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From the Rudolph Magnus Institute of Neurosciences, Departments of Neurology (Drs. Notermans, Teunissen, Jennekens, Van den Berg, and Wokke), Hematology (Dr. Lokhorst), Clinical Neurophysiology (Dr. Franssen), and Epidemiology (Dr. Van der Graaf), University Hospital, Utrecht, the Netherlands.
Received November 27, 1995. Accepted in final form March 27, 1996.
Address correspondence and reprint requests to Dr Notermans, Department of Neuromuscular Disorders, University Hospital Utrecht C03.236, P.O. Box 85500, 3508 GA Utrecht, the Netherlands.
In an open prospective study, we analyzed the effect of cyclophosphamide (300 mg/m2 body surface daily for 4 days) combined with prednisone (40 mg/m2 body surface daily for 5 days) at 4-week intervals during 6 months in 16 patients with polyneuropathy associated with monoclonal gammopathy of undetermined significance (MGUS). Eleven patients had an IgM-MGUS and five an IgG-MGUS. During a follow-up period of 3 years, eight patients had improvement and six patients stabilized, based on quantitative neurologic examination, the Rankin disability scale, and electrophysiologic studies. These 14 patients had neuropathy with demyelinating and axonal features. One patient with a purely axonal neuropathy had deterioration despite therapy. One other patient developed severe leukopenia as side effect of cyclophosphamide, necessitating withdrawal of treatment. A difference in response was not present in patients with IgM- or IgG-MGUS, nor in patients with or without autoantibodies against myelin-associated glycoprotein. Nine patients had a bone marrow biopsy before and 1 year after treatment. In eight patients, the monoclonal lymphoid IgM or plasma cell IgG infiltration decreased, while in four the monoclonality disappeared after treatment. In the patient who had neurologic deterioration, repeated bone marrow biopsy showed deposits of amyloid. In conclusion, short-term treatment with intermittent cyclophosphamide and prednisone may have a long-term favorable effect in patients with demyelinating polyneuropathy associated with MGUS.
NEUROLOGY 1996;47: 1227-1233
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