Anti-angiogéniques : mécanisme d’action et néphrotoxicité (notice n° 760123)
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| fixed length control field | 04106cam a2200301 4500500 |
| 005 - DATE AND TIME OF LATEST TRANSACTION | |
| control field | 20250123102121.0 |
| 041 ## - LANGUAGE CODE | |
| Language code of text/sound track or separate title | fre |
| 042 ## - AUTHENTICATION CODE | |
| Authentication code | dc |
| 100 10 - MAIN ENTRY--PERSONAL NAME | |
| Personal name | Clou, Emmanuelle |
| Relator term | author |
| 245 00 - TITLE STATEMENT | |
| Title | Anti-angiogéniques : mécanisme d’action et néphrotoxicité |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. | |
| Date of publication, distribution, etc. | 2022.<br/> |
| 500 ## - GENERAL NOTE | |
| General note | 9 |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | Dans le processus tumoral, l’angiogenèse va permettre l’approvisionnement mais aussi la dissémination des cellules cancéreuses. Le développement des anti-angiogéniques et plus particulièrement des anti- Vascular Endothelial Growth Factor (VEGF) a amélioré le pronostic et la survie de nombreux patients atteints de cancer. Le bévacizumab (anticorps monoclonal), l’aflibercept (VEGF-trap) et certains inhibiteurs de tyrosine kinase comme le sunitinib ont un mécanisme d’action similaire, basé sur une inhibition de la voie de signalisation du Vascular Endothelial Growth Factor. Ces traitements peuvent être associés à une chimiothérapie conventionnelle et sont de tolérance variable selon l’état général du patient et les facteurs de comorbidités associés. Les anti-angiogéniques ont une toxicité potentielle vasculaire et rénale, et sont donc soumis à une surveillance accrue pendant la durée du traitement. L’hypertension artérielle et la protéinurie sont les effets indésirables les plus fréquents, généralement contrôlables et réversibles à l’arrêt du traitement. Néanmoins, des toxicités plus sévères ont été rapportées comme des insuffisances rénales aiguës par atteinte glomérulaire ou vasculaire à type de microangiopathie thrombotique, mais aussi, plus rarement, par atteinte tubulo-interstitielle. Cet article vise à décrire les mécanismes d’action des anti-angiogéniques et leurs toxicités potentielles, en particulier rénales. |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | Tumoral angiogenesis is a key mechanism involved in the growth and spread of cancer cells. The development of angiogenesis inhibitors, particularly those targeting the Vascular Endothelial Growth Factor (VEGF) pathway, has improved the prognosis and survival of many cancer patients since they were approved in 2005 in France. Vascular Endothelial Growth Factor inhibitors have different mechanisms of action, targeting either the ligand (e.g. bevacizumab, anti-Vascular Endothelial Growth Factor monoclonal antibody; aflibercept, recombinant anti-Vascular Endothelial Growth Factor fusion protein), or its receptors such as tyrosine kinase inhibitors (e.g. sunitinib or sorafenib). These treatments can be combined with conventional chemotherapy, or other anti-cancer therapies, and are associated with variable tolerance depending on the patient's clinical condition and comorbidities. Additionally, angiogenesis inhibition may be associated with cardiovascular and/or kidney toxicity and therefore special monitoring is needed during the treatment duration. Development of hypertension and proteinuria are the commonest renal side effects; these are generally manageable and reversible when treatment is stopped. However, more severe toxicities have been reported such as acute kidney injury, glomerular and/or vascular insults such as thrombotic microangiopathy, and more rarely tubulointerstitial damage. The prescribing physician should be aware of these potentially serious. This article describes the mechanisms of action of antiangiogenic agents and their potential toxicities, with particular respect to the kidneys. |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Protéinurie |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Microangiopathie thrombotique |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Néphrotoxicité |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Anti-Vascular Endothelial Growth Factor |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Hypertension |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Nephrotoxicity |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Proteinuria |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Vascular Endothelial Growth Factor targeted therapies |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Hypertension |
| 690 ## - LOCAL SUBJECT ADDED ENTRY--TOPICAL TERM (OCLC, RLIN) | |
| Topical term or geographic name as entry element | Thrombotic microangiopathy |
| 700 10 - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Luque, Yosu |
| Relator term | author |
| 786 0# - DATA SOURCE ENTRY | |
| Note | Néphrologie & Thérapeutique | Volume 18 | 1 | 2022-01-26 | p. 1-6 | 1769-7255 |
| 856 41 - ELECTRONIC LOCATION AND ACCESS | |
| Uniform Resource Identifier | <a href="https://shs.cairn.info/revue-nephrologie-et-therapeutique-2022-1-page-1?lang=fr&redirect-ssocas=7080">https://shs.cairn.info/revue-nephrologie-et-therapeutique-2022-1-page-1?lang=fr&redirect-ssocas=7080</a> |
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