Abstract
A 39-year-old male, who had a history of Osserman type II myasthenia gravis and underwent thymectomy 5 years ago, was admitted to the hospital because of bulbar symptoms. On admission, laboratory data showed remarkable high titer of anti-Ach-R antibody (108 nM/l) and high percentage of CD8 cells and low percentage of CD4 cells in peripheral blood. Further study by two color analysis using various anti-lymphocyte antibodies revealed that the high percentage of CD8 cells was dependent on the increment of CD8(+)CD11(-) cells (cytotoxic T cells) and the low percentage of CD4 cells was dependent of CD4(+)2H4(+) cells (suppressor/inducer T cells). Anti-lymphocyte antibodies in serum detected by the microcytotoxicity test were found and their activities were mainly to CD4 cells rather than to CD8 cells. These antibodies were considered to be associated with the alteration of T cell subsets in this patient. Therefore, the immunoadsorption trial with IM-T was done and the excellent improvement was observed in the clinical symptoms and in the abnormal laboratory data including anti-Ach-R antibody and Tcell subsets. Afterwards, he was in good condition for one year. However, he was attacked again by myasthenic crisis and was maintained on mechanical ventilation. Thus, the second immunoadsorption therapy was instituted and resulted in good response. Accordingly, we presumed that reduced number of peripheral CD4(+)2H4(+) cells in this case might be associated with the destruction of CD4 cells by the anti-lymphocyte antibody in serum, but the pathogenic relevanse of increased number of parpheral CD 8 cells was not clarified. Concerning about the immunoadsorption therapy, it could induce the clinical improvement, but post-immunosuppressive treatment was needed for the prevention of immunological rebound phenomenon.
