This Article  • References  • Full text PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Contact me when this article is cited  Related Content  • Similar articles in this journal

William C. Koller, MD, PhD; Louisa K. Gehlmann, MD; Frederick D. Malkinson, MD; Floyd A. Davis, MD

Arch Neurol. 1977;34(10):644-646.

Abstract
• Peripheral neuropathy is a rare complication of dapsone therapy. This neuropathy appears primarily to be of the motor type, and recovery occurs on discontinuation of the drug therapy. The patient in this report developed a marked motor deficit as well as a selective marked loss of vibration sense shortly after the initiation of a relatively low dose of dapsone. Recovery was rapid on cessation of the therapy. This patient was found to be a slow acetylator of isoniazid, and therefore is probably a slow acetylator of dapsone. The possible mechanisms of the neurotoxicity of dapsone and the role of altered metabolism are discussed.

Author Affiliations
From the Departments of Neurology (Drs Koller and Davis) and Dermatology (Drs Gehlmann and Malkinson), Rush-Presbyterian-St Luke's Medical Center, Chicago.

Footnotes
Accepted for publication May 20, 1977.

Reprint requests to Department of Neurology, Rush-Presbyterian-St Luke's Medical Center, 1753 W Congress Pkwy, Chicago, IL 60612 (Dr Koller).