Clinical Trial Details
— Status: Completed
Administrative data
NCT number |
NCT00280345 |
Other study ID # |
Pigmentary Glaucoma |
Secondary ID |
|
Status |
Completed |
Phase |
N/A
|
First received |
|
Last updated |
|
Start date |
February 2006 |
Est. completion date |
May 2009 |
Study information
Verified date |
December 2023 |
Source |
University of Oklahoma |
Contact |
n/a |
Is FDA regulated |
No |
Health authority |
|
Study type |
Interventional
|
Clinical Trial Summary
Based on these recent observations and findings in this new animal model of pigmentary
glaucoma in the DBA/2J mouse, we propose that immune system abnormalities in the anterior
chamber may play a possible role in the development of pigmentary glaucoma and possibly
primary open-angle glaucoma (POAG) in humans.
Description:
The aim is to establish, through tissue and aqueous analysis of patients with pigmentary
glaucoma, POAG and normal controls, that markers for anterior chamber autoimmune dysfunction
occur in significantly different amounts in patients with these conditions when compared to
normal controls. We also will attempt to establish, through proven methodologies of tissue
gene expression, that the source of these differences in markers, notably PEDF and IL-18, is
from the uveal tissues of the anterior chamber, most importantly the iris and possibly the
trabecular meshwork as well.
The actual etiology at the cellular level of elevated intraocular pressure and the
development of pigmentary glaucoma is not well understood in humans. If anterior chamber
immune dysfunction were shown to be an important factor in the development of this disease in
humans, which apparently is demonstrated by the DBA/2J mouse, it would lead to an important
area of further investigation and possible novel approaches in treating or preventing this
disease in humans.
We hypothesize that in patients with pigmentary glaucoma, the amount of PEDF in the aqueous
is significantly reduced while IL-18 is significantly elevated when compared to the aqueous
of normal controls. In patients with POAG, we hypothesize similar results for PEDF, although
significantly less reduction of PEDF when compared to the pigmentary glaucoma patients may be
an interesting finding as well. With regard to IL-18, it is possible that amounts would be
significantly elevated in the pigmentary glaucoma patients when compared to both normal
controls and POAG patients. In view of the results from the DBA/2J mouse model, we hope to
determine whether expression of PEDF could be down regulated in the iris and/or trabecular
meshwork of pigmentary glaucoma patients when compared to POAG patients and whether IL-18
expression in these tissues could be up regulated in pigmentary glaucoma patients when
compared to POAG patients.
Such findings would strongly suggest that anterior chamber immune abnormalities play a role
in the etiology of pigmentary glaucoma in humans. It already has been suggested that
decreased amounts and expression of PEDF are found in patients with glaucoma and other
neurodegenerative diseases of the eye. However, the source of the decreased expression has
not been identified. If IL-18 production is elevated in pigmentary glaucoma and is up
regulated in the anterior chamber structures of the eye in human patients with the disease,
this also would be highly suggestive that localized anterior chamber immune dysfunction plays
a role in the development of this disease.
Depending on our findings, additional investigations of autoimmune dysregulation in
pigmentary glaucoma (and perhaps other secondary glaucomas) may help determine the predictive
value of such markers in identifying whether or not patients with pigment dispersion syndrome
develop glaucomatous damage.