Bartoccioni E, Evoli A, Casali C, Scoppetta C, Tonali P, Provenzano C
J Neuroimmunol. 1986 Aug;12(2):155-61. doi: 10.1016/0165-5728(86)90028-7.
We studied 7 mothers with myasthenia gravis (MG) and their infants. We confirmed that the development of neonatal MG was not related to the serum titer of maternal anti-acetylcholine receptor antibody (anti-AChR ab). To investigate the possibility that specific immunization of the newborn infant had occurred, serial serum determinations of total and 'specific' anti-AChR IgG and IgM were performed. We found that: the decay in total IgG was within the normal range in all the babies; there was a shorter half-life of 'specific' IgG, compared to total IgG, in 3 of the cases, 2 of which did have neonatal MG; no difference was found between the decay of anti-AChR ab in the babies who had neonatal MG and those who did not; there was no anti-AChR IgM-associated activity. Our data suggest that neonatal MG is due to maternal anti-AChR abs and that affected infants do not produce specific antibodies.
我们研究了7名重症肌无力（MG）母亲及其婴儿。我们证实新生儿MG的发生与母亲抗乙酰胆碱受体抗体（抗AChR抗体）的血清滴度无关。为了研究新生儿是否发生了特异性免疫，我们对总抗AChR IgG和IgM以及“特异性”抗AChR IgG和IgM进行了系列血清测定。我们发现：所有婴儿的总IgG衰减均在正常范围内；在3例病例中，“特异性”IgG的半衰期比总IgG短，其中2例确实患有新生儿MG；患有新生儿MG的婴儿和未患新生儿MG的婴儿之间，抗AChR抗体的衰减没有差异；不存在与抗AChR IgM相关的活性。我们的数据表明，新生儿MG是由母亲的抗AChR抗体引起的，受影响的婴儿不会产生特异性抗体。
