Dry eye is a multifactorial disease of the ocular surface characterized by loss of homeostasis of the tear film; and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles. The ocular surface environment is maintained by immune regulation which fights exogenous and endogenous pathogens while maintaining tolerance to self-antigens and commensals. In autoimmune diseases like SLE and RA, immune regulation gets disturbed by multiple triggers which may be environmental, microbial or genetic culminating in aberrant activation of the immune system. Dry eye disease (DED) in SLE and RA occurs due to immune dysregulation leading to self-reactive immune cells producing abnormally elevated levels of pro-inflammatory cytokines which impair secretory function, increase corneal permeability, apoptosis of surface epithelial cells, and in severe cases, loss of goblet cells or due to secondary Sjogren’s syndrome is caused by CD4+ T cell infiltration of lacrimal glands. In SLE and RA patients, the prevalence of DED is reported as 16 % and 25-65%, respectively, previously.  None of them reports on patients from India. Antibodies to Ro(SS-A) and La(SS-B) occur in a subset of patients constituting 50% and 20% in SLE, and 29% and 7% in RA, respectively. They are more prevalent in primary Sjogren’s syndrome(SS). Patients with SLE and RA having overlap syndrome with SS possess both antibodies. It may be useful to assess if SLE and RA patients with DED have a higher prevalence of these antibodies.

The following evaluation will be done for all patients. 1. Ocular symptom score, 2. Tear film breakup time (TBUT), 3. Ocular Surface Staining Score (NEI), 4. Schirmer’s test, 5. Serum SS-A and SS-B autoantibody levels.