Once SO is developed, immunosuppressive therapy is the mainstay of treatment. When initiated promptly following injury, it is effective in controlling the inflammation and improving the prognosis. Mild cases may be treated with local application of corticosteroids and pupillary dilators. More severe or progressive cases require high-dose systemic corticosteroids for months to years. Patients who become resistant to corticosteroids or develop side effects of long-term corticosteroid therapy (osteoporosis and pathologic fractures, mental status changes, etc. ), may be candidates for therapy with chlorambucil, cyclophosphamide, or ciclosporin. Epidemiology
Sympathetic ophthalmia is rare, affecting 0.2% to 0.5% of non-surgical eye wounds, and less than 0.01% of surgical penetrating eye wounds. There are no gender or racial differences in incidence of SO. History
Although descriptions of sympathetic ophthalmia can be found in ancient Greek texts, modern understanding of SO derives from the works of Scotlands William MacKenzie who characterized and named the disease sympathetic ophthalmitis. At MacKenzies time, oral mercury and leeches applied to the conjunctiva were the treatments of choice for SO.It is thought that Louis Braille, who injured one of his eyes as a child, lost vision in his other eye owing to SO. James Thurbers adult blindness was also diagnosed as sympathetic ophthalmia deriving from the loss of an eye when he was six years old. See also
Vogt–Koyanagi–Harada disease

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Through osmosis (water movement from a low solute concentration to an area of high solute concentration) water is reabsorbed back into the blood from nephron tubules in the kidney. This maintenance of water concentration in the blood is essential for maintaining blood pressure and is affected in nephritis. Diagnosis
The cardinal symptom in Epstein syndrome is thrombocytopaenia with giant platelets (macrothrombocytopenia). A peripheral blood smear is taken from the patient and a light microscope is used to these identify giant platelets. Leukocyte inclusions are also examined for, because approximately 41.1% of R207 mutations have leukocyte inclusions. These are often abnormal neutrophils with a small size of approximately less than 0.7 um and have an abnormallocation on the non-muscle myosin heavy chain IIA (NMMHC-II). These inclusion bodies have RNA and no DNA. RNA in these inclusion bodies can be located in immunofluorescence analysis with the anti nonmuscle heavy chain IIA antibody.Hematology analysers or a hemocytometer can be used to determine the amount of platelets. A sample of blood is drawn from a patients arm. A small amount of platelets in blood smears compared to the normal range of 150,000 to 450,000 platelets in microliter of blood suggest thrombocytopaenia, which is a common symptom in Epstein syndrome.A urine sample is often collected where a urinalysis can be used to determine the volume of proteins excreted in urine. Abnormal amounts of protein detected means the patient has proteinuria. Patients with Epstein syndrome often have large proteinuria where they excrete above 3.5g of protein in their urine in a day.