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

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...

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Bibliographic Details
Published in:Experimental dermatology 2017-10, Vol.26 (10), p.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: Article
Language:English
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
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Summary: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.
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.13343