diclofenac
Sources réglementaires consultées
Indications approuvées
- Traitement de la kératose actinique.
Contre-indications
Absolues
- Hypersensibilité au diclofénac ou aux excipients.
- Antécédent d’asthme, de rhinite allergique ou d’urticaire provoqué par l’aspirine ou d’autres AINS.
- Troisième trimestre de la grossesse.
Mises en garde cliniques
- Mise en garde majeure · Ne pas appliquer sur des plaies, infections ou dermatite exfoliative ; éviter les yeux, les muqueuses, l’ingestion, le soleil direct et les pansements occlusifs. Arrêter en cas d’éruption généralisée ou de sensibilité cutanée. — CIMA/AEMPS, ficha técnica 89632
- Mise en garde majeure · Bien que l’absorption systémique soit faible, utiliser avec prudence en cas d’hémorragie ou d’ulcère digestif, d’insuffisance cardiaque, hépatique ou rénale et de diathèse hémorragique, surtout sur de grandes surfaces ou pendant une longue durée. — CIMA/AEMPS, ficha técnica 89632
Effets indésirables
Communs (≥1%)
Dermatite, eczéma, sécheresse, érythème, œdème, prurit ou éruption · Inflammation, irritation, douleur, paresthésie ou vésicules au site d’application · Hyperesthésie, hypertonie ou paresthésie localisée · Conjonctivite
Rares mais graves
Hémorragie gastro-intestinale · Insuffisance rénale · Angio-œdème ou hypersensibilité systémique · Asthme
Grossesse et allaitement
Contre-indiqué au troisième trimestre. Aux premier et deuxième trimestres, utiliser seulement si absolument nécessaire, à la dose minimale, sur moins de 30 % de la surface corporelle et pendant 3 semaines au maximum. Pendant l’allaitement, utiliser uniquement sur avis professionnel ; ne pas appliquer sur les seins, de grandes surfaces ni pendant une période prolongée.
Bibliographie récente (PubMed)
Myofascial pain syndrome (MPS) is a chronic regional pain condition characterized by trigger points-hyperirritable spots within taut bands of muscle fibers that cause both localized and referred pain. The pathogenesis, diagnostic criteria, and classification of MPS are still under investigation, which complicates the development of standardized treatment protocols. Although diagnostic tools have improved, MPS often remains underrecognized due to symptom overlap with other pain disorders, such as fibromyalgia, neuropathic pain, and joint disorders. Factors contributing to its onset and persistence include muscle overuse, postural imbalance, systemic conditions, and psychological and behavioral influences. This narrative review explores the primary risk factors, current hypotheses on pathogenesis, diagnosis and differential diagnosis, and both conventional and emerging treatments. Sufficient evidence supports the use of local anesthetic injections for MPS. Some evidence suggests that dry needling, acupuncture, magnetic stimulation, ultrasound therapy, laser therapy, extracorporeal shock wave therapy, and manual therapy may be effective, particularly compared to sham or placebo. However, non-steroidal anti-inflammatory drugs, diclofenac, botulinum toxin, and transcutaneous electrical nerve stimulation show insufficient evidence, while the effectiveness of muscle relaxants, antidepressants, gabapentin, opioids, topical lidocaine, capsaicin, EMLA cream, and kinesio taping remains inconclusive. Effective management of MPS requires a patient-centered approach that integrates empirically supported and evidence-based treatments tailored to individual needs. This review synthesizes the current understanding of MPS and highlights the need for high-quality research to improve clinical decision-making in managing this complex condition.
To assess the effectiveness and safety of different preparations and doses of non-steroidal anti-inflammatory drugs (NSAIDs), opioids, and paracetamol for knee and hip osteoarthritis pain and physical function to enable effective and safe use of these drugs at their lowest possible dose. Systematic review and network meta-analysis of randomised trials. Cochrane Central Register of Controlled Trials (CENTRAL), Medline, Embase, regulatory agency websites, and ClinicalTrials.gov from inception to 28 June 2021. Randomised trials published in English with ≥100 patients per group that evaluated NSAIDs, opioids, or paracetamol (acetaminophen) to treat osteoarthritis. The prespecified primary outcome was pain. Physical function and safety outcomes were also assessed. Two reviewers independently extracted outcomes data and evaluated the risk of bias of included trials. Bayesian random effects models were used for network meta-analysis of all analyses. Effect estimates are comparisons between active treatments and oral placebo. 192 trials comprising 102 829 participants examined 90 different active preparations or doses (68 for NSAIDs, 19 for opioids, and three for paracetamol). Five oral preparations (diclofenac 150 mg/day, etoricoxib 60 and 90 mg/day, and rofecoxib 25 and 50 mg/day) had ≥99% probability of more pronounced treatment effects than the minimal clinically relevant reduction in pain. Topical diclofenac (70-81 and 140-160 mg/day) had ≥92.3% probability, and all opioids had ≤53% probability of more pronounced treatment effects than the minimal clinically relevant reduction in pain. 18.5%, 0%, and 83.3% of the oral NSAIDs, topical NSAIDs, and opioids, respectively, had an increased risk of dropouts due to adverse events. 29.8%, 0%, and 89.5% of oral NSAIDs, topical NSAIDs, and opioids, respectively, had an increased risk of any adverse event. Oxymorphone 80 mg/day had the highest risk of dropouts due to adverse events (51%) and any adverse event (88%). Etoricoxib 60
Pain is one of the most burdensome symptoms in people with cancer, and opioid analgesics are considered the mainstay of cancer pain management. For this review, the authors evaluated the efficacy and toxicities of opioid analgesics compared with placebo, other opioids, nonopioid analgesics, and nonpharmacologic treatments for background cancer pain (continuous and relatively constant pain present at rest), and breakthrough cancer pain (transient exacerbation of pain despite stable and adequately controlled background pain). They found a paucity of placebo-controlled trials for background cancer pain, although tapentadol or codeine may be more efficacious than placebo (moderate-certainty to low-certainty evidence). Nonsteroidal anti-inflammatory drugs including aspirin, piroxicam, diclofenac, ketorolac, and the antidepressant medicine imipramine, may be at least as efficacious as opioids for moderate-to-severe background cancer pain. For breakthrough cancer pain, oral transmucosal, buccal, sublingual, or intranasal fentanyl preparations were identified as more efficacious than placebo but were more commonly associated with toxicities, including constipation and nausea. Despite being recommended worldwide for the treatment of cancer pain, morphine was generally not superior to other opioids, nor did it have a more favorable toxicity profile. The interpretation of study results, however, was complicated by the heterogeneity in the study populations evaluated. Given the limited quality and quantity of research, there is a need to reappraise the clinical utility of opioids in people with cancer pain, particularly those who are not at the end of life, and to further explore the effects of opioids on immune system function and quality of life in these individuals.
Hand-foot syndrome (HFS) is a dose-limiting side effect of capecitabine. Celecoxib prevents HFS by inhibiting cyclooxygenase-2 (COX-2) that is upregulated because of the underlying associated inflammation. However, systemic side effects of celecoxib have limited routine prescription. Topical diclofenac inhibits COX-2 locally with minimal risk of systemic adverse events. Therefore, we conducted this study to assess the efficacy of topical diclofenac in the prevention of capecitabine-induced HFS. In this single-site phase III randomized double-blind trial, we enrolled patients with breast or GI cancer who were planned to receive capecitabine-based treatment. Participants were randomly assigned in a 1:1 ratio to receive topical diclofenac or placebo gel for 12 weeks or until the development of HFS, whichever occurred earlier. The primary end point was the incidence of grade 2 or 3 HFS (Common Terminology Criteria for Adverse Events version 5), which was compared between the two groups using simple logistic regression. In total, 264 patients were randomly assigned to receive topical diclofenac gel (n = 131) or placebo (n = 133). Grade 2 or 3 HFS was observed in 3.8% of participants in the diclofenac group compared with 15.0% in the placebo group (absolute difference, 11.2%; 95% CI, 4.3 to 18.1; P = .003). Grade 1-3 HFS was lower in the diclofenac group than in the placebo group (6.1% v 18.1%; absolute risk difference, 11.9%; 95% CI, 4.1 to 19.6). Capecitabine dose reductions because of HFS were less frequent in the diclofenac group (3.8%) than in the placebo group (13.5%; absolute risk difference, 9.7%; 95% CI, 3.0 to 16.4). Topical diclofenac prevented HFS in patients receiving capecitabine. This trial supports the use of topical diclofenac to prevent capecitabine-associated HFS.