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The role of hypoxia and inflammation in the regulation of iron metabolism and erythropoiesis in COVID-19: The IRONCOVID study
American Journal of Hematology ( IF 10.1 ) Pub Date : 2022-08-05 , DOI: 10.1002/ajh.26679
Diletta Maira 1 , Lorena Duca 1 , Fabiana Busti 2 , Dario Consonni 3 , Michela Salvatici 4 , Alice Vianello 2 , Angelo Milani 5, 6 , Amedeo Guzzardella 7 , Elena Di Pierro 1 , Stefano Aliberti 8 , Itala Marina Baldini 1 , Alessandra Bandera 9, 10 , Francesco Blasi 10, 11 , Elena Cassinerio 1 , Matteo Cesari 12, 13 , Anna Ludovica Fracanzani 10, 14 , Giacomo Grasselli 7, 10 , Giovanna Graziadei 1 , Rosa Lombardi 10, 14 , Giacomo Marchi 2 , Nicola Montano 13, 15 , Valter Monzani 16 , Flora Peyvandi 10, 17 , Marco Proietti 12, 13, 18 , Maria Sandri 4 , Luca Valenti 10, 19 , Maria Domenica Cappellini 1 , Domenico Girelli 2 , Alessandro Protti 5, 6 , Irene Motta 1, 13
Affiliation  

Coronavirus Disease (COVID-19) can be considered as a human pathological model of inflammation combined with hypoxia. In this setting, both erythropoiesis and iron metabolism appear to be profoundly affected by inflammatory and hypoxic stimuli, which act in the opposite direction on hepcidin regulation. The impact of low blood oxygen levels on erythropoiesis and iron metabolism in the context of human hypoxic disease (e.g., pneumonia) has not been fully elucidated. This multicentric observational study was aimed at investigating the prevalence of anemia, the alterations of iron homeostasis, and the relationship between inflammation, hypoxia, and erythropoietic parameters in a cohort of 481 COVID-19 patients admitted both to medical wards and intensive care units (ICU). Data were collected on admission and after 7 days of hospitalization. On admission, nearly half of the patients were anemic, displaying mild-to-moderate anemia. We found that hepcidin levels were increased during the whole period of observation. The patients with a higher burden of disease (i.e., those who needed intensive care treatment or had a more severe degree of hypoxia) showed lower hepcidin levels, despite having a more marked inflammatory pattern. Erythropoietin (EPO) levels were also lower in the ICU group on admission. After 7 days, EPO levels rose in the ICU group while they remained stable in the non-ICU group, reflecting that the initial hypoxic stimulus was stronger in the first group. These findings strengthen the hypothesis that, at least in the early phases, hypoxia-driven stimuli prevail over inflammation in the regulation of hepcidin and, finally, of erythropoiesis.

中文翻译:


缺氧和炎症在调节 COVID-19 铁代谢和红细胞生成中的作用:IRONCOVID 研究



冠状病毒病(COVID-19)可以被认为是炎症与缺氧相结合的人类病理模型。在这种情况下,红细胞生成和铁代谢似乎都受到炎症和缺氧刺激的深刻影响,这对铁调素的调节作用相反。在人类缺氧疾病(例如肺炎)的背景下,低血氧水平对红细胞生成和铁代谢的影响尚未完全阐明。这项多中心观察性研究旨在调查 481 名入住内科病房和重症监护病房 (ICU) 的 481 名 COVID-19 患者的贫血患病率、铁稳态的变化以及炎症、缺氧和红细胞生成参数之间的关系。 )。数据在入院时和住院 7 天后收集。入院时,近一半患者患有贫血,表现为轻至中度贫血。我们发现铁调素水平在整个观察期间有所增加。疾病负担较高的患者(即需要重症监护治疗或缺氧程度较严重的患者)尽管具有更明显的炎症模式,但铁调素水平较低。入院时 ICU 组的促红细胞生成素 (EPO) 水平也较低。 7天后,ICU组的EPO水平上升,而非ICU组的EPO水平保持稳定,反映出第一组最初的低氧刺激更强。这些发现强化了这样的假设:至少在早期阶段,缺氧驱动的刺激在铁调素以及最终红细胞生成的调节中胜过炎症。
更新日期:2022-08-05
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