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S. Grover, G. Adamus, G.A. Fishman; Is There an Association of Anti–Retinal Antibodies and Cystoid Macular Edema in Patients With Retinitis Pigmentosa? . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5795.
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Cystoid macular edema (CME) has been well documented in patients with retinitis pigmentosa (RP). Although the exact pathogenesis for the development of cysts is not known, some studies have suggested an autoimmune basis. This is mainly based on the findings of one study that has described anti–retinal antibodies in 90% of patients with CME and RP including those against carbonic anhydrase II, enolase, arrestin, recoverin and interphotoreceptor retinoid binding protein. The aim of the present study was to attempt to further evaluate if there was an autoimmune basis for the development of CME in patients with RP.
Sixteen patients (mean age, 39 years; range 15 – 62 years) with CME and different genetic subtypes of RP participated in this prospective study. The diagnosis of RP was established based on detailed fundus examination. All patients showed evidence of CME by either fluorescein angiography or optical coherence tomography. After obtaining consent from all patients, blood was drawn and sera tested for anti–retinal antibodies.
We found anti–retinal antibodies in 6 out of 16 (38%) patients. All six patients showed retinal antibodies selectively to carbonic anhydrase II. None of the other antibodies that have been described earlier were detected in our group of patients. In a control group of 79 sera from healthy subjects with no visual loss, anti–retinal antibodies have been reported in 15 (19%) sera – 5 (6%) sera had antibodies to carbonic anhydrase II.
There was a notable difference in the percentage of patients with the anti–retinal antibodies and the antibody specificities that were found between the present study and an earlier study. Possible factors may include the genetic makeup of the population of patients, possible presence of other systemic factors in these patients, and methodologies employed to detect these antibodies. Our findings suggest that more studies are warranted to clarify the role of an autoimmune basis for development of CME in patients with RP.
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