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I. Bonaventura, MD; J. PONSETI, MD; E. Arnau, MD; J. Matias-Guiu, MD; A. Codina Puiggros, MD
Barcelona, Spain

Arch Intern Med. 1987;147(2):207-211.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—We have read with interest the article by Arsura et al¹ concerning 12 cases that were treated with high-dose intravenous immunoglobulin therapy for exacerbations of generalized myasthenia gravis. As all of their patients had elevated acetylcholine-receptor antibody (AChR) titers, the authors theorized that a possible mechanism of this therapy is the interference of the interaction of the acetylcholine receptor with AChR antibody. Nevertheless, we have recently described² a 14-year-old patient with myasthenia gravis without AChR antibody who was successfully treated with high-dose intravenous immunoglobulin therapy. A diagnosis of congenital myasthenic syndrome had been excluded. Our patient was classified as grade III according to the criteria of Osserman. She experienced a severe exacerbation of the disease. High-dose prednisone and anticholinesterase therapies failed to improve her condition within 45 days. Intravenous 7S immunoglobulin was administered with a loading dose of 400 mg/kg daily over five consecutive days. . . . [Full Text PDF of this Article]

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