Peripheral multifocal chorioretinitis with panuveitis: clinical and immunogenetic characterization in older patients.
Kata kunci
Abstrak
BACKGROUND
The etiology of peripheral multifocal chorioretinitis with panuveitis (MCP) is unclear. Characteristic signs of MCP are punched-out, white chorioretinal lesions of the lower fundus periphery, chronic smoldering chorioretinal inflammation, vitritis, and mild inflammation of the anterior chamber. In this retrospective study we investigated clinical and immunogenetic abnormalities in MCP in older patients.
METHODS
20 patients (18 women, 2 men), median age 70.5 years, were investigated clinically by ophthalmologists and were typed for HLA class I antigens using the standard microlymphocytotoxicity test. Typing for HLA-DR antigens was performed by polymerase chain reaction with sequence-specific primers (PCR-SSP). The HLA controls consisted of healthy people (108 for HLA class I, 114 for HLA class II).
RESULTS
MCP was bilateral in 18 patients. Disease-related symptoms were present for 8 months (median) before diagnosis. The main presenting symptoms or findings were glaucoma (in 11 patients), visual loss (7), iritis (5), and vitritis (2). Anterior segment changes were frequently seen: keratitic precipitates (32 eyes), anterior chamber cells (25 eyes), aqueous flare (26 eyes), posterior synechiae (22 eyes), secondary glaucoma (15 eyes), and iris neovascularization (8 eyes). All patients had vitritis and typical chorioretinal fundus lesions. Fourteen patients developed cystoid macular edema (bilateral in seven cases). Subretinal neovascularization occurred in three patients. Although systemic medication was given to 17 patients and surgical treatment was performed in 25 eyes, improvement in vision was found in only 6 eyes, but 18 eyes deteriorated markedly (median 5 lines) during follow-up (median 24.5 months). Immunogenetically significant reduced frequencies of HLA-B7 and HLA-DR1 were found; also HLD-DR15(2) was reduced. However, several alleles were increased in MCP, although not significantly: HLA-A31; HLA-B57, HLA-B62; HLA-Cw3, HLA-Cw6; HLA-DR4, HLA-DR7, and HLA-DR8.
CONCLUSIONS
MCP is clinically and immunogenetically open to speculation. The present diagnosis and treatment of MCP are insufficient. Further DNA typing methods should clarify, whether HLA-DQ antigens are associated with the disease.
