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© 1990 American Academy of Neurology Suramin-induced polyneuropathyMedicine Branch, Clinical Oncology Program, National Cancer Institute (Drs. La Rocca, Stein, and Myers, and Ms. Cassidy), and the National Institute of Neurological Disorders and Stroke (Drs. Meer, Gilliatt, and Dalakas), National Institutes of Health, Bethesda, MD. We report the development of a severe polyneuropathy in 4 of 38 patients who were receiving parenteral suramin therapy for the treatment of various underlying malignancies. In 2 of these patients, the neuropathy progressed to generalized flaccid paralysis with bulbar and respiratory involvement, requiring endotracheal intubation and ICU monitoring. EMG and nerve conduction studies showed evidence of conduction block, suggestive of a demyelinating polyneuropathy. After several weeks, both patients improved clinically. The other 2 patients developed a reversible neuropathy with flaccid paresis of the limbs but without bulbar or respiratory compromise. No immediate response to plasmapheresis was noted. All 4 patients demonstrated an elevated CSF protein in the acute phase of their neuropathy, which declined or returned to normal during recovery. The development of polyneuropathy correlated with the maximum plasma suramin level, with an estimated 40% risk of developing neurotoxicity in those patients whose maximum level was 350 µg/ml or greater. No correlation could be made with the total dose of suramin administered or with the duration of therapy. Two of these 4 patients manifested tumor shrinkage while receiving suramin therapy. We conclude that suramin, a promising antineoplastic agent, is capable of inducing a severe sensorimotor polyneuropathy which appears to be related to the plasma concentration of suramin. Serial measurement of the plasma concentration during suramin therapy is recommended. Address correspondence and reprint requests to Dr. Renato V. La Rocca, Medicine Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 12N-226, Bethesda, MD 20892. Presented in part at the 41st annual meeting of the American Academy of Neurology, Chicago, IL, April 1989. Received August 29, 1989. Accepted for publication in final form November 22, 1989.
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