocation: Non-Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Open Label
Primary Purpose: Diagnostic
Glaucoma
Procedure: Blood Sample
A single venous blood sample will be taken (10 ml).
  • 1
    Patients with primary open angle glaucoma
    Intervention: Procedure: Blood Sample
  • 2
    Age- and sex-matched control subjects
    Intervention: Procedure: Blood Sample
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
400
December 2009
November 2009   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Men and women older than 39 years
  • Primary open angle glaucoma as evidenced from characteristic visual field loss and optic disc cupping (POAG group)
  • Healthy subjects matched by age, sex and ethnicity to the POAG patients group (control group)

Exclusion Criteria:

  • Exfoliation glaucoma, pigmentary glaucoma
  • History of acute angle closure
Both
40 Years and older
Yes
Contact information is only displayed when the study is recruiting subjects
Austria
 
NCT00312403
OPHT-300505
Yes
Gabriele Fuchsjaeger-Mayrl, Department of Clinical Pharmacology, Medical University of Vienna
Medical University of Vienna
Not Provided
Principal Investigator: Gabriele Fuchsjaeger-Mayrl, M.D. Department of Clinical Pharmacology, Medical University of Vienna
Medical University of Vienna
January 2010

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP