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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Niesters, M. Proto, P. L. Aarts, L. Sarton, E. Y. Drewes, A. M. Dahan, A. |
| Description | Country affiliation: Netherlands Author Affiliation: Niesters M ( Department of Anesthesiology, Leiden University Medical Center, P5-Q, PO Box 9600, 2300 RC Leiden, The Netherlands m.niesters@lumc.nl.); Proto PL ( Department of Anesthesiology, Leiden University Medical Center, P5-Q, PO Box 9600, 2300 RC Leiden, The Netherlands.); Aarts L ( Department of Anesthesiology, Leiden University Medical Center, P5-Q, PO Box 9600, 2300 RC Leiden, The Netherlands.); Sarton EY ( Department of Anesthesiology, Leiden University Medical Center, P5-Q, PO Box 9600, 2300 RC Leiden, The Netherlands.); Drewes AM ( Mech-Sense, Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark.); Dahan A ( Department of Anesthesiology, Leiden University Medical Center, P5-Q, PO Box 9600, 2300 RC Leiden, The Netherlands.) |
| Abstract | BACKGROUND: Tapentadol is an analgesic agent for treatment of acute and chronic pain that activates the µ-opioid receptor combined with inhibition of neuronal norepinephrine reuptake. Both mechanisms are implicated in activation of descending inhibitory pain pathways. In this study, we investigated the influence of tapentadol on conditioned pain modulation (CPM, an experimental measure of endogenous pain inhibition that gates incoming pain signals as a consequence of a preceding tonic painful stimulus) and offset analgesia (OA, a test in which a disproportionally large amount of analgesia becomes apparent upon a slight decrease in noxious heat stimulation). METHODS: Twenty-four patients with diabetic polyneuropathy (DPN) were randomized to receive daily treatment with tapentadol sustained-release (SR) [average daily dose 433 (31) mg] or placebo for 4 weeks. CPM and OA were measured before and on the last day of treatment. RESULTS: Before treatment, none of the patients had significant CPM or OA responses. At week 4 of treatment, CPM was significantly activated by tapentadol SR and coincided with significant analgesic responses. CPM increased from 9.1 (5.4)% (baseline) to 14.3 (7.2)% (placebo) and 24.2 (7.7)% (tapentadol SR, P<0.001 vs placebo); relief of DPN pain was also greater in patients treated with tapentadol than placebo (P=0.028). Neither placebo nor tapentadol SR treatment had an effect on the magnitude of the OA responses (P=0.78). CONCLUSIONS: Tapentadol's analgesic effect in chronic pain patients with DPN is dependent on activation of descending inhibitory pain pathways as observed by CPM responses. CLINICAL TRIAL REGISTRATION: The study was registered at trialregister.nl under number NTR2716. |
| File Format | HTM / HTML |
| ISSN | 00070912 |
| e-ISSN | 14716771 |
| Journal | British Journal of Anaesthesia |
| Issue Number | 1 |
| Volume Number | 113 |
| Language | English |
| Publisher | Oxford University Press |
| Publisher Date | 2014-07-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Discipline Anesthesiology Analgesics, Opioid Therapeutic Use Chronic Pain Drug Therapy Diabetic Neuropathies Phenols Administration & Dosage Pharmacology Physiopathology Delayed-action Preparations Double-blind Method Drug Administration Schedule Neural Pathways Drug Effects Nociception Physiology Pain Measurement Receptors, Opioid, Mu Agonists Randomized Controlled Trial Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Anesthesiology and Pain Medicine |
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