Could Hypokalemia explain COVID-19 mortality?

THAILAND MEDICAL NEWS has reported that a new research study by researchers from Wenzhou Medical University in Zhejiang province lead by Dr Don Chen ‘revealed that almost all Covid-19 patients exhibited hypokalemia and that supplementation with potassium ions was one of the many factors that assisted in their recovery.

The study apparently found that as the SARS-CoV-2 coronavirus attacks human cells via the ACE2 (Angiotensin- converting enzyme-2) receptors, it also attacks the renin–angiotensin system (RAS), causing low electrolyte levels in particularly potassium ions.

The study involving 175 patients in collaboration with Wenzhou Hospital found that ‘almost all patients exhibited hypokalemia and for those who already had hypokalemia, the situation even drastically worsened as the disease progressed.’

However, it was found from the study that ‘patients responded well to potassium ion supplements and had a better chance of recovery.’

The study has yet to be peer reviewed and has been published in the open platform medRvix : (https://www.medrxiv.org/content/10.1101/2020.02.27.20028530v1.full.pdf+html)

Meanwhile another medical paper theorises why COVID19 starves patients of oxygen and produces crushed glass imagery

UPDATE: The heme theory has apparently been debunked see below,

COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism.

The attack apparently will cause less and less hemoglobin that can carry oxygen and carbon dioxide.The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images.

Another paper published by a group of Italian doctors claims ‘Covid-19 Does Not Lead to a “Typical” Acute Respiratory Distress Syndrome’ and is cause for concern.

while the clinical approach to these patients is the one typically applied to severe ARDS, namely high Positive End Expiratory Pressure (PEEP) and prone positioning. However, the patients with Covid-19 pneumonia, fulfilling the Berlin criteria of ARDS, present an atypical form of the syndrome. Indeed, the primary characteristics we are observing (confirmed by colleagues in other hospitals), is the dissociation between their relatively well preserved lung mechanics and the severity of hypoxemia.

A New York City doctor explains why COVID19 is a ‘new disease requiring new treatment’ is not viral pneumonia, requires oxygen not ventilation, different protocols.

The past 48 hours or so have seen a huge revelation: COVID-19 causes prolonged and progressive hypoxia (starving your body of oxygen) by binding to the heme groups in hemoglobin in your red blood cells. People are simply desaturating (losing o2 in their blood), and that’s what eventually leads to organ failures that kill them, not any form of ARDS or pneumonia. All the damage to the lungs you see in CT scans are from the release of oxidative iron from the hemes, this overwhelms the natural defenses against pulmonary oxidative stress and causes that nice, always-bilateral ground glass opacity in the lungs. Patients returning for re-hospitalization days or weeks after recovery suffering from apparent delayed post-hypoxic leukoencephalopathy strengthen the notion COVID-19 patients are suffering from hypoxia despite no signs of respiratory ‘tire out’ or fatigue. Source

A blood test result more typically seen in disorders associated with bone marrow diseases was found in a patient with COVID-19, a viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The findings were published March 25 in the American Journal of Hematology.

Reviewing the currently published literature, I am unable to find any evidence for significant SARS-CoV-2 entry into red blood cells. writes Matthew Amdahl, MD, PhD in Covid-19: Debunking the Hemoglobin Story

2 comments
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