Dry eye syndrome (DES) is a” disorder of the tear film attributable to tear deficiency or excessive evaporation that causes damage to the interpalpebral ocular surface and is associated with symptoms of discomfort”. This disease is associated with a broad spectrum of ocular symptoms ranging from mild transient to persistent irritation such as burning, itching, redness, pain, ocular fatigue, and visual disturbances.

About 14% to 33% of the worldwide population suffers from dry eye.

Dry eye conditions have been classified into 2 main categories by the National Eye Institute- aqueous tear deficiency (ATD) and evaporative dry eye. Tear deficient dry eye can be further separated into Sjogren syndrome (SS) dry eye, an autoimmune disorder affecting the lacrimal and salivary glands, and non-SS dry eye that encompasses the range of other causes of tear deficiency. Evaporative dry eye is caused by deficiency and/or alterations in lipid secretions by the meibomian glands resulting in increased evaporation of aqueous tears from the ocular surface. The leading cause is meibomian gland dysfunction (MGD).

 Recent studies have shown that dry eye is an inflammatory disease that has many features in common with autoimmune disease. Stress to the ocular surface (environmental factors, infection, endogenous stress, antigens, genetic factors) is postulated as the pathogenetic triggering mechanism. Pro-inflammatory cytokines, chemokines, and matrix metalloproteinases lead to the expansion of autoreactive T helper cells which infiltrate the ocular surface and lacrimal gland . The result is a vicious circle of damage to the ocular surface and inflammation.

 Around 10% of patients with dry eye have a solely aqueous-deficient disorder. Hyper evaporative disorders, mostly caused by dysfunction of the meibomian glands, and mixed hyper evaporative/aqueous-deficient forms account for more than 80% of cases. Based on this new insight, novel diagnostic procedures and therapeutic approaches have evolved.

Goals for treatment of patients with dry eye syndrome are to improve the patient’s ocular comfort and quality of life and to return the ocular surface and tear film to the normal homeostatic state. Current therapies for the management of dry eye include drugs for tear supplementation, retention, and stimulation; anti-inflammatory; environmental therapies like tear substitutes are currently the most common choice of treatment but have failed to yield high success rates because they give only symptomatic improvement but do not treat underlying cause of disease. The major anti-inflammatory agents currently in use include topical corticosteroids and immunomodulatory agents.

Chloroquine is a well-known anti-inflammatory drug used in the treatment of rheumatoid arthritis , discoid lupus erythematosus ), malaria and amoebic hepatitis . Dry eye patients were found with higher levels of proinflammatory cytokines such as IL1-alpha , along with IL1- beta, IL-6, IL-8 and TNF-alpha in the tear film. Studies suggest that chloroquine is known to block TNF-alpha and IL-6 synthesis in lipopolysaccharide stimulated inflammation in mouse macrophages; additionally it is also a known modulator of autophagy. It is suggested that topical therapy with chloroquine can not only alleviate the symptoms of dry eye but also target the inflammatory processes contributing to disease pathogenesis . It has recently been added in to dry eye armamentarium.

Cyclosporine A is a calcineurin inhibitor that exerts immunomodulatory effects by blocking T cell infiltration, activation, and the subsequent release of inflammatory Cytokines , IL-2 and IL-4. The subsequent reduction in IL-2 levels further reduces the function of effector T cells. Moreover, cyclosporine A protects human conjunctival epithelial cells via its anti-apoptotic action, as well as improves conjunctival goblet cell density and corneal surface integrity via its immunomodulatory activities . In a case series of patients with recurrent corneal erosions and refractory persistent epithelial defects, treatment with cyclosporine A 0.05% improved tear film stability, reduced recurrent corneal erosions, and completely healed areas of previous epithelial loss.

In this study, we aim to assess the clinical profile and quality of life in patients after  with topical chloroquine versus topical cyclosporine.