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Clinical Management of Neuropathic Itch

To identify the key insights or developments described in this article
1 Credit CME

Neuropathic itch refers to disorders characterized by chronic itching caused by dysfunction or damage to pruriceptors, nerves involved in itch transmission. In these conditions, itch is not triggered by external stimuli (eg, irritants or allergens), but rather arises spontaneously. Neuropathic itch can occur through nerve damage from mechanical, metabolic, inflammatory, or cytopathic injury. It is often accompanied by neural hypersensitivity manifesting as alloknesis (itch) or dysesthesia (eg, burning, stinging) in response to innocuous mechanical stimuli. Although pruritus arising from nerve damage in the central nervous system can occur, most common itch conditions arise peripherally. Further, although many generalized itch conditions exhibit neuropathic qualities (eg, prurigo nodularis, diabetic itch), the extent to which neuropathy alone is the primary driver remains controversial. Thus, we will focus on the mechanisms underlying and therapeutic management of peripheral sensory itch conditions in this review.

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CME Disclosure Statement: Unless noted, all individuals in control of content reported no relevant financial relationships. If applicable, all relevant financial relationships have been mitigated.

Article Information

Corresponding Author: Brian S. Kim, MD, MTR, Icahn Medical Institute, 1425 Madison Ave, Room L12-75A, New York, NY 10029 (brian.kim3@mountsinai.org).

Published Online: September 20, 2023. doi:10.1001/jamadermatol.2023.3384

Conflict of Interest Disclosures: Dr Kim is founder of KliRNA Biotech; he has served as a consultant for 23andMe, ABRAX Japan, AbbVie, Almirall, Amagma Therapeutics, Amgen, Arcutis Biotherapeutics, Arena Pharmaceuticals, argenx, AstraZeneca, Boehringer Ingelheim, Bristol Myers Squibb, Cara Therapeutics, Clexio Biosciences, Eli Lilly and Company, Escient Pharmaceuticals, Evommune, Galderma, Genentech, GlaxoSmithKline, Granular Therapeutics, Incyte Corporation, Innovaderm Research, Janssen, Kiniksa, LEO Pharma, Maruho, Novartis, Pfizer, Recens Medical, Regeneron Pharmaceuticals, Sanofi, Septerna, Teva, Vial, WebMD; he has stock in ABRAX Japan, KliRNA Biotech, Locus Biosciences, and Recens Medical; he holds a patent for the use of JAK1 inhibitors for chronic pruritus; and he has a patent pending for the use of JAK inhibitors for interstitial cystitis. No other disclosures were reported.

Funding/Support: Research in the Kim Lab is funded by National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR070116, R01AR077007) and National Institute of Allergy and Infectious Diseases (R01AI167933, R21AI167047).

Role of the Funder/Sponsor: The funders had no role in the preparation, review, or approval of the manuscript and decision to submit the manuscript for publication.

AMA CME Accreditation Information

Credit Designation Statement: The American Medical Association designates this Journal-based CME activity activity for a maximum of 1.00  AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Successful completion of this CME activity, which includes participation in the evaluation component, enables the participant to earn up to:

  • 1.00 Medical Knowledge MOC points in the American Board of Internal Medicine's (ABIM) Maintenance of Certification (MOC) program;;
  • 1.00 Self-Assessment points in the American Board of Otolaryngology – Head and Neck Surgery’s (ABOHNS) Continuing Certification program;
  • 1.00 MOC points in the American Board of Pediatrics’ (ABP) Maintenance of Certification (MOC) program;
  • 1.00 Lifelong Learning points in the American Board of Pathology’s (ABPath) Continuing Certification program; and
  • 1.00 credit toward the CME of the American Board of Surgery’s Continuous Certification program

It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting MOC credit.

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