Ignite Creation Date:
2024-10-26 @ 3:41 PM
Last Modification Date:
2024-10-26 @ 3:41 PM
Study NCT ID:
NCT06610422
Status:
NOT_YET_RECRUITING
Last Update Posted:
None
First Post:
2024-09-20
Brief Title:
Association Between Neuropathy and Some Autoantibodies in Systemic Lupus Erythematosus SLE Patients
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Association Between Neuropathy and Some Autoantibodies in Systemic Lupus Erythematosus SLE Patients With Lupus Nephritis in Assiut University Hospital
Status:
NOT_YET_RECRUITING
Status Verified Date:
2024-09
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
1 Frequency of peripheral neuropathy associated with lupus nephritis
2 Sensitivity and specificity of some biomarkers used in diagnosis and follow up of SLE with lupus nephritis and peripheral neuropathy
2 Sensitivity and specificity of some biomarkers used in diagnosis and follow up of SLE with lupus nephritis and peripheral neuropathy
Detailed Description:
Systemic lupus erythematosus SLE is a chronic inflammatoryautoimmune disease that is characterized by multisystemic involvement with diverse clinical presentation
Peripheral neuropathy is a well-documented clinical manifestation of systemic lupus erythematosus SLE with a prevalence rate ranging from 2 to 278 Several lines of evidence link the risk of neuropathy with the antiphospholipid antibody and rheumatoid factor as well as neuropsychiatric lupus with anti-Ro Some evidence links anti-ganglioside antibodies with neuropathy but other studies do not Peripheral neuropathy may be slowly progressive or acutely devastating Lupus nephritis LN a more definite and specific subgroup of lupus is a major cause of morbidity and mortality in SLE and can affect up to 60 of SLE patients Furthermore the presence of peripheral neuropathy in LN patients may be relevant for improving their lives Such complex situation poses a therapeutic challenge The clinical presentation of PN relies upon the diameter of the affected nerve the sort of demyelinating or axonal lesions and their acute or chronic occurrence Routine nerve conduction studies just mirror the activity of the fast conducting myelinated A nerve fibers which are physiologically irrelevant to pain Hence quantitative sensory testing can evaluate small nerve fiber function The pathogenesis of SLE-related neuropathy is obscure and the few pathological studies of the peripheral nerves in SLE have revealed axonal degeneration inflammatory changes and vasculitis
The major inflammatory mediators released from immune cells act on sensory neurons inducing peripheral sensitization and hyperalgesic phenomena In addition after damage this natural inflammatory response could encourage the pathogenetic activity of antineural autoantibodies in addition to ischemic vascular mechanism by vasa nervorum vascularitis or by microthrombi linked to antiphospholipid antibodies
The other legitimate mechanisms are immunologic cause by a direct aggression by antibodies entraining obliteration of the peripheral nerve component
Furthermore the PN has not been well prescribed in SLE in terms of onset severity clinical associations and electrophysiological characteristics Therefore we are going to characterize PN in SLE with respect to the patients clinical lupus properties serologic markers disease activity and electrophysiological data
Peripheral neuropathy is a well-documented clinical manifestation of systemic lupus erythematosus SLE with a prevalence rate ranging from 2 to 278 Several lines of evidence link the risk of neuropathy with the antiphospholipid antibody and rheumatoid factor as well as neuropsychiatric lupus with anti-Ro Some evidence links anti-ganglioside antibodies with neuropathy but other studies do not Peripheral neuropathy may be slowly progressive or acutely devastating Lupus nephritis LN a more definite and specific subgroup of lupus is a major cause of morbidity and mortality in SLE and can affect up to 60 of SLE patients Furthermore the presence of peripheral neuropathy in LN patients may be relevant for improving their lives Such complex situation poses a therapeutic challenge The clinical presentation of PN relies upon the diameter of the affected nerve the sort of demyelinating or axonal lesions and their acute or chronic occurrence Routine nerve conduction studies just mirror the activity of the fast conducting myelinated A nerve fibers which are physiologically irrelevant to pain Hence quantitative sensory testing can evaluate small nerve fiber function The pathogenesis of SLE-related neuropathy is obscure and the few pathological studies of the peripheral nerves in SLE have revealed axonal degeneration inflammatory changes and vasculitis
The major inflammatory mediators released from immune cells act on sensory neurons inducing peripheral sensitization and hyperalgesic phenomena In addition after damage this natural inflammatory response could encourage the pathogenetic activity of antineural autoantibodies in addition to ischemic vascular mechanism by vasa nervorum vascularitis or by microthrombi linked to antiphospholipid antibodies
The other legitimate mechanisms are immunologic cause by a direct aggression by antibodies entraining obliteration of the peripheral nerve component
Furthermore the PN has not been well prescribed in SLE in terms of onset severity clinical associations and electrophysiological characteristics Therefore we are going to characterize PN in SLE with respect to the patients clinical lupus properties serologic markers disease activity and electrophysiological data
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None