Ignite Creation Date:
2024-05-05 @ 4:37 PM
Last Modification Date:
2024-10-26 @ 9:22 AM
Study NCT ID:
NCT00280345
Status:
COMPLETED
Last Update Posted:
2023-12-15
First Post:
2006-01-19
Brief Title:
Autoimmune Dysregulation in Pigmentary Glaucoma
Sponsor:
University of Oklahoma
Organization:
University of Oklahoma
Study Overview
Official Title:
Autoimmune Dysregulation in Pigmentary Glaucoma
Status:
COMPLETED
Status Verified Date:
2023-12
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Based on these recent observations and findings in this new animal model of pigmentary glaucoma in the DBA2J 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
Detailed 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 DBA2J 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 DBA2J mouse model we hope to determine whether expression of PEDF could be down regulated in the iris andor 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
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 DBA2J 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 DBA2J mouse model we hope to determine whether expression of PEDF could be down regulated in the iris andor 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
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None