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晶体诱导性炎症发病机制与治疗的最新进展。

Recent developments in crystal-induced inflammation pathogenesis and management.

作者信息

Lioté Frédéric, Ea Hang-Korng

机构信息

Fédération de Rhumatologie (pôle appareil locomoteur), INSERM U606, Paris 7 Medical University, centre Viggo Petersen (Assistance Publique- Hôpitaux de Paris), hôpital Lariboisière, 2, rue Ambroise Paré, 75010 PARIS, France.

出版信息

Curr Rheumatol Rep. 2007 Jun;9(3):243-50. doi: 10.1007/s11926-007-0039-5.

Abstract

Crystal-induced inflammation pathogenesis is undergoing a transition with respect to monosodium urate, calcium pyrophosphate dihydrate, and even basic calcium phosphate crystals. It is now recognized that innate immunity could be involved in the earlier pathogenic events and that the inflammasome, along with other signaling pathways, is activated and results in interleukin-1 processing and secretion, ultimately activating cells as a paracrine or autocrine cytokine. Management of acute and chronic monosodium urate crystal-induced inflammation, namely gout, has been critically reviewed by a dedicated European working group, and on the behalf of the European League against Rheumatism, 12 evidence-based recommendations have been reported. Calcium pyrophosphate dihydrate chronic inflammation could benefit from colchicine and from methotrexate as an anti-inflammatory agent.

摘要

关于尿酸钠、二水焦磷酸钙甚至碱性磷酸钙晶体,晶体诱导的炎症发病机制正在发生转变。现在人们认识到,先天免疫可能参与早期致病事件,炎性小体与其他信号通路一起被激活,导致白细胞介素-1的加工和分泌,最终作为旁分泌或自分泌细胞因子激活细胞。一个专门的欧洲工作组对急性和慢性尿酸钠晶体诱导的炎症(即痛风)的管理进行了严格审查,代表欧洲抗风湿病联盟,报告了12条循证建议。二水焦磷酸钙慢性炎症可能受益于秋水仙碱和作为抗炎剂的甲氨蝶呤。

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