pentoxifylline
Sources réglementaires consultées
Indications approuvées
- Elorgan (Espagne) : artériopathie périphérique oblitérante ; troubles circulatoires d'origine artérioscléreuse, diabétique, inflammatoire ou fonctionnelle ; troubles trophiques, ulcères distaux des membres inférieurs et gangrène.
- États-Unis : claudication intermittente due à une artériopathie oblitérante chronique des membres. Elle peut améliorer la fonction et les symptômes, mais ne remplace pas un traitement définitif tel qu'un pontage ou la levée d'une obstruction artérielle.
Contre-indications
Absolues
- Hypersensibilité ou intolérance à la pentoxifylline, aux excipients ou à d'autres méthylxanthines telles que la caféine, la théophylline ou la théobromine.
- Elorgan : hémorragie massive ou hémorragie rétinienne étendue. États-Unis : hémorragie cérébrale ou rétinienne récente.
Mises en garde cliniques
- Mise en garde majeure · Arrêter immédiatement dès les premiers signes de réaction anaphylactique ou anaphylactoïde. — CIMA ficha técnica 54635; DailyMed setid cd840a2c-2a0e-4b2b-84ff-a0406bb6fa37
- Mise en garde majeure · Surveiller les saignements chez les patients ayant subi une chirurgie récente, présentant un ulcère gastroduodénal, un trouble de la coagulation ou recevant un anticoagulant ou un antiagrégant ; contrôler l'hémoglobine, l'hématocrite et l'activité anticoagulante selon le risque. — CIMA ficha técnica 54635; DailyMed setid cd840a2c-2a0e-4b2b-84ff-a0406bb6fa37
- Mise en garde majeure · Une surveillance étroite est requise en cas d'arythmie sévère, d'infarctus du myocarde, d'hypotension, d'insuffisance rénale sévère ou d'insuffisance hépatique sévère ; l'exposition à la pentoxifylline ou à ses métabolites augmente en cas d'atteinte rénale ou hépatique. — CIMA ficha técnica 54635; DailyMed setid cd840a2c-2a0e-4b2b-84ff-a0406bb6fa37
Interactions médicamenteuses
- SévèreAntagonistes de la vitamine K et autres anticoagulants
Mécanisme: Une augmentation de l'activité anticoagulante, un allongement du temps de prothrombine et des hémorragies ont été rapportés.
Recommandation: Surveiller plus fréquemment le temps de prothrombine, l'INR, l'activité anticoagulante et les signes de saignement lors de l'instauration ou d'un changement de dose.
CIMA ficha técnica 54635DailyMed setid cd840a2c-2a0e-4b2b-84ff-a0406bb6fa37
- SévèreAntiagrégants plaquettaires et AINS
Mécanisme: Les effets antihémostatiques additifs augmentent le risque hémorragique.
Recommandation: Utiliser avec prudence et renforcer la surveillance clinique des saignements.
CIMA ficha técnica 54635
- SévèreThéophylline ou aminophyllineR03DA04
Mécanisme: La pentoxifylline peut augmenter les concentrations de théophylline et sa toxicité.
Recommandation: Surveiller l'état clinique et les concentrations de théophylline ; adapter sa dose pendant et après l'association.
CIMA ficha técnica 54635DailyMed setid cd840a2c-2a0e-4b2b-84ff-a0406bb6fa37
- ModéréeCiprofloxacine, fluvoxamine ou autres inhibiteurs puissants du CYP1A2
Mécanisme: Ils peuvent augmenter l'exposition à la pentoxifylline et intensifier les effets indésirables.
Recommandation: Surveiller la tolérance et les effets indésirables ; adapter le traitement selon la réponse clinique.
CIMA ficha técnica 54635DailyMed setid cd840a2c-2a0e-4b2b-84ff-a0406bb6fa37
- ModéréeAntihypertenseurs ou antidiabétiques
Mécanisme: La pentoxifylline peut majorer la baisse de la pression artérielle ou l'effet hypoglycémiant.
Recommandation: Surveiller la pression artérielle et la glycémie ; ajuster le médicament associé si nécessaire.
CIMA ficha técnica 54635
- ModéréeCimétidineA02BA01
Mécanisme: La cimétidine augmente d'environ 25 % la concentration plasmatique moyenne à l'état d'équilibre de pentoxifylline et de 30 % celle de son métabolite I actif.
Recommandation: Surveiller la tolérance et les effets indésirables pendant l'administration concomitante.
CIMA ficha técnica 54635DailyMed setid cd840a2c-2a0e-4b2b-84ff-a0406bb6fa37
Effets indésirables
Communs (≥1%)
Dyspepsie (2,8 % avec les comprimés à libération prolongée) · Nausées (2,2 % avec les comprimés à libération prolongée) · Vertiges (1,9 % avec les comprimés à libération prolongée) · Céphalées (1,2 % avec les comprimés à libération prolongée) · Vomissements (1,2 % avec les comprimés à libération prolongée)
Rares mais graves
Fréquence indéterminée : hémorragie · Fréquence indéterminée : réaction anaphylactique ou choc anaphylactique · Fréquence indéterminée : angio-œdème ou bronchospasme · Fréquence indéterminée : thrombopénie, pancytopénie ou anémie aplasique · Fréquence indéterminée : hépatite, ictère ou cholestase · Fréquence indéterminée : arythmie ou angor
Grossesse et allaitement
Elorgan n'est pas recommandé pendant la grossesse en raison d'une expérience insuffisante. La pentoxifylline est excrétée en faibles quantités dans le lait maternel ; pendant l'allaitement, mettre en balance le bénéfice maternel et les risques possibles.
Bibliographie récente (PubMed)
Cardiogenic pulmonary edema (CPE) is characterized by the development of acute respiratory failure associated with the accumulation of fluid in the lung's alveolar spaces due to an elevated cardiac filling pressure. All cardiac diseases, characterized by an increasing pressure in the left side of the heart, can cause CPE. High capillary pressure for an extended period can also cause barrier disruption, which implies increased permeability and fluid transfer into the alveoli, leading to edema and atelectasis. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of procoagulant processes, cell death, and mechanical stretch. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance. Some studies claim that these patients may have higher levels of surfactant protein B in the bloodstream. The correct approach to patients with CPE should include a detailed medical history and a physical examination to evaluate signs and symptoms of CPE as well as potential causes. Second-level diagnostic tests, such as pulmonary ultrasound, natriuretic peptide level, chest radiograph, and echocardiogram, should occur in the meantime. The identification of the specific CPE phenotype is essential to set the most appropriate therapy for these patients. Non-invasive ventilation (NIV) should be considered early in the treatment of this disease. Diuretics and vasodilators are used for pulmonary congestion. Hypoperfusion requires treatment with inotropes and occasionally vasopressors. Patients with persistent symptoms and diuretic resistance might benefit from additional approaches (i.e., beta-agonists and pentoxifylline). This paper reviews the pathophysiology, clinical presentation, and management of CPE.
The α-Klotho protein (henceforth denoted Klotho) has antiaging properties, as first observed in mice homozygous for a hypomorphic Klotho gene (kl/kl). These mice have a shortened lifespan, stunted growth, renal disease, hyperphosphatemia, hypercalcemia, vascular calcification, cardiac hypertrophy, hypertension, pulmonary disease, cognitive impairment, multi-organ atrophy and fibrosis. Overexpression of Klotho has opposite effects, extending lifespan. In humans, Klotho levels decline with age, chronic kidney disease, diabetes, Alzheimer's disease and other conditions. Low Klotho levels correlate with an increase in the death rate from all causes. Klotho acts either as an obligate coreceptor for fibroblast growth factor 23 (FGF23), or as a soluble pleiotropic endocrine hormone (s-Klotho). It is mainly produced in the kidneys, but also in the brain, pancreas and other tissues. On renal tubular-cell membranes, it associates with FGF receptors to bind FGF23. Produced in bones, FGF23 regulates renal excretion of phosphate (phosphaturic effect) and vitamin D metabolism. Lack of Klotho or FGF23 results in hyperphosphatemia and hypervitaminosis D. With age, human renal function often deteriorates, lowering Klotho levels. This appears to promote age-related pathology. Remarkably, Klotho inhibits four pathways that have been linked to aging in various ways: Transforming growth factor β (TGF-β), insulin-like growth factor 1 (IGF-1), Wnt and NF-κB. These can induce cellular senescence, apoptosis, inflammation, immune dysfunction, fibrosis and neoplasia. Furthermore, Klotho increases cell-protective antioxidant enzymes through Nrf2 and FoxO. In accord, preclinical Klotho therapy ameliorated renal, cardiovascular, diabetes-related and neurodegenerative diseases, as well as cancer. s-Klotho protein injection was effective, but requires further investigation. Several drugs enhance circulating Klotho levels, and some cross the blood-brain barrier to potentially act in the brain. In c
Mandibular osteoradionecrosis (MORN) is a morbid complication of head and neck radiation therapy. Recent advances in surgical and medical therapies underscore the need for a shift in traditional treatment paradigms and a disease grading system that can guide appropriate management. Pubmed/MEDLINE. We conducted a detailed review of publications related to MORN, specifically focusing on its staging and management techniques. Articles meeting inclusion criteria were synthesized into a final narrative review. There has been a paradigm shift away from hyperbaric oxygen therapy in the management of MORN. Growing evidence for the efficacy of pentoxifylline and tocopherol in early-stage disease and novel surgical techniques to manage moderate and late-stage disease warrant an updated staging stratification which is proposed. This review summarizes the clinical efficacy of established and novel therapeutic modalities currently available in treating MORN, emphasizing the significant advances achieved over the last decade. It introduces a contemporary staging and treatment algorithm which incorporates traditional, evidence-supported surgical and medical management with effective early intervention strategies.
Diabetic kidney disease (DKD) is a major cause of chronic kidney disease (CKD), and it heightens the risk of cardiovascular incidents. The pathogenesis of DKD is thought to involve hemodynamic, inflammatory, and metabolic factors that converge on the fibrotic pathway. Genetic predisposition and unhealthy lifestyle practices both play a significant role in the development and progression of DKD. In spite of the recent emergence of angiotensin receptors blockers (ARBs)/angiotensin converting enzyme inhibitor (ACEI), sodium-glucose cotransporter 2 (SGLT2) inhibitors, and nonsteroidal mineralocorticoid receptors antagonists (NS-MRAs), current therapies still fail to effectively arrest the progression of DKD. Glucagon-like peptide 1 receptor agonists (GLP-1RAs), a promising class of agents, possess the potential to act as renal protectors, effectively slowing the progression of DKD. Other agents, including pentoxifylline (PTF), selonsertib, and baricitinib hold great promise as potential therapies for DKD due to their anti-inflammatory and antifibrotic properties. Multidisciplinary treatment, encompassing lifestyle modifications and drug therapy, can effectively decelerate the progression of DKD. Based on the treatment of heart failure, it is recommended to use multiple drugs in combination rather than a single-use drug for the treatment of DKD. Unearthing the mechanisms underlying DKD is urgent to optimize the management of DKD. Inflammatory and fibrotic factors (including IL-1, MCP-1, MMP-9, CTGF, TNF-a and TGF-β1), along with lncRNAs, not only serve as diagnostic biomarkers, but also hold promise as therapeutic targets. In this review, we delve into the potential mechanisms and the current therapies of DKD. We also explore the additional value of combing these therapies to develop novel treatment strategies. Drawing from the current understanding of DKD pathogenesis, we propose HIF inhibitors, AGE inhibitors, and epigenetic modifications as promising therapeutic targe
Keloids are an aberrant fibroproliferative response to wound healing of the skin, leading to scar tissue that expands above and beyond the original cutaneous injury. Keloids can be difficult to treat because of their tendency to recur after treatments, including after excision. There is a myriad of treatment modalities used, which can be used as monotherapy or in combination with surgical excision or other treatment methods. This review covers many treatment approaches including surgical excision, compression, silicone sheets, steroid-impregnated tape, imiquimod, intralesional injections, cryotherapy, laser, radiation, pentoxifylline, and dupilumab.