Reply: Iron chelation may harm patients with COVID-19
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LETTER TO THE EDITOR
Reply: Iron chelation may harm patients with COVID-19 Anis Abobaker 1 Received: 12 August 2020 / Accepted: 27 August 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Dear Editor A strikingly high level of ferritin has been reported in patients with the novel coronavirus disease 2019 (COVID-19) [1]. One of the possible explanations of this observation is inflammation induced by COVID-19 infection which increases the hepcidin level, the main regulator of tissue iron store, as discussed by Garrick and Ghio [2]. Moreover, the novel coronavirus (SARS-CoV-2) spike protein has hepcidin-like action, which means that the virus can directly increase ferritin level regardless of the inflammatory effect [1]. I agree with Garrick and Ghio that the release of free iron secondary to interaction between SARS-CoV-2 and haemoglobin molecule as an explanation of high ferritin level in COVID-19 remains a theoretical possibility, and it has not been practically confirmed as yet. It is believed that ferritin protein generated by inflammation has less iron content than normal ferritin [3]. Therefore, a test measuring serum ferritin iron content could differentiate between high ferritin secondary to inflammation or other causes, such as an iron overload state [3]. Although this test is useful in understanding the pathophysiology of SARS-CoV-2 infection, in my opinion, it has a limited value to ascertain the safety and effectiveness of iron chelation in management of COVID-19, and this is because of two reasons. First of all, a high ferritin level, regardless of the cause, has been linked with poor prognosis in COVID-19 [4]. The level of ferritin in COVID-19 non-survivors is higher than that of the survivors by twofold [5]. Intracellular iron generates reactive oxygen species in the lung by interacting with oxygen molecules which could predispose to the development of adult respiratory distress syndrome ( A R D S ) [ 5 ] . I n a d d it i o n , i n t r a c e l l u l a r i r o n a n d hyperferritinemia increase the risk of coagulopathy and
* Anis Abobaker [email protected] 1
Spire Fylde Coast Hospital, St Walburgas Road, Blackpool FY3 8BP, UK
oxidative stress and induce endothelial inflammation which could predispose to disseminated coagulation and multiorgan failure [1, 5]. Secondly, iron chelation drugs are not only able to bind free iron but they can also remove iron from iron-containing proteins, which means that iron chelation can have an anti-ferritin effect [6]. In fact, deferoxamine increases degradation of ferritin by lysosomes [4]. Other iron chelators, such as deferasirox, bind cytosolic iron released from ferritin [4]. In addition, deferoxamine decreases the production of free radicals generated by intracellular iron, which limits the chance of development of ARDS and subsequent tissue fibrosis [4]. Garrick and Ghio suggested that hepcidin antagonist could be a potential future possible approach in supportive management of COVID-19. Interestingly, it is stated that one of the addit
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