Cutaneous nerve fiber and peripheral Nav1.7 assessment in a large cohort of patients with postherpetic neuralgia.


Journal

Pain
ISSN: 1872-6623
Titre abrégé: Pain
Pays: United States
ID NLM: 7508686

Informations de publication

Date de publication:
01 11 2023
Historique:
received: 03 11 2022
accepted: 25 04 2023
medline: 23 10 2023
pubmed: 27 6 2023
entrez: 27 6 2023
Statut: ppublish

Résumé

The mechanisms of pain in postherpetic neuralgia (PHN) are still unclear, with some studies showing loss of cutaneous sensory nerve fibers that seemed to correlate with pain level. We report results of skin biopsies and correlations with baseline pain scores, mechanical hyperalgesia, and the Neuropathic Pain Symptom Inventory (NPSI) in 294 patients who participated in a clinical trial of TV-45070, a topical semiselective sodium 1.7 channel (Nav1.7) blocker. Intraepidermal nerve fibers and subepidermal Nav1.7 immunolabeled fibers were quantified in skin punch biopsies from the area of maximal PHN pain, as well as from the contralateral, homologous (mirror image) region. Across the entire study population, a 20% reduction in nerve fibers on the PHN-affected side compared with that in the contralateral side was noted; however, the reduction was much higher in older individuals, approaching 40% in those aged 70 years or older. There was a decrease in contralateral fiber counts as well, also noted in prior biopsy studies, the mechanism of which is not fully clear. Nav1.7-positive immunolabeling was present in approximately one-third of subepidermal nerve fibers and did not differ on the PHN-affected vs contralateral sides. Using cluster analysis, 2 groups could be identified, with the first cluster showing higher baseline pain, higher NPSI scores for squeezing and cold-induced pain, higher nerve fiber density, and higher Nav1.7 expression. While Nav1.7 varies from patient to patient, it does not seem to be a key pathophysiological driver of PHN pain. Individual differences in Nav1.7 expression, however, may determine the intensity and sensory aspects of pain.

Identifiants

pubmed: 37366590
doi: 10.1097/j.pain.0000000000002950
pii: 00006396-990000000-00340
pmc: PMC10578423
doi:

Banques de données

ClinicalTrials.gov
['NCT02365636']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2435-2446

Informations de copyright

Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain.

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Auteurs

Michael Fetell (M)

Teva Pharmaceuticals, West Chester, PA, United States.

Manon Sendel (M)

Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital of Schleswig-Holstein, Campus Kiel, Germany.

Thomas Li (T)

Teva Pharmaceuticals, West Chester, PA, United States.

Leslie Marinelli (L)

Teva Pharmaceuticals, West Chester, PA, United States.

Jan Vollert (J)

Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital of Schleswig-Holstein, Campus Kiel, Germany.
Pain Research, MSk Lab, Department of Surgery and Cancer, Imperial College, London, United Kingdom.
Department of Neurophysiology, Mannheim Center for Translational Neuroscience MCTN, Medical Faculty Mannheim, Ruprecht Karls University, Heidelberg, Germany.
Department of Anaesthesiology, Intensive Care and Pain Medicine, University Hospital Muenster, Muenster, Germany.

Elizaeth Ruggerio (E)

Integrated Tissue Dynamics LLC, Rensselaer, NY, United States.

George Houk (G)

Integrated Tissue Dynamics LLC, Rensselaer, NY, United States.

Marilyn Dockum (M)

Integrated Tissue Dynamics LLC, Rensselaer, NY, United States.

Phillip J Albrecht (PJ)

Integrated Tissue Dynamics LLC, Rensselaer, NY, United States.

Frank L Rice (FL)

Integrated Tissue Dynamics LLC, Rensselaer, NY, United States.

Ralf Baron (R)

Division of Neurological Pain Research and Therapy, Department of Neurology, University Hospital of Schleswig-Holstein, Campus Kiel, Germany.

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