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NEUROLOGY 1995;45:1302-1304
© 1995 American Academy of Neurology

Inclusion body myositis

Explanation for poor response to immunosuppressive therapy

R. J. Barohn, MD, A. A. Amato, MD, Z. Sahenk, MD, J. T. Kissel, MD and J. R. Mendell, MD

From the Department of Neurology (Dr. Barohn), University of Texas Southwestern Medical Center, Dallas, Tx, the Department of Neurology (Dr. Amato), Wilford Hall USAF Medical Center, San Antonio, Tx; and the Department of Neurology (Drs. Sahenk, Kissel, and Mendell), Ohio State University School of Medicine, Columbus, OH.

Address correspondence and reprint requests to Dr. Richard J. Barohn, Department of Neurology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, Dallas, TX 75235-8897.

We treated eight patients who had inclusion body myositis (IBM) with oral prednisone therapy, and we performed muscle biopsies before and after treatment. We documented the patients' clinical response to therapy and changes in serum CK. Although the serum CK level fell, muscle strength worsened after prednisone treatment. In addition, while inflammation decreased in the muscle biopsy specimens, the number of vacuolated and amyloid-positive fibers increased after oral prednisone therapy. These observations indicate that the inflammatory response in IBM may play a secondary role in the pathogenesis of IBM. The unique findings of intracellular amyloid deposits and rimmed vacuoles distinguishing IBM from other inflammatory myopathies, and recognition that suppression of inflammation has no effect on the clinical course, suggest that IBM may represent a degenerative muscle disorder.

Fkceived October 13, 1994. Accepted in final form December 13,1994.




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