Treatment for dry eye syndrome

Abstract

A novel formulation for the treatment of the many underlying inflammatory processes that cause dry eye syndrome. In particular, the formulation, which is orally administered includes the optimal blend of omega-3 and omega-6 essential fatty acids, and nutrient cofactors necessary to enhance the metabolic conversion associated with the tear-specific series E-one anti-inflammatory prostaglandin (PGE1). As used herein, the term “nutrient cofactor” refers to a compound that supports and enhances the conversion of linoleic acid to gamma-linolenic acid. Additionally, the formulation inhibits the production of pro-inflammatory compounds, as well as the growth of viral and bacterial pathogens of the three-layer tear film.

Description

FIELD OF THE INVENTION [0001] The present invention relates generally to the treatment of eye disorders, and, in particular, to an orally administered treatment for dry eye syndrome. BACKGROUND OF THE INVENTION [0002] Sufficient lubricating tears are critical to good eye health. Because tears provide the same functions for the cornea of the eye that the blood provides for the body, any abnormalities in tear production can results in eye disorders. One such disorder is dry eye syndrome. Dry eye syndrome, commonly referred to as “dry eyes,” is a prevalent eye condition affecting approximately 20 million Americans. Specifically, dry eye syndrome is a disorder resulting generally from any abnormality in the tear production process, such as decreased tear production, excessive tear evaporation, or an abnormality in mucin or lipid component of the tear film that covers the normal ocular surface. [0003] Although dry eye syndrome may have many different etiologies, the common denominator in...

AI Technical Summary

Benefits of technology

[0024] A unique feature of the present invention is the use of vitamin E in proper combination with the other components of the formulation. Vitamin E is an important regulator of prostaglandin E2 (PGE2), which plays a key role in inflammation and diseases associated with inflammation. Specifically, vitamin E inhibits cyclooxygenase-2 (COX-2) enzyme activity that promotes inflammatory response by catalyzing the synthesis of PGE2. Further, vitamin E enhances the T-cell function needed to inhibit the production of the pro-inflammatory Interleukin-1, which is responsible for inhibiting lacrimal aqueous secretion. Finally, vitamin stabilizes and prevents the oxidation of the omega-3 and omega-6 EFAs that are needed to generate anti-inflammatory PGE1.

[0036] Another feature of the present invention is the use of an immune system modulator to reduce the production of Interleukin 1 (IL-1), a metabolite of the pro-inflammatory PGE2, thereby lessening the need for potentially dangerous corticosteroids, which are now commonly used to reduce the IL-1 inflammatory process in the dry eye patient.

Problems solved by technology

Because tears provide the same functions for the cornea of the eye that the blood provides for the body, any abnormalities in tear production can results in eye disorders.

Mucin deficiency, or mucopolysaccharide abnormalities, can lead to poor wetting or glycation of the corneal surface with subsequent desiccation and epithelial damage, even in the presence of adequate aqueous tear production.

A decrease in circulating androgen hormones can result in loss of the oil layer, which exacerbates the evaporative tear loss.

Because EFAs cannot be synthesized by the human body, they must be obtained from the diet.

A disruption in this overall process is also believed to be an underlying cause of dry eye syndrome.

In extreme cases of dry eye, patients may become unusually sensitive to light, experience severe eye pain, and start to notice diminished vision.

The normal aging of tear glands, for example, can result in dryness, because tear volume decreases from age 18 as much as 60% by age 65.

Computer use can also cause dry eye, as most people blink less frequently (about 7 times per minute vs. a normal rate of around 22 times / minute) that leads to increased evaporation along with fatigue and eye-strain associated with staring at a computer monitor.

Inflammation of the ocular surface may also disturb the nerve endings, which in turn would disrupt the neural feedback mechanism and adversely affect tear production and cellular renewal.

The resultant absence of tear film will expose the epithelial surface to drying, mechanical damage, and the release of agonal chemicals from within the cells.

This result initiates an inflammatory process.

Even minimal levels of dry eye will result in a low-level ocular surface inflammatory component.

If left untreated, smoldering inflammation can cause damage over time and increase susceptibility to bacterial conjunctivitis and viral conjunctivitis.

As a result, epithelial cells die at a greater rate and release chemicals, which cause damage and inflammation.

Extended use of contact lens can result in dry eye from corneal oxygen and nutrient deficiency.

Protein build-up on contact lens can produce a breeding ground for bacterial growth and surface roughness, further contributing to inflammatory changes.

Also, medications such as antibiotics, blood pressure medications, antidepressants, diuretics, over-the-counter vasoconstrictors, antihistamines, birth control pills, appetite suppressants, and ulcer medications, refractive surgery, autoimmune diseases and disorders such as those mentioned above, hormonal changes, and nutritional deficiencies can cause disruption in the tear production and retention process.

Although artificial tears may provide temporary relief, they merely palliate the symptoms.

Furthermore, the preservatives used in the artificial tears can actually aggravate the condition, and can even kill corneal cells.

Artificial tears that promise to “get the red out” actually reduce circulation in the eye by vessel constriction, decreasing production of the tear film, and worse, eventually make the eyes drier.

Thus far, there have been few approaches to the treatment of dry eye disorders that have been effective in addressing all the issues regarding dry eye syndrome.

However, the HYDROEYE® treatment focused only on the production of the anti-inflammatory PGE1 and mucin.

For example, the formulation did not address the inhibition of pro-inflammatory compounds, such as PGE2 and Interleukin-1.

Further, the formulation did not address the inhibition of the growth of viral and bacterial pathogens in the three-layer tear film through the production of lactoferrin, which is a natural antibiotic.

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