Summary: New research reveals how elevated eye pressure distorts blood vessels and disrupts oxygen delivery, potentially accelerating the progression of glaucoma, a leading cause of irreversible vision loss. Using advanced 3D modeling and fluorescent dyes, scientists found that even mild increases in eye pressure can restrict blood flow in the optic nerve region.
This hypoxia may damage cells and lead to vision loss, even when pressure-lowering treatments are used. The findings could lead to earlier glaucoma detection by identifying blood flow disruptions before irreversible damage occurs.
Key Facts:
- Vascular Damage: Elevated eye pressure can deform optic nerve vessels and reduce oxygen delivery.
- Early Detection Potential: Blood flow changes may predict glaucoma before symptoms appear.
- Treatment Gap: Many patients still lose vision despite reduced eye pressure, signaling need for better therapies.
Source: University of Mississippi
One of the world’s leading causes of irreversible vision loss could begin with elevated eye pressure, according to a recent study published by the American Academy of Ophthalmology.
Yi Hua, a biomedical engineering professor at the University of Mississippi, partnered with researchers at the University of Pittsburgh to study how ocular hypertension – elevated eye pressure – affects the eye.
“We wanted to see how intraocular pressure changes and deforms the blood vessels in the eye,” Hua said. “If we can understand that, we can inform drug delivery to improve blood flow in the back of the eye. That can slow down the progression of glaucoma.”
Glaucoma damages the optic nerve, leading to irreversible vision loss. It is a leading cause of blindness worldwide. Glaucoma is sometimes called the “silent thief of sight,” with symptoms often not becoming apparent until the damage is extensive.
“This can lead us to a new way to diagnose glaucoma earlier,” said Yuankai Lu, a postdoctoral researcher at the University of Pittsburgh and co-author of the study. “If this finding holds true, then we can use blood flow supply to predict the development of this disease.”
Pressure inside the eye can increases when aqueous humor – a clear fluid produced by the eye – does not properly drain. The buildup of fluid increases pressure on the lamina cribrosa, a mesh-like structure in the optic nerve head, which can constrict blood vessels, reducing oxygen flow to nerve cells and other parts of the eye.
Without oxygen, these cells can die, leading to loss of sight.
“We want to understand this problem so we can develop new drug pathways for patients,” Hua said. “We still do not have an efficient way to slow down the progression of glaucoma. The only way is to reduce eye pressure.
“But for some patients, even though we’ve reduced the eye pressure, the damage progresses, and they still lose vision. So, we need better methods.”
The researchers used a combination of 3D modeling and fluorescent dye to trace the path of blood flow through the eye under various amounts of pressure. They found even mildly elevated eye pressure can distort blood vessels and lead to hypoxia, an oxygen deficit. Extreme eye pressure led to hypoxia in approximately 30% of the lamina cribrosa tissue.
“The eye can weather a short-lived increase in eye pressure,” said Ian Sigal, associate professor of ophthalmology and bioengineering at the University of Pittsburgh.
“For instance, when we rub our eyes lightly. But a chronic increase of weeks, months or years can cause substantial damage.
“The vision loss resulting from this damage cannot be recovered. Hence, it is crucial to find ways to detect the disease and prevent the damage before it happens.”
Previous research has correlated elevated eye pressure with glaucoma, but did not explain how those issues were related, Lu said.
“Most glaucoma research is based on statistics, which can give you a correlation,” he said. “But it was actually very difficult to discover the mechanics of it.
“By combining imaging techniques with 3D modeling, we gained a more comprehensive understanding of blood flow and oxygen distribution in the eye.”
Treatment options are available for elevated eye pressure, but they are most effective for patients who undergo regular eye examinations and are diagnosed early, especially if they are at risk of developing glaucoma, Hua said.
Risk factors include medical conditions like high blood pressure or diabetes, a family history of the disease and race, as studies show that Black and Latino individuals are more likely to be affected.
“We really want to raise awareness of this issue,” Hua said. “A lot of people know the risk of high blood pressure, but we want to also raise the importance of elevated eye pressure.”
Funding: This material is based on work supported by the National Institutes of Health grant nos. R01-EY023966, R01-EY031708, R01-HD083383, P30-EY008098 and T32-EY017271.
About this glaucoma and visual neuroscience research news
Author: Clara Turnage
Source: University of Mississippi
Contact: Clara Turnage – University of Mississippi
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Association of Dipeptidyl Peptidase-4 Inhibitors with Glaucoma Risk in Patients with Type 2 Diabetes: A Nationwide Cohort Study” by Yi Hua et al. Ophthalmology Science
Abstract
Association of Dipeptidyl Peptidase-4 Inhibitors with Glaucoma Risk in Patients with Type 2 Diabetes: A Nationwide Cohort Study
Purpose
To investigate the association between Dipeptidyl Peptidase-4 Inhibitors (DPP4i) and the risk of primary open-angle glaucoma (POAG) and normal-tension glaucoma (NTG) in patients with type 2 diabetes mellitus (T2DM).
Design
Retrospective cohort study.
Subjects
A total of 582,710 T2DM patients treated with either DPP4i (exposure group) or non-DPP4i medications (control group) were analyzed between 2008 and 2021.
Methods
Patients were one-to-one matched by propensity scores on demographic and clinical characteristics. Cox proportional hazards models were applied to estimate hazard ratios for POAG and NTG, adjusting for age, sex, comorbidities, and concurrent antidiabetic medications.
Main Outcome Measures
Incidences of POAG and NTG.
Results
DPP4i users demonstrated a significantly lower risk of POAG (adjusted HR [aHR], 0.53; 95% CI, 0.50-0.56) and NTG (aHR, 0.55; 95% CI, 0.50-0.62) compared to non-DPP4i users on first-generation diabetes medication.
Subgroup analysis revealed a consistent risk reduction across all age groups (18–39: aHR, 0.56; 95% CI, 0.51-0.62; 40–64: aHR, 0.52; 95% CI, 0.47-0.57; ≥65 years: aHR, 0.51; 95% CI, 0.47-0.56) and among patients with or without diabetic-related complications, including diabetic retinopathy (DR), diabetic kidney disease (DKD), and diabetic neuropathy (DN) (aHR: without vs. with DR (0.54 vs. 0.43), without vs. with DKD (0.53 vs. 0.49), without vs. with DN (0.54 vs.0.43)), with all comparisons showing statistical significance (p < 0.001).
Cumulative incidence analyses revealed a sustained lower risk for DPP4i users throughout the study period (log-rank p < 0.001).
Conclusions
Exposure to DPP4i was associated with a reduced risk of developing POAG and NTG compared to users of first-generation diabetes medication. Further research is needed to explore the underlying mechanisms and their implications for glaucoma prevention and management.
