Iron deficiency anemia and COVID-19

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a significant health and financial issue in the current century. Despite significant attempts to manage the illness, the transmission routes of the virus and its widespread genomic mutations have led to an increasing number of new infections and mortality rates. In the absence of specific treatment for this new virus, identifying and managing factors affecting the prognosis of the disease is one of the critical strategies to reduce disease mortality. Patients with iron deficiency anemia (IDA), who account for an estimated half a billion people globally, are more prone to infections due to immune system disorders. Since they visit hospitals more frequently for follow-up care and diagnosis, they are more susceptible to becoming infected with SARS-CoV-2. Once infected with SARS-CoV-2, low hemoglobin (Hb) levels and compromised immune systems disrupt the restriction of infection in these individuals, ultimately leading to severe complications of COVID-19.

Different Dimensions of the Effects of SARS-CoV-2 in Causing Fluctuations in the Blood Pressure of Patients

In late 2019, SARS-CoV-2 was transmitted from animal to human in China. Subsequently, the virus spread rapidly throughout the world by human-to-human transmission and caused high mortality the people with underlying diseases, especially hypertension. This virus binds to its receptor, angiotensin-converting enzyme-2 (ACE2), via the S protein. ACE2 has a negative regulatory function in the renin-angiotensin system (RAS) and degrades angiotensin 2 (Ang II) as a vasoconstrictor which causes blood pressure regulation. It also converts Ang II to Ang1-7, which has anti-inflammatory and anti-oxidative effects. SARS-CoV-2 infection in patients with hypertension reduces ACE2 levels due to virus binding, which decreases Ang II degradation. Consequently, the complications associated with hypertension are raised, and blood pumping from the lungs into the left atrium lowers. On the other hand, the final product, Ang1-7, is reduced, and its related anti-inflammatory activity is also eliminated. The virus multiplies and damages lung cells, causing inflammation and edema of the lung tissue through the function of immune cells and cytokines, which eventually leads to lung damage, reduced oxygen delivery, and death. Careful care of patients with hypertension can prevent their infection and reduce their death with appropriate oxygen therapy and possibly using exogenous ACE2 supplements. © 2022 by the authors.