Ignite Creation Date:
2024-05-06 @ 12:40 PM
Last Modification Date:
2024-10-26 @ 1:02 PM
Study NCT ID:
NCT03815578
Status:
COMPLETED
Last Update Posted:
2023-05-06
First Post:
2019-01-11
Brief Title:
Evaluation of Pain Sensitization in Rheumatoid Arthritis Analysis on a Cohort of Tofacitinib Treated Patients
Sponsor:
University Hospital Bordeaux
Organization:
University Hospital Bordeaux
Study Overview
Official Title:
Evaluation of Pain Sensitization in Rheumatoid Arthritis Analysis on a Cohort of Tofacitinib Treated Patients
Status:
COMPLETED
Status Verified Date:
2023-05
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
TOPRA
Brief Summary:
Persistent pain and chronic fatigue are very common complaints in rheumatoid arthritis RA patients whatever the anti-inflammatory treatment response Interestingly pain remaining despite good clinical response was associated with high disability and low inflammation at baseline suggesting a mechanism of pain independent of inflammation in these patients Such patients with discordantly high patient-reported DAS28 components fatigue and mood disturbance might represent a subgroup of RA patients who have specific clinical needs not resolved by classical conventional or biologic DMARDs In this way neuropathic pain and pain sensitization have been demonstrated in 20 to 30 of RA patients neuropathic pain scores being associated with worsen disease activity scores Thus pain sensitization may contribute to amplification of pain in active RA and should be responsible for persisting pain and fatigue even after inflammation has resolved
Pain sensitization is associated with neuroplastic changes in sensory pathways at peripheral and central levels Interestingly major mediators responsible for this neuroplasticity operate via a JAKSTAT signaling pathway which is specifically targeted by new RA treatments New drug targeting JAKSTAT signalling pathway have been recently designed for RA treatment based on the implication of this pathway on the signaling of various cytokines implicated in the pathophysiology of RA such as IL-6 IL-12 IL-23 and IFNs Two Jak-inhibitors have been put on the market Tofacitinib and Baricitinib In randomized clinical trials Tofacitinib have shown a remarkable efficacy on pain and other patient reported outcomes suggesting a specific effect or jak-inhibitors on pain control Recent data suggest that Jak-inhibitors could have a direct effect on sensory neurons
Pain sensitization is associated with neuroplastic changes in sensory pathways at peripheral and central levels Interestingly major mediators responsible for this neuroplasticity operate via a JAKSTAT signaling pathway which is specifically targeted by new RA treatments New drug targeting JAKSTAT signalling pathway have been recently designed for RA treatment based on the implication of this pathway on the signaling of various cytokines implicated in the pathophysiology of RA such as IL-6 IL-12 IL-23 and IFNs Two Jak-inhibitors have been put on the market Tofacitinib and Baricitinib In randomized clinical trials Tofacitinib have shown a remarkable efficacy on pain and other patient reported outcomes suggesting a specific effect or jak-inhibitors on pain control Recent data suggest that Jak-inhibitors could have a direct effect on sensory neurons
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None