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Probing the Role of Sodium Channels in Painful Neuropathies

Probing the Role of Sodium Channels in Painful Neuropathies: Observational Study

Status
UNKNOWN
Phases
Unknown
Study type
Observational
Source
ClinicalTrials.gov
Registry ID
NCT02243475
Enrollment
1500
Registered
2014-09-18
Start date
2014-09-30
Completion date
Unknown
Last updated
2014-09-18

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Painful Peripheral Neuropathy, Painless Peripheral Neuropathy

Brief summary

Neuropathic pain is a frequent feature of peripheral neuropathy causing a significant impact on patients' quality of life and health care costs. Not all individuals with neuropathy develop pain and it is not possible to predict who is more or less susceptible among those with similar risk exposure. Current inability to identify high-risk individuals hinders development and application of therapies to counteract neuropathic pain and to address targeted prevention strategies. Recently, the investigators Consortium has identified novel pathogenic mutations in genes encoding for two sodium channels (Nav1.7 and Nav1.8) known to play a critical role in the generation and conduction of action potentials in nociceptors and their terminal axons. This study was undertaken in a carefully selected group of patients with painful neuropathy using a candidate gene approach and directly revealed targets for new therapeutic strategies. This discover widened the spectrum of sodium channel-related pain disorders including conditions more common in the general population than those known so far. PROPANE STUDY, starting from the hypothesis of a common origin of neuropathic pain in a cohort of patients with predominantly small fibre neuropathy, aims to develop this original idea in a larger and well characterized study population, to provide evidence for the reliable stratification of patients at high risk and potential new treatments tailored on patients' clinical features, in order to improve their quality of life.

Interventions

None listed

Sponsors

Maastricht University
CollaboratorOTHER
Yale University
CollaboratorOTHER
University of Manchester
CollaboratorOTHER
Deutsche Diabetes Gesellschaft
CollaboratorOTHER
Centre National de la Recherche Scientifique, France
CollaboratorOTHER
Ospedale San Raffaele
CollaboratorOTHER
Fondazione I.R.C.C.S. Istituto Neurologico Carlo Besta
Lead SponsorOTHER

Study design

Observational model
COHORT
Time perspective
PROSPECTIVE

Eligibility

Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No

Inclusion criteria

* diagnosis of sensory neuropathy, including pure small fibre neuropathy (SFN), based on established clinical, nerve conduction study (NCS) and skin biopsy findings (Tesfaye et al. Diab Care 2010) caused by 1. type 1 or type 2 diabetes (World Health Organization criteria) with stable metabolic control for \>6 months (haemoglobin A1C \<9%); or 2. idiopathic aetiology after ruling out all known causes of neuropathy including vitamin deficiencies, malignancies, toxic, drugs

Exclusion criteria

* any other cause of neuropathy

Design outcomes

Primary

MeasureTime frame
Number of patients with novel mutations in the genes encoding for Nav1.7, Nav1.8, Nav1.9, Nav1.6, and Nav1.3 sodium channels2 years

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 20, 2026