Determination of acetylcholine receptor antibody in myasthenia gravis: clinical usefulness and pathogenetic implications.

Anti-Acetylcholine Receptor Antibody in Myasthenia Gravis

“…Regarding our data, when the mean value of anti-AChR antibody concentrations was estimated as a percentage of preoperative values at every month since thymectomy in 19 MG patients without thymoma, anti-AChR antibody titer revealed a rapid decline within 1 month followed by fluctuation up to several postoperative months and stably gentle fall later correlated with the clinical state. These findings in Japanese MG are similar to the results by Lefvert et al [3], Scadding et al [16], and Vincent et al [20]. Not only the examination of a large number of patients but also the long-term followup measurement at regular intervals seems to be necessary for the evaluation of the effect of thymectomy on MG.…”

“…There have been conflicting reports of the effects of thymectomy on anti-AChR antibody levels in patients without thymoma [3,[16][17][18][19][20][21]. Regarding our data, when the mean value of anti-AChR antibody concentrations was estimated as a percentage of preoperative values at every month since thymectomy in 19 MG patients without thymoma, anti-AChR antibody titer revealed a rapid decline within 1 month followed by fluctuation up to several postoperative months and stably gentle fall later correlated with the clinical state.…”

“…AChR antibodies [1][2][3][4]. Moreover, anti-AChR antibodies have been reported to bring about not only a defect in neuromuscular transmission, but also a loss of available AChRs on the postsynaptic membrane [5][6][7].…”

“…Thymectomy increases the chance of clinical remission or improvement, particularly if performed in the early stage of the disease [11,12]. Although it has been suggested that the effects of thymectomy may be due to the suppression of cell-mediated and/or humoral immunity to auto-AChR through the alteration of T-cell subsets, the reports have not come to an agreement in regard to the actual effects on T-cell subsets [13][14][15] or concentration of anti-AChR antibody [3,[16][17][18][19][20][21].…”

CDS1 and promoter single nucleotide polymorphisms of the CTLA-4 gene in human myasthenia gravis

“…Antibodies against the acetylcholine receptor (AChR) were analysed by radioimmunoassay. 18 The level of IL-1␤ (a) is related to the genotypes at position 49 + in the CDS1 region of Ctla-4 (P Ͻ 0.05). There were no associations with IL-12 (b) and anti-AChR (c) levels.…”