Pathogenesis and Management of Dry Eye Disease

Dry eye is a multifactorial illness that affects the preocular tear film such that there is insufficient production of tears. As a result, patients end up suffering from eye discomfort, visual disturbance, and even damage to the ocular surface. The disease has been commonly diagnosed by ophthalmologists such 5 to 35 percent of those diagnosed are adults (Wei & Asbell, 2014). Also, researchers have found out that the triggering factors for the disease include age, gender, autoimmune disorders, and some hormones among others. However, there have been some controversies on the pathogenic process and the exact treatment of the disease.

Based on the recent studies, dry eye is a chronic inflammatory disease which results after some intrinsic and extrinsic factors initiate a destructive effect on the preocular tear film. The resultant changes in tear composition combined with other systemic factors trigger an inflammatory cycle which then causes ocular surface epithelial disease and neural stimulation. This process is stimulated by inflammatory mediators which lead to the release of metalloprotease, dendritic cell maturation, and inflammatory cell recruitment (Bhavsar, Bhavsar, & Jain, 2011). A combination of the above processes with autoantigens leads to a mediated T-cell response which leads disruption of the tear film and the normal production of tears in interrupted.

Diagnosis of eye disease involves observation of possible symptoms such as dryness of the eyes, feeling a foreign body in eyes, pain and soreness, and increased blinking among other symptoms (Baudouin et al., 2018). Physical acuity measurements and imaging approaches are also used to diagnose the disease (Phadatare, Momin, Nighojkar, Askarkar, & Singh, 2015). After the diagnosis of the condition in patients, treatment can be initiated. Since it has been confirmed that the disease is caused by inflammation, anti-inflammatory therapies such as corticosteroids can be initiated. Other therapies include tear substitutes and applying tear conservation techniques like avoiding much light while using computers and taking breaks while reading.

 

Reference

Baudouin, C., Irkeç, M., Messmer, E. M., Benítez‐del‐Castillo, J. M., Bonini, S., Figueiredo, F. C., … & Van Setten, G. (2018). Clinical impact of inflammation in dry eye disease: proceedings of the ODYSSEY group meeting. Acta ophthalmologica, 96(2), 111-119.

Bhavsar, A. S., Bhavsar, S. G., & Jain, S. M. (2011). A review of recent advances in dry eye: Pathogenesis and management. Oman Journal of Ophthalmology, 4(2), 50.

Phadatare, S. P., Momin, M., Nighojkar, P., Askarkar, S., & Singh, K. K. (2015). A comprehensive review of dry eye disease: diagnosis, medical management, recent developments, and future challenges. Advances in Pharmaceutics, 2015.

Wei, Y., & Asbell, P. A. (2014). The core mechanism of dry eye disease (DED) is inflammation. Eye & contact lens, 40(4), 248.

 
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