parotid duct) and the amount of saliva that flows into the mouth.For Sjögrens syndrome, sudomotor function through electrochemical skin conductance may help in the diagnosis process.Sjögrens syndrome can be excluded from people with past head and neck radiation therapy, acquired immunodeficiency syndrome, pre-existing lymphoma, sarcoidosis, graft-versus-host disease, and use of anticholinergic drugs. Prevention
No prevention mechanism exists for Sjögrens syndrome (SS) because of its complexity as an autoimmune disorder, but lifestyle changes can reduce the risk factors related to developing SS or reduce the severity of the condition for patients who have already been diagnosed. Diet is strongly associated with the inflammation seen in many autoimmune related diseases, including SS. An experimental study concluded that SS patients often show high sensitivity to gluten that directly relates to inflammation. Moderate exercise is also helpful in SS patients, mainly reducing the effect of lung inflammation. Treatment
Neither a cure nor a specific treatment for Sjögrens syndrome is known to permanently restore gland secretion. Instead, treatment is generally symptomatic and supportive. Eye care
Moisture replacement therapies such as artificial tears may ease the symptoms of dry eyes. Some patients with more severe problems use goggles to increase local humidity or have punctal plugs inserted to help retain tears on the ocular surface for a longer time.Additionally, cyclosporine (Restasis) is available by prescription to treat chronic dry eye by suppressing the inflammation that disrupts tear secretion. Prescription drugs are also available that help to stimulate salivary flow, such as cevimeline (Evoxac) and pilocarpine.
Studies on the polymorphisms of human leukocyte antigen (HLA)-DR and HLA-DQ gene regions in Sjögrens patients show differential susceptibility to the syndrome as the result of different types of the resulting autoantibody production. Hormones
Since Sjögrens syndrome is associated with a high prevalence in women, sex hormones, especially estrogen, are believed to affect humoral and cell-mediated immune responses affecting susceptibility to the syndrome. Androgens are generally considered to prevent autoimmunity. Studies on mice models suggest estrogen deficiency stimulates presentation of autoantigens, inducing Sjögrens-like symptoms. Microchimerism
Microchimerism of fetal cells (offspring lymphoid cells in maternal circulation) may generate autoimmunity in women who have previously been pregnant. Generation of an autoimmune potential via microchimerism may lead to a switch from a silent form of autoimmunity with age-dependent decrease in self-tolerance. Environment
Viral proteins, engulfed molecules, or degraded self-structures may initiate autoimmunity by molecular mimicry and increase the chances of Sjögrens syndrome development. Epstein–Barr virus, hepatitis C, and human T-cell leukemia virus-1 are among the most studied infectious agents in Sjögrens syndrome. To date, no direct causes and effect relationship has been identified between these pathogens and the development of Sjögrens syndrome. Damaged self-structures targeted for apoptosis may be mistakenly exposed to the immune system, triggering autoimmunity in exocrine glands, which are often prone to autoimmune responses. Pathogenesis
The pathogenetic mechanisms of Sjögrens syndrome have not been fully elucidated, resulting in the lack of pathophysiology knowledge of the management of this autoimmune exocrinopathy.