A new hypothesis is coming up for lung involvement in COVID 19

There is a new hypothesis is coming up for lung involvement in COVID 19. Based on observations from the different studies published recently: Most of the postmortem analysis revealed pulmonary thrombosis, not typical ARDS. Also patient hypoxemia is not responding to PEEP, but high Fio2 .
Like methemoglobin, the virus structural protein sticks to heme - displaces oxygen - displaces iron - free iron toxicity causes inflammation of alveolar macrophages- leads to CT scan changes. No benefit of invasive ventilation . May require frequent blood transfusions.
The virus attacks beta chain, dissociates heme, removing iron & -convert-ing it to porphyrin.
Virus can dissociate oxy-Hb, carboxy-Hb and glycosylated Hb. Lung inflammation from inability of both oxygen & CO2 exchange, ground glass x rays, like CO2 poisoning.
Chloroquine competes for binding to porphyrin. Favipiravir binds to the virus envelope protein with very high affinity, prevents entry into the cells as well as binding of structural protein to porphyrin.

To summarize
COVID doesn’t cause pneumonia´-or-ARDs .. We are treating a presumed wrong disease
SARS2 Corona Virus binds to hemoglobin in a certain way that releases the iron ion into the circulation
Hb looses its capacity to bind with oxygen thus oxygen is not supplied to major organs. Which is why we see resistant hypoxia coupled with very rapid multi-organ failures.

* To simplify it more, we can take the example of CO-poision where Hb is unable to carry oxygen.

* The free iron released into the circulation is so toxic as it causes a powerful oxidative damage to the lungs (which explain the bilateral -and always bilateral- ground glass opacities seen on Chest CT of those patients, that was mistakenly treated as bilateral pneumonia)

* The body tries to compensate by elevating the rate of Hb synthesis which explains why Hb is high in those patients
* Other compensatory mechanisms to deal with the iron load such as increasing ferritin level explain the very high ferritin observed in those patients

* This hypothesis could explain why we are losing patients so rapidly and why mechanical ventilation is not so much effective in treatment and using ARDS mechanical ventilation protocol is not causing much benefit. Actually it could be causing more lung damage

* Sure more research is needed to understand the exact pathogenesis because this is the only hope for proper treatment . You can not treat what you do not actually know.

- This also could explain why the high ferritin as a bad prognosis marker (too much iron means too much Hb lost its O2 carrying capacity)

-Why there is monocytosis as the body needs excess macrophages to engulf the excess iron load. Also why there is lymphopenia as the WBCs differentiation is favored towards monocytes line rather than lymphocytes line.
-Why liver injury exists with high levels of transaminases and why it is associated with worse prognosis.

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