RESULTS WITH ACTH AND SPIRONOLACTONE IN SEVERE CASES OF MYASTHENIA GRAVIS

Myasthenia gravis has since its description by Thomas Willis in 1672 been the subject of many endocrinological speculations. This applies above all to notions that the thymus may become hyperplastic and neoplastic in this disease and its removal is considered, by many authors, the best treatment in certain cases. The thyroid has also been thought to play a part in the origin of myasthenia. This is quite natural as pathologic anatomic findings may be similar in thyrotoxicosis and myasthenia gravis (lymphorrhagias, thymic hyperplasias etc.) (cf. Ringertx 1951). The muscular insufficiency also may be similar with inter alia improvements following neostigmine injections and, finally, both diseases have been found to occur in the same individual. Naturally i t has been attempted to relate the disease to the hypophysisadrenal cortex system. Clinicians working with the disease nil1 soon notice that exacerbations of the symptoms arise in connection with situations of stress of various kinds, e.g. infections, fatiguing periods such as breast feeding, etc. To this may be added the very distinct effect of ACTH and corticosteroids on lymphatic tissue. It was, thus, quite natural that when ACTH f i t for clinical use became available it was promptly tried in myasthenia gravis. Torda and Wolff were in 1951 able to describe the results from 15 cases of myasthenia gravis treated in this way. In their summary they reported: 1. The administration of 500 mg of ACTH to 15 patients with myasthenia gravis induced in 10 a significant partial remission of variable duration. The occurrence of a real remission could not be established in four patients mildly ill with myasthenia gravis. 2. During administration of ACTH severe symptoms may develop and one patient with bulbar manifestations died during the third day of ACTH administration. The severity of symptoms developed seemed to be reduced by the concurrent administration of potassium chloride. 3. Repeated courses of ACTH (500 mg per course) induced further remissions. 4. The beneficial effects of ACTH in myasthenia gravis cannot be fully duplicated by cortisone.