There is no functional small‐fibre neuropathy in prurigo nodularis despite neuroanatomical alterations

• Published in: Experimental dermatology Vol. 26; no. 10; pp. 969 - 971
• Main Authors: Pereira, Manuel P., Pogatzki‐Zahn, Esther, Snels, Chantal, Vu, Thai‐Ha, Üçeyler, Nurcan, Loser, Karin, Sommer, Claudia, Evers, Andrea Walburga Maria, Laarhoven, Antoinette I. M., Agelopoulos, Konstantin, Ständer, Sonja
• Format: Journal Article
• Language: English
• Published: Denmark Wiley Subscription Services, Inc 01.10.2017
• Subjects: Adult; Anatomy; Case-Control Studies; chronic pruritus; Epidermis - innervation; Female; Gene Expression; Humans; Interleukins - genetics; interleukin‐31; Male; Middle Aged; Nerve Fibers - pathology; Nerve Fibers - physiology; Nerve growth factor; Nerve Growth Factor - genetics; Neuropathy; Peripheral Nerves - pathology; Peripheral Nerves - physiopathology; Prurigo - genetics; Prurigo - immunology; Prurigo - pathology; quantitative sensory testing; SEMA3A; Semaphorin-3A - genetics; Semaphorins; Skin diseases; Skin tests; small‐fibre neuropathy; interleukin-31; small-fibre neuropathy; chronic pruritus; SEMA3A; quantitative sensory testing
• ISSN: 0906-6705; 1600-0625; 1600-0625
• DOI: 10.1111/exd.13343

Prurigo nodularis (PN) is a pruritic condition with altered epidermal neuroanatomy as demonstrated previously. Here we elucidated neuroimmunological mechanisms by combining functional, morphological and gene expression experiments in twelve subjects with PN and eight healthy controls. Subjects with PN showed a reduced intra‐epidermal nerve fibre density (IENFD) in lesional skin. Quantitative sensory testing indicated maintenance of somatosensory function compared to controls. None of the tested molecular markers including the neuron‐distracting SEMA3A and neuron‐attracting NGF were altered in lesional vs non‐lesional skin in PN subjects. Accordingly, we speculate that scratching may contribute to reduced IENFD rather than an authentic endogenous neuropathy.