Dry Eye Drops

Maintaining Ocular Surface Health and Comfort

Dry eye diseases (DED) have exploded world-wide largely because of increased time spent at tasks requiring prolonged steady fixation with reduced blinking (sitting in front of computers, reading, driving). This has now reached a prevalence of 5% to 33% of the adult population worldwide1 with greater than 60% in those over age 60.2 The surface disease process results in patients experiencing eye irritation, stinging, dryness, ocular fatigue, and fluctuating vision3. All can lead to significant functional impairment in daily work as well as during social activities, resulting in diminished quality of life, and productivity… often with ensuing depression.4

DED is now recognized to be a complex condition characterized by inflammation of the ocular surface and glands that results in scarring with reductions in the quantity and quality of the tear components.5,6,7  This results in diminished protection of the ocular surfaces between blinks causing erosions of the corneal and conjunctival surfaces with associated inflammation on the back surface and within the lids8.

The cause of the inflammation is now recognized to be multifactorial. Hyperosmolarity, caused by a reduction in the lipid tear layer with increased tear evaporation and instability, has traditionally been thought to be a primary trigger of the acute inflammatory response, irrespective of the dry eye subtype,6,7 and has resulted in treatments primarily of frequently administered hypo-osmolar tear drops or anti-inflammatory medications (steroids, cyclosporine A, etc) but without understanding or measuring the underlying, causations of the inflammation.

More recently the focus of the inflammation has been redirected toward understanding the chronic blepharitis intimately associated with all cases of DED presenting initially as intense erythema of the mucosa behind the lids, which then spreads to the ocular surface behind the lids and onto the central conjunctiva and cornea. The inflammation occurs, not only of the mucosa on the back surface as well as lid margins, but also penetrates through to the underlying meibomian glands within the lids as well as the Goblet cells on the ocular surface and the lacrimal glands and ducts. This has been shown to be associated with abnormal colonization by pathogenic bacteria or even disproportionate colonization by normal strains8.9.

GSXPharma has been investigating a naturally occurring molecule, that cannot be metabolized by many bacterial strains and has been shown to significantly reduce the growth of multiple pathogens within the mucosa with normalization of the normal bacterial and fungal colonies. In addition, this molecule also disturbs the binding process of pathogens to epithelial surfaces and improves the glycosylation of O-glycans that results in thickening improvement of the mucosal protective surface that is altered in a number of DED syndromes.10,11  Solutions utilizing this natural occurring ingredient have been developed by GSXPharma for the ocular surface to re-establish the mucin layer protection, reduce the inflammation, especially behind the lids and improve the tear meibum spreading over the ocular surface. GSX Pharma holds a pending patent on the topical use of the molecule for surface ocular diseases including multiple types of DED, inflammation caused by CTL wearing and blepharitis.

References

  1. DEWS. The epidemiology of dry eye disease: report of the Epidemiology Subcommittee of the International Dry Eye WorkShop (2007). Ocul Surf. 2007;5(2):93–107.
  2. Stapleton, F., Alves, M., Bunya, V., & et al. (2017). TFOS DEWS II epidemiology report. Ocul Surf, 15, 334-365. doi:10.1016/j.jtos.2017.05.003
  3. Johnson ME. The association between symptoms of discomfort and signs in dry eye. Ocul Surf. 2009;7(4):199–211.
  4. Miljanovic B, Dana R, Sullivan DA, Schaumberg DA. Impact of dry eye syndrome on vision-related quality of life. Am J Ophthalmol. 2007; 143(3):409–415.
  5. Baudouin C, Messmer EM, Aragona P. Revisiting the vicious circle of dry eye disease: a focus on the pathophysiology of meibomian gland dysfunction. Br J Ophthalmol 2016; 100: 300–306. doi: 10.1136/bjophthalmol-2015-307415
  6. Bron AJ, de Paiva CS, Chauhan SK et al. TFOS DEWS II pathophysiology report. Ocul Surf 2017; 15: 438–510. doi:10.1016/j.jtos.2017.05.011
  7. Ganesalingam, K., Ismail, S., Sherwin, T., & Craig, J. (2019). Molecular evidence for the role of inflammation in dry eye disease. Clin Exp Optom, 102, 446-454.doi:10.1111/cxo.12849
  8. Dougherty, J., & McCulley, J. (1986). Analysis of the free fatty acid component of meibomian secretions in chronic blepharitis. Invest Ophthalmol Vis Sci, 27, 52-56.
  9. Graham JE, Moore JE, Jiru X, et al. Ocular pathogen or commensal: A PCR-based study of surface bacterial flora in normal and dry eyes. Invest Ophthalmol Vis Sci 2007;48:12:5616.
  10. Gipson, I., & Argueso, P. (2003). Role of mucins in the function of the corneal and conjunctival epithelia. Internatinal rev Cytology, 231, 1-49.
  11. Gipson, I. (2007). The Ocular surface: The challenge to enable and protect vision. The Friedenwald lecture. Invest Ophthalmol Vis Sci, 48, 4391-4398.