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诱导性炎性小体激活与凝血紊乱。

Induced Inflammasome Activation and Coagulation Derangements.

作者信息

Mattana Marta, Tomasello Riccardo, Cammarata Claudia, Di Carlo Paola, Fasciana Teresa, Giordano Giulio, Lucchesi Alessandro, Siragusa Sergio, Napolitano Mariasanta

机构信息

Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (ProMISE), University of Palermo, 90141 Palermo, Italy.

Division of Internal Medicine, Hematology Service, Regional Hospital "A. Cardarelli", 86100 Campobasso, Italy.

出版信息

Microorganisms. 2022 Aug 10;10(8):1624. doi: 10.3390/microorganisms10081624.

DOI:10.3390/microorganisms10081624
PMID:36014040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9416296/
Abstract

enterocolitis (CDAC) is the most common hospital infection, burdened by an increased incidence of coagulation-related complications such as deep vein thrombosis (DVT) and disseminated intravascular coagulation (DIC) as well as a significant sepsis-related mortality. In this review, we analyzed the available data concerning the correlation between coagulation complications related to infection (CDI) and inflammasome activation, in particular the pyrin-dependent one. The little but solid available preclinical and clinical evidence shows that inflammasome activation increases the risk of venous thromboembolism (VTE). As proof of this, it has been observed that in vitro inhibition of the molecules (e.g., tissue factor) mainly involved in coagulation activation could block the process. In vivo studies show that it could be possible to reduce the incidence of complications associated with infection (CDI) and mortality due to a state of hypercoagulability. A personalized therapeutic approach to reduce the inflammatory activity and prevent thromboembolic complications could be preliminarily defined to reduce mortality.

摘要

艰难梭菌相关性肠炎(CDAC)是最常见的医院感染,其负担在于凝血相关并发症(如深静脉血栓形成(DVT)和弥散性血管内凝血(DIC))的发病率增加,以及与脓毒症相关的显著死亡率。在本综述中,我们分析了有关感染相关性凝血并发症(CDI)与炎性小体激活之间相关性的现有数据,尤其是与吡啉依赖性炎性小体激活之间的相关性。现有的少量但确凿的临床前和临床证据表明,炎性小体激活会增加静脉血栓栓塞(VTE)的风险。作为对此的证明,已经观察到,在体外抑制主要参与凝血激活的分子(如组织因子)可以阻断这一过程。体内研究表明,降低与感染(CDI)相关的并发症发生率以及因高凝状态导致的死亡率是有可能的。可以初步确定一种个性化治疗方法,以降低炎症活性并预防血栓栓塞并发症,从而降低死亡率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/6eda3830878d/microorganisms-10-01624-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/978ebe72013b/microorganisms-10-01624-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/70cec817f01e/microorganisms-10-01624-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/8b71c20f479b/microorganisms-10-01624-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/114c1ddc1be9/microorganisms-10-01624-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/dfd048299b50/microorganisms-10-01624-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/6eda3830878d/microorganisms-10-01624-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/978ebe72013b/microorganisms-10-01624-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/70cec817f01e/microorganisms-10-01624-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/8b71c20f479b/microorganisms-10-01624-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/114c1ddc1be9/microorganisms-10-01624-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/dfd048299b50/microorganisms-10-01624-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16b3/9416296/6eda3830878d/microorganisms-10-01624-g006.jpg

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