sildenafil
Sources réglementaires consultées
Indications approuvées
- Traitement de la dysfonction érectile chez l’homme adulte ; une stimulation sexuelle est nécessaire.
Contre-indications
Absolues
- Utilisation de dérivés nitrés ou donneurs de monoxyde d’azote ; utilisation de stimulateurs de la guanylate cyclase tels que le riociguat ; hypersensibilité.
Mises en garde cliniques
- Mise en garde majeure · Ne pas utiliser si l’activité sexuelle est déconseillée en raison de l’état cardiovasculaire. Une érection durant plus de 4 heures nécessite une prise en charge urgente. — FDA/DailyMed, set_id 00ee09dd-2de0-4dc4-85f6-b51ed6eabd5b
- Mise en garde majeure · Arrêter et consulter immédiatement en cas de perte soudaine de la vision ou de diminution/perte soudaine de l’audition. — FDA/DailyMed, set_id 00ee09dd-2de0-4dc4-85f6-b51ed6eabd5b
Interactions médicamenteuses
- SévèreDérivés nitrés, donneurs de monoxyde d’azote ou riociguat
Mécanisme: La vasodilatation additive peut provoquer une hypotension sévère.
Recommandation: Association contre-indiquée.
FDA/DailyMed, set_id 00ee09dd-2de0-4dc4-85f6-b51ed6eabd5bhttps://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=00ee09dd-2de0-4dc4-85f6-b51ed6eabd5b
- ModéréeAlpha-bloquants ou antihypertenseurs
Mécanisme: Ils peuvent provoquer une hypotension symptomatique additive.
Recommandation: Stabiliser le traitement, commencer à faible dose et surveiller la pression artérielle et les symptômes.
FDA/DailyMed, set_id 00ee09dd-2de0-4dc4-85f6-b51ed6eabd5bhttps://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=00ee09dd-2de0-4dc4-85f6-b51ed6eabd5b
- SévèreRitonavir ou inhibiteurs puissants du CYP3A4
Mécanisme: Ils augmentent fortement l’exposition au sildénafil.
Recommandation: Avec le ritonavir, ne pas dépasser 25 mg en 48 heures ; avec d’autres inhibiteurs puissants, envisager de commencer à 25 mg.
FDA/DailyMed, set_id 00ee09dd-2de0-4dc4-85f6-b51ed6eabd5bhttps://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=00ee09dd-2de0-4dc4-85f6-b51ed6eabd5b
Effets indésirables
Communs (≥1%)
Céphalées · Bouffées vasomotrices · Dyspepsie · Troubles visuels · Congestion nasale · Vertiges
Rares mais graves
Priapisme · Neuropathie optique ischémique antérieure non artéritique · Perte auditive soudaine · Événement cardiovasculaire grave
Grossesse et allaitement
Non indiqué chez la femme.
Bibliographie récente (PubMed)
Pulmonary arterial hypertension (PAH) is a subtype of pulmonary hypertension (PH), characterized by pulmonary arterial remodeling. The prevalence of PAH is approximately 10.6 cases per 1 million adults in the US. Untreated, PAH progresses to right heart failure and death. Pulmonary hypertension is defined by a mean pulmonary artery pressure greater than 20 mm Hg and is classified into 5 clinical groups based on etiology, pathophysiology, and treatment. Pulmonary arterial hypertension is 1 of the 5 groups of PH and is hemodynamically defined by right heart catheterization demonstrating a mean pulmonary artery pressure greater than 20 mm Hg, a pulmonary artery wedge pressure of 15 mm Hg or lower, and a pulmonary vascular resistance of 3 Wood units or greater. Pulmonary arterial hypertension is further divided into subgroups based on underlying etiology, consisting of idiopathic PAH, heritable PAH, drug- and toxin-associated PAH, pulmonary veno-occlusive disease, PAH in long-term responders to calcium channel blockers, and persistent PH of the newborn, as well as PAH associated with other medical conditions including connective tissue disease, HIV, and congenital heart disease. Early presenting symptoms are nonspecific and typically consist of dyspnea on exertion and fatigue. Currently approved therapy for PAH consists of drugs that enhance the nitric oxide-cyclic guanosine monophosphate biological pathway (sildenafil, tadalafil, or riociguat), prostacyclin pathway agonists (epoprostenol or treprostinil), and endothelin pathway antagonists (bosentan and ambrisentan). With these PAH-specific therapies, 5-year survival has improved from 34% in 1991 to more than 60% in 2015. Current treatment consists of combination drug therapy that targets more than 1 biological pathway, such as the nitric oxide-cyclic guanosine monophosphate and endothelin pathways (eg, ambrisentan and tadalafil), and has shown demonstrable improvement in morbidity and mortality compared with the previ
The establishment and maintenance of pregnancy depend on endometrial competence. Asherman syndrome (AS) and intrauterine adhesions (IUA), or endometrial atrophy (EA) and thin endometrium (TE), can either originate autonomously or arise as a result from conditions (i.e. endometritis or congenital hypoplasia), or medical interventions (e.g. surgeries, hormonal therapies, uterine curettage or radiotherapy). Affected patients may present an altered or inadequate endometrial lining that hinders embryo implantation and increases the risk of poor pregnancy outcomes and miscarriage. In humans, AS/IUA and EA/TE are mainly treated with surgeries or pharmacotherapy, however the reported efficacy of these therapeutic approaches remains unclear. Thus, novel regenerative techniques utilizing stem cells, growth factors, or tissue engineering have emerged to improve reproductive outcomes. This review comprehensively summarizes the methodologies and outcomes of emerging biotechnologies (cellular, acellular, and bioengineering approaches) to treat human endometrial pathologies. Regenerative therapies derived from human tissues or blood which were studied in preclinical models (in vitro and in vivo) and clinical trials are discussed. A systematic search of full-text articles available in PubMed and Embase was conducted to identify original peer-reviewed studies published in English between January 2000 and September 2023. The search terms included: human, uterus, endometrium, Asherman syndrome, intrauterine adhesions, endometrial atrophy, thin endometrium, endometritis, congenital hypoplasia, curettage, radiotherapy, regenerative therapy, bioengineering, stem cells, vesicles, platelet-rich plasma, biomaterials, microfluidic, bioprinting, organoids, hydrogel, scaffold, sheet, miRNA, sildenafil, nitroglycerine, aspirin, growth hormone, progesterone, and estrogen. Preclinical and clinical studies on cellular, acellular, and bioengineering strategies to repair or regenerate the human endo
To update the existing European Alliance of Associations for Rheumatology (EULAR) points to consider (PtC) for use of antirheumatic drugs in reproduction, pregnancy, and lactation, including additional drugs and adverse outcomes as well as paternal drug safety. According to the EULAR standardised operating procedures, an international task force (TF) defined the questions for a systematic literature review, followed by formulation of the updated statements. A predefined voting process was applied to each overarching principle and statement. Level of evidence and strength of recommendation were assigned, and participants finally provided their level of agreement for each item. The TF proposes 5 overarching principles and 12 recommendations for the use of antirheumatic drugs before and during pregnancy, through lactation, and in male patients. The current evidence indicates that synthetic disease-modifying antirheumatic drugs (DMARDs) compatible with pregnancy include antimalarials, azathioprine, colchicine, cyclosporine, sulfasalazine, and tacrolimus. Regarding nonsteroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids, a more restrictive approach to their use during pregnancy is recommended. Based on an individualised risk-benefit assessment, all tumour necrosis factor inhibitor (TNFi) biologic DMARDs (bDMARDs) can be used throughout pregnancy, and non-TNFi bDMARDs may be used if needed. In relation to lactation, compatible drugs include antimalarials, azathioprine, colchicine, cyclosporine, glucocorticoids, intravenous immunoglobulin (IVIG), NSAIDs, sulfasalazine, and tacrolimus. All bDMARDs are considered compatible with breastfeeding. Concerning the use of drugs in men, compatible options include antimalarials, azathioprine, colchicine, cyclosporine, IVIG, leflunomide, methotrexate, mycophenolate, NSAIDs, glucocorticoids, sildenafil, sulfasalazine, tacrolimus, and bDMARDs. The updated recommendations provide consensus guidance and will help to improve the