Abstract

Late onset myasthenia gravis (MG) is defined as the onset of the disease after the age of 50 in a patient with no clinical or paraclinical evidence of a thymoma. Myasthenia gravis has a bimodal appearance for both sexes with a peak age of onset located in the early onset group and another peak for late onset of MG. Early onset of MG in men is approximately 10 years later than in females. In late onset MG, the thymus is smaller than in early onset and much of the lymphoid tissue has been substituted with fat. There is no morphological evidence that the thymus atrophy seen in late onset MG is any different from the thymus involution which is age‐related. The AChR antibody concentration is lower in cases with late onset MG than it is in early onset and in thymoma‐associated MG. Sera from late onset MG patients can be divided in 2 groups; those with and those without striated muscle (MGT 30) antibodies. Their presence is not an effect of age since they are not detected among old healthy individuals. Nor is it an effect of long MG duration, since there is no relation between titre and duration. Non‐thymoma MG patients who demonstrate an immune response to titin identical to that observed in thymoma, have a worse prognosis and seem to do less well after thymectomy than late onset MG patients without muscle antiboides.

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