الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Dry eye disease (DED) is one of the most frequently encountered ocular morbidities and one of the most common conditions seen by eye care practitioners.
In 2007, the International Dry Eye Workshop (DEWS) revised the original definition and classification scheme of DED and developed a new definition, as well as a three-part classification of DED based on etiology, mechanism, and severity of the disease. The two major classes are aqueous tear-deficient dry eye and evaporative dry eye.
There is an increasing evidence that dry eye is an inflammatory disease. Disease or dysfunction of the tear secretory glands leads to changes in tear composition, such as hyperosmolarity that stimulate the production of inflammatory mediators on the ocular surface(6). Inflammation may in turn cause dysfunction or disappearance of cells responsible for tear secretion or retention. Inflammation can also be initiated by chronic irritative stress (e.g. contact lenses) and systemic inflammatory/autoimmune disease (e.g. rheumatoid arthritis). Regardless of the initiating cause, a vicious cycle of inflammation may develop on the ocular surface in dry eye that leads to ocular surface disease.
Due to a newer understanding of the pathogenesis of DED, use of antiinflammatory medications is a paradigm shift in the treatment of dry eye. It addresses the root cause of the dry eye instead of giving symptomatic relief as done by lubricants. Antiinflammatory therapy is considered to be the first “causative therapeutic approach” in the treatment of dry eye, since its objective is to interrupt the inflammatory cascade.
In December 2002, the US Food and Drug Administration approved CsA 0.05% ophthalmic emulsion for treatment of dry eye disease and it has been a record number of prescriptions in the USA and worldwide.
The mechanism of action of CsA is the inhibition of calcineurin, with subsequent restriction in the expression of certain genes involved in T-cell activation (IL-2, IL-4, IL-12p40).
Our study was designed to determine the efficacy of topical CsA 0.05% b.i.d. in treatment of moderate to severe dry eye.
This study included eighty eyes of forty patients with moderate to severe dry eye divided into two groups, I and II. Group I received topical CsA 0.05% for 3 months, and group II didn’t receive the study drug. The age range was 30.0 - 65.0 years for group I, and 32.0 – 63.0 years for group II.
The protocol was composed of a 2-week washout phase, a 12-week treatment phase, and a 12-week post treatment phase. Patients were evaluated at weeks 1, 4, 12 during the treatment phase. During these visits, patients were evaluated for changes from the base line in Schirmer test, TBUT, fluorecein staining of ocular surface, LIPCOF, subjective symptoms of ocular discomfort, OSDI scores, and visual acuity. After completion of the treatment phase, patients were also evaluated at post treatment week 12 for the assessment of the same outcome measures.