AIM: To investigate whether presumed ocular histoplasmosis syndrome in the Netherlands is caused by Histoplasma capsulatum and whether other risk factors might play a role in the pathogenesis of this syndrome. METHODS: 23 patients were clinically diagnosed as having presumed ocular histoplasmosis syndrome based on the following criteria: peripapillary atrophy, punched out lesions, a macular disciform lesion or scar in one eye without vitritis. As controls, 66 sex and age matched healthy volunteers were used. Serum samples from both patients and controls were tested for the presence of antibodies against H capsulatum, Toxoplasma gondii, Toxocara canis et cati, Ascaris sp, and for the presence of antigens of Cryptococcus neoformans. Serum samples were also tested for the presence of autoantibodies against retinal or choroidal proteins. To investigate other risk factors, patients and controls were asked to fill in a health and travel related questionnaire. Ten patients with ocular toxoplasmosis were used as a disease control group. RESULTS: None of the patients with presumed ocular histoplasmosis syndrome or controls had circulating antibodies directed against H capsulatum. No risk factors could be identified and no indications for autoimmunity and no evidence for the role of the other infectious agents could be demonstrated. CONCLUSIONS: In a Dutch group of patients fulfilling the criteria of a disease currently named presumed ocular histoplasmosis syndrome, no risk factors or relation with the fungus H capsulatum could be detected.
AIM: To investigate whether presumed ocular histoplasmosis syndrome in the Netherlands is caused by Histoplasma capsulatum and whether other risk factors might play a role in the pathogenesis of this syndrome. METHODS: 23 patients were clinically diagnosed as having presumed ocular histoplasmosis syndrome based on the following criteria: peripapillary atrophy, punched out lesions, a macular disciform lesion or scar in one eye without vitritis. As controls, 66 sex and age matched healthy volunteers were used. Serum samples from both patients and controls were tested for the presence of antibodies against H capsulatum, Toxoplasma gondii, Toxocara canis et cati, Ascaris sp, and for the presence of antigens of Cryptococcus neoformans. Serum samples were also tested for the presence of autoantibodies against retinal or choroidal proteins. To investigate other risk factors, patients and controls were asked to fill in a health and travel related questionnaire. Ten patients with ocular toxoplasmosis were used as a disease control group. RESULTS: None of the patients with presumed ocular histoplasmosis syndrome or controls had circulating antibodies directed against H capsulatum. No risk factors could be identified and no indications for autoimmunity and no evidence for the role of the other infectious agents could be demonstrated. CONCLUSIONS: In a Dutch group of patients fulfilling the criteria of a disease currently named presumed ocular histoplasmosis syndrome, no risk factors or relation with the fungus H capsulatum could be detected.