|- candidate number||2952|
|- NTR Number||NTR1193|
|- ISRCTN||ISRCTN wordt niet meer aangevraagd|
|- Date ISRCTN created|
|- date ISRCTN requested|
|- Date Registered NTR||17-dec-2007|
|- Secondary IDs||15023 (METC) |
|- Public Title||Psychophysiological stress mechanisms in chronic inflammatory diseases.|
|- Scientific Title||Psychophysiological stress mechanisms in chronic inflammatory diseases.|
|- ACRONYM||psychophysiology, stress, chronic inflammatory disease,|
|- hypothesis||Particularly in patients at risk, the stress-management intervention affect self-reported, immune and neuroendocrine indicators of stress reactivity.|
|- Healt Condition(s) or Problem(s) studied||Rheumatoid arthritis|
|- Inclusion criteria||Patients diagnosed with rheumatoid arthritis.
|- Exclusion criteria||1. Severe physical comorbid conditions (e.g. psoriatic arthritis, malignancy, renal insufficiency); |
2. Psychiatric disturbances that interfere with the study protocol;
4. Non-Dutch speakers.
|- mec approval received||yes|
|- multicenter trial||no|
|- Type||2 or more arms, randomized|
|- planned startdate ||1-nov-2007|
|- planned closingdate||1-nov-2009|
|- Target number of participants||64|
|- Interventions||1. Stress management intervention + usual care (intervention group);|
2. Usual care (control group).
|- Primary outcome||Psychological distress.|
|- Secondary outcome||Cortisol and IL-6.|
|- Timepoints||3 measurement points for the intervention group:|
1. T1: at study entry (i.e. 1 week prior to treatment);
2. T2: 1 month follow-up (i.e. 1 week post treatment);
3. T3: 3 months follow-up.
3 measurement points for the control group:
1. T1: at study entry;
2. T2: 1 month follow-up;
3. T3: 3 months follow-up.
|- Trial web site||N/A|
|- status||inclusion stopped: follow-up|
|- CONTACT FOR PUBLIC QUERIES||Prof. Dr. A.W.M. Evers|
|- CONTACT for SCIENTIFIC QUERIES||Prof. Dr. A.W.M. Evers|
|- Sponsor/Initiator ||University Medical Center St. Radboud|
(Source(s) of Monetary or Material Support)
|- Brief summary||There is increasing evidence for the idea that psychological stress factors can influence chronic inflammatory diseases, such as RA. These relationships are assumed to be (at least partly) mediated by immune and neuroendocrine function. In addition, our and other previous work suggests that stress mechanisms affecting disease activity and immunological parameters are primarily evident in patients with a psychological risk profile for stress. |
The effects of a short-term stress-management intervention are investigated in 64 RA patients. It is expected that, particularly in patients at risk, the stress-management intervention affect self-reported, immune and neuroendocrine indicators of stress-reactivity, which in turn affect disease activity and physical symptoms of pain. The study might contribute to improved diagnosis and treatment of RA and other chronic inflammatory diseases.
|- Main changes (audit trail)|
|- RECORD||17-dec-2007 - 16-mei-2010|