Acute glaucoma is largely an inflammatory disease, say researchers

Acute glaucoma is largely an inflammatory disease, say researchers -

Researchers at the University of California, San Diego School of Medicine and the Sun Yat University sen in China have shown that acute glaucoma in mice is largely an inflammatory disease, and the high pressure in the eye causes vision loss by setting in motion an inflammatory response similar to that caused by bacterial infections.

The study, published in this week's issue of Proceedings of the National Academy of Sciences has immediate clinical relevance in treating tens of millions of people around the world of what is known as acute angle-closure glaucoma.

"Our research is the first to show by which high eye pressure inflammatory mechanism causes vision loss in patients with acute glaucoma," said co-senior author Kang Zhang, MD, Ph. D. and Professor of ophthalmology.

The second leading cause of irreversible blindness worldwide, glaucoma refers to a group of eye diseases associated with elevated intraocular pressure generally classified as open-angle or acute angle. In open angle is sometimes called the silent thief of sight because of his slow, progress often overlooked. In contrast, acute angle-closure glaucoma is often a painful ophthalmic emergency in which there is a sudden increase in eye pressure and immediate damage to the eye.

Less than 10 percent of America glaucoma patients have an acute angle form, but in some parts of Asia, it represents almost half of all cases. The higher prevalence of angle closure glaucoma among Asians and women is believed to be due to ocular chamber (front) shallower anterior.

In the study, the researchers showed that rapid, sustained strong increase in eye pressure the mouse turns on a gene (TLR4) which activates a protein known as the caspase-8. This protein signaling in turn triggers the production of inflammatory proteins which normally assist mammals to combat microbial infections.

"This immune response is a double edged sword because while these proteins protect us from infection in a normal situation, they stimulate apoptosis (programmed cell death) in retinal cells in cases of acute glaucoma, "said Zhang, who is also a physician health system staff of former San Diego fighters.

To further confirm the mechanism linking high eye pressure in retinal damage, the researchers showed they could slow the cell death of the retina in mice with acute glaucoma by removing either the TLR4 gene or caspace-8 proteins.

latter is particularly important because caspace-8 inhibitors are currently in clinical trials for the treatment of cancer and stroke. "By injecting these inhibitors in the eyes of patients with acute glaucoma, it is possible to evaluate and bring the vision saving treatment more quickly," said co-author Robert N. Weinreb, MD, chairman and professor emeritus ophthalmology.