Abstract
Summary Sjogren's syndrome is a chronic immunomodulatory, connective tissue disorder. The major target organs are lacrimal glands and salivary glands where prominent lymphocytic infiltration occurs, which may induce varying levels of autoantibody production. Multiple factors, including environmental stress, viral infection, oncogenes and genes regulating lymphocyte apoptosis and neuroendocrine factors are thought to be involved in the pathogenesis of Sjogren's syndrome. Production of anti-SS-A/Ro and anti-SS-B/La antibodies is thought to be regulated by the presentation of autoantigens in context with an aberrant expression pattern of human leukocyte antigen (HLA) in situ. Autoantibody to Glutamic Acid Decarboxylase (GAD) are also found in some diabetic patients who initially present as type 2 diabetes but becomes insulin dependent later on. It is likely that diabetes associated GAD antibodies recognize a confirmation- dependent middle GAD 65 region. A case of Sjogren's syndrome associated with autoimmune diabetes mellitus in a 45 year old housewife is being discussed.
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