oxybutynin
Sources réglementaires consultées
Indications approuvées
- Traitement symptomatique de l’incontinence par impériosité, de la pollakiurie et de l’urgence mictionnelle chez l’adulte présentant une vessie instable.
Contre-indications
Absolues
- Rétention urinaire, trouble gastro-intestinal sévère, myasthénie, glaucome à angle fermé ou risque de ces affections ; hypersensibilité.
Mises en garde cliniques
- Mise en garde majeure · Surveiller les effets anticholinergiques centraux, notamment confusion, hallucinations, troubles de la mémoire ou somnolence chez les personnes âgées ; envisager l’arrêt s’ils apparaissent. — CIMA/AEMPS, ficha técnica 03270001
- Mise en garde majeure · Utiliser avec prudence en cas d’insuffisance rénale ou hépatique, d’obstruction vésicale, de diminution de la motilité gastro-intestinale et d’exposition à une chaleur intense. — CIMA/AEMPS, ficha técnica 03270001
Interactions médicamenteuses
- ModéréeAutres anticholinergiques ou médicaments à activité anticholinergique
Mécanisme: Ils peuvent augmenter la sécheresse, la constipation, la somnolence et les effets cognitifs.
Recommandation: Éviter une charge anticholinergique inutile et surveiller étroitement.
CIMA/AEMPS, ficha técnica 03270001https://cima.aemps.es/cima/dochtml/ft/03270001/FT_03270001.html
- ModéréeInhibiteurs du CYP3A4
Mécanisme: Ils peuvent augmenter l’exposition à l’oxybutynine.
Recommandation: Surveiller la tolérance anticholinergique et ajuster le traitement.
CIMA/AEMPS, ficha técnica 03270001https://cima.aemps.es/cima/dochtml/ft/03270001/FT_03270001.html
Effets indésirables
Communs (≥1%)
Réaction ou prurit au site d’application · Sécheresse buccale · Constipation ou diarrhée · Céphalées ou somnolence · Vertiges ou vision trouble
Rares mais graves
Rétention urinaire · Délire ou hallucinations · Angio-œdème
Grossesse et allaitement
Utiliser pendant la grossesse uniquement si cela est clairement nécessaire. L’utilisation n’est pas recommandée pendant l’allaitement.
Bibliographie récente (PubMed)
Multiple sclerosis (MS) is a chronic autoimmune disease with demyelination, inflammation, neuronal loss, and gliosis (scarring). Our object to review MS pathophysiology causes and treatment. A Narrative Review article was conducted by searching on Google scholar, PubMed, Research Gate about relevant keywords we exclude any unique cases and case reports. The destruction of myelinated axons in the central nervous system reserves this brunt. This destruction is generated by immunogenic T cells that produce cytokines, copying a proinflammatory T helper cells1-mediated response. Autoreactive cluster of differentiation 4 + cells, particularly the T helper cells1 subtype, are activated outside the system after viral infections. T-helper cells (cluster of differentiation 4+) are the leading initiators of MS myelin destruction. The treatment plan for individuals with MS includes managing acute episodes, using disease-modifying agents to decrease MS biological function of MS, and providing symptom relief. Management of spasticity requires physiotherapy, prescription of initial drugs such as baclofen or gabapentin, secondary drug options such as tizanidine or dantrolene, and third-line treatment such as benzodiazepines. To treat urinary incontinence some options include anticholinergic medications such as oxybutynin hydrochloride, tricyclic antidepressants (such as amitriptyline), and intermittent self-catheterization. When it comes to bowel problems, one can try to implement stool softeners and consume a high roughage diet. The review takes about MS causes Pathophysiology and examines current treatment strategies, emphasizing the advancements in disease-modifying therapies and symptomatic treatments. This comprehensive analysis enhances the understanding of MS and underscores the ongoing need for research to develop more effective treatments.
To update the evidence-based Nonhormonal Management of Menopause-Associated Vasomotor Symptoms: 2015 Position Statement of The North American Menopause Society. An advisory panel of clinicians and research experts in women's health were selected to review and evaluate the literature published since the Nonhormonal Management of Menopause-Associated Vasomotor Symptoms: 2015 Position Statement of The North American Menopause Society. Topics were divided into five sections for ease of review: lifestyle; mind-body techniques; prescription therapies; dietary supplements; and acupuncture, other treatments, and technologies. The panel assessed the most current and available literature to determine whether to recommend or not recommend use based on these levels of evidence: Level I, good and consistent scientific evidence; Level II, limited or inconsistent scientific evidence, and Level III, consensus and expert opinion. Evidence-based review of the literature resulted in several nonhormone options for the treatment of vasomotor symptoms. Recommended: Cognitive-behavioral therapy, clinical hypnosis, selective serotonin reuptake inhibitors/serotonin-norepinephrine reuptake inhibitors, gabapentin, fezolinetant (Level I); oxybutynin (Levels I-II); weight loss, stellate ganglion block (Levels II-III). Not recommended: Paced respiration (Level I); supplements/herbal remedies (Levels I-II); cooling techniques, avoiding triggers, exercise, yoga, mindfulness-based intervention, relaxation, suvorexant, soy foods and soy extracts, soy metabolite equol, cannabinoids, acupuncture, calibration of neural oscillations (Level II); chiropractic interventions, clonidine; (Levels I-III); dietary modification and pregabalin (Level III). Hormone therapy remains the most effective treatment for vasomotor symptoms and should be considered in menopausal women within 10 years of their final menstrual periods. For women who are not good candidates for hormone therapy because of contraindications (eg
Menopausal hormone therapy (HT) is highly effective against vasomotor symptoms (VMS). When HT is contraindicated, ineffective, or unacceptable, alternatives have included antidepressants, antiseizure, and antihypertensive formulations. Novel pharmacologic treatments for VMS have emerged in recent decades, some of which are already approved by the U.S. Food and Drug Administration (FDA) (eg, fezolinetant, a neurokinin 3B antagonist), and others are poised to seek FDA approval (eg, elinzanetant, a dual neurokinin 1B and 3B antagonist, and estetrol, a natural estradiol derivative that is unique to the pregnant state). Oxybutynin was shown to be effective for VMS and could provide additional benefits against overactive bladder, but long-term safety data are needed before wider utilization can be recommended.
Obstructive sleep apnea syndrome (OSAS) is characterized by intermittent hypoxia (IH) during sleep due to recurrent upper airway obstruction. The derived oxidative stress (OS) leads to complications that do not only concern the sleep-wake rhythm but also systemic dysfunctions. The aim of this narrative literature review is to investigate molecular alterations, diagnostic markers, and potential medical therapies for OSAS. We analyzed the literature and synthesized the evidence collected. IH increases oxygen free radicals (ROS) and reduces antioxidant capacities. OS and metabolic alterations lead OSAS patients to undergo endothelial dysfunction, osteoporosis, systemic inflammation, increased cardiovascular risk, pulmonary remodeling, and neurological alterations. We treated molecular alterations known to date as useful for understanding the pathogenetic mechanisms and for their potential application as diagnostic markers. The most promising pharmacological therapies are those based on N-acetylcysteine (NAC), Vitamin C, Leptin, Dronabinol, or Atomoxetine + Oxybutynin, but all require further experimentation. CPAP remains the approved therapy capable of reversing most of the known molecular alterations; future drugs may be useful in treating the remaining dysfunctions.