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Dry eye; Tear hyper-osmolarity; Allergic eye disease

Introduction

Dry eye is a multifactorial condition affecting millions worldwide, with its prevalence steadily increasing due to factors such as aging, digital device usage, and environmental stressors. While tear deficiency and instability remain key contributors, mounting evidence supports the involvement of inflammation as a primary driver of dry eye pathogenesis. Inflammation markers have emerged as essential tools in understanding the disease's underlying mechanisms and devising personalized treatment strategies [1].

The definition of DED which includes etiology, pathophysiology, and symptoms was recently improved in the light of new findings about the role of tear hyperosmolarity and ocular surface inflammation in dry eye and its effect on visual function. According to current knowledge dry eye can be defined as a multifactorial disease of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability, with potential damage to the ocular surface. It is accompanied by increased osmolarity of the tear film and inflammation of the ocular surface [2].

The term “tear-deficient dry eye” implies that this condition is caused by the lacrimal acinar destruction or dysfunction with reduced lacrimal tear secretion and volume. This in turn causes tear hyperosmolarity, since water evaporates from a reduced aqueous tear pool. Tear film hyperosmolarity causes hyperosmolarity of the ocular surface epithelial cells which stimulates a cascade of inflammatory events. Aqueous-deficient dry eye has two major groupings: Sjogren’s syndrome and non-Sjogren’s syndrome dry eye [3]. Sjogren’s syndrome is an exocrinopathy in which the lacrimal and salivary glands as well as other organs are affected by autoimmune processes and can be divided into two subgroups: primary and secondary Sjogren’s syndrome.

Evaporative dry eye may be intrinsic as a result of meibomian lipid deficiency, poor lid congruity and lid dynamics, low blink rate, and the effects of drug use. Extrinsic evaporative dry eye embraces those etiologies that increase evaporation including vitamin A deficiency, the action of toxic topical agents such as preservatives, and topical anesthesia. Patient wearing contact lenses is more prone to have dry eye symptoms. Disease of the exposed ocular surface including allergic eye disease may lead to destabilization of the tear film and add a dry eye component to the ocular surface.

Inflammation and dry eye

The ocular surface is continuously exposed to environmental challenges, and when the protective tear film is compromised, it triggers an inflammatory response. Inflammation disrupts the balance of cytokines, chemokines, and immune cells, leading to chronic ocular surface damage. Prolonged inflammation can exacerbate dry eye symptoms and contribute to disease progression [4].

Role of inflammatory markers in dry eye diagnosis

Tear cytokine profiling: Analyzing the composition of proinflammatory and anti-inflammatory cytokines in tears can provide insights into the inflammatory status of the ocular surface. Elevated levels of interleukins, tumor necrosis factor-alpha (TNF-α), and matrix metalloproteinases (MMPs) are commonly associated with dry eye.

Ocular surface staining: The assessment of ocular surface staining with vital dyes, such as fluorescein and lissamine green, helps identify areas of epithelial damage caused by inflammation [5].

Inflammatory cell count: Measuring the number of inflammatory cells, particularly on the conjunctiva, can aid in determining the severity of inflammation in dry eye.

Correlation between inflammation and dry eye symptoms

Studies have revealed a strong correlation between inflammatory markers and dry eye symptom severity. Patients with higher levels of inflammation tend to experience more severe discomfort, foreign body sensation, and blurred vision.

Targeted anti-inflammatory approaches for dry eye management

Topical anti-inflammatory medications: Steroids and cyclosporine A are commonly prescribed to reduce inflammation and improve symptoms in severe cases of dry eye. Prolonged use of steroids, however, may lead to adverse effects [6].

Omega-3 fatty acids: Supplementation with omega-3 fatty acids has shown promise in reducing inflammation and alleviating dry eye symptoms.

Lifitegrast: Lifitegrast, a lymphocyte function-associated antigen-1 (LFA-1) antagonist, has been approved for the treatment of dry eye. It targets the inflammatory cascade and reduces symptoms by inhibiting T-cell activation [7].

Symptoms

It is often incorrectly assumed that symptoms of dry eye are the main feature of this disease, whereas unfortunately they do not always correspond with diagnostic test results except in severe cases. The symptoms that patients describe are the same ocular sensations felt in other ocular surface disorders, namely, reports of a gritty, sandy foreign body sensation and visual disturbances. Visual complaints are highly prevalent among dry eye patients usually described as blurry vision that clears temporarily upon blinking [8]. These transient changes, resulting from disrupted tear film in the central cornea, can be profound with marked drops in contrast sensitivity and visual acuity thereby affecting workplace productivity and vision-related quality of life.

Treatment The prime goal of treatment of the ocular surface disorders includes relief of symptoms, improvement of visual acuity and quality of life, restoration of ocular surface and tear film, and correction of underlying defects. Treatment options comprise of hygiene and life style changes, artificial or autologous serum tear use, and antiinflammatory drug therapy, as well as physical and surgical procedures to increase tear retention. Treatment should be adjusted to incorporate the patient’s response and must maintain a balance between efficacy, safety, and patient convenience [9]. The simplest and most effective way to relieve symptoms of dry eye is a lifestyle change. Patients should be advised to avoid long exposure to computers, TV, and reading which is associated with a reduced blink rate and thus increased evaporation. The use of artificial tears and short breaks during these activities are recommended. Humidification of air in the home and work place could also alleviate undesirable effects. Avoidance of hot, windy, lowhumidity, and high-altitude environments as well as smog and smoke is also advisable.

Eyelid hygiene, warm compresses, and topical antibiotics when needed are essential for chronic blepharitis and meibomian gland dysfunction treatment which can be associated with tear dysfunction. These measures reduce bacterial induced changes in the lipid component of the tear film, which in turn reduces evaporative tear loss. It has been shown that a higher dietary intake of omega3 fatty acids with lower dietary ratio of omega-6 to omega-3 fatty acids as well as use of supplements containing linoleic and gamma-linoleic acid decreases the risk associated with dry eye symptoms. Tear supplements provide only temporary relief of dry eye symptoms and usually contain preservatives which can irritate the eye and additionally exacerbate symptoms. Thus patients requiring tear supplements more than 4 times a day should be prescribed preservative-free products. Artificial tears cannot replace the cytokines and growth factors which are comprised in normal tears and produced by normal functioning lacrimal glands and thus do not have direct anti-inflammatory effect [10].

Future directions

The identification of specific biomarkers associated with dry eye inflammation holds great promise for personalized medicine. Advancements in molecular biology and proteomics may pave the way for novel and more targeted therapeutic interventions.

Conclusion

Inflammation plays a central role in the pathogenesis of dry eye syndrome, significantly impacting symptom severity and disease progression. Integrating inflammation markers into the diagnostic process allows for a more comprehensive understanding of the disease and enables ophthalmologists to tailor treatment plans accordingly. By addressing the inflammatory component, new avenues for effective and personalized dry eye management are being explored, offering hope for improved patient outcomes and a better quality of life for those affected by this common ocular condition.

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