At the end of March, a New York City doctor drew massive attention with his claim, published in a YouTube video, that COVID-19 was more similar to altitude sickness than to acute respiratory distress syndrome (ARDS), and that it was being treated the wrong way.
At the root of his claim was that ARDS patients typically have muscles that can no longer support their own breathing, thus requiring mechanical ventilation. By contrast, COVID-19 patients can breathe fine, but they are starving for oxygen.
On Twitter, I pointed out that the Italians had already beat him too it, publishing about this in a peer-reviewed journal. They wrote that COVID-19 patients have an “atypical form” of ARDS, where the mechanical function of their lungs is preserved, but they have severe hypoxemia, meaning severely low levels of oxygen in their blood.
The Italians published new research today as a preprint* shedding light on how the hypoxemia might develop. This is the first release of findings from a large number of post-mortem analyses conducted on the lungs of people who died from COVID-19.
They found increased numbers of megakaryocytes in the lung capillaries, which are bone marrow cells responsible for making the platelets that are needed to form blood clots. 33 out of 38 patients had blood clots in the lung arteries. Had they been able to observe the clotting in real-time over the course of the disease, they may have seen these blood clots in all 38 patients. They suggested that the blood clots interfere with the delivery of oxygen to the blood and explain the hypoxemia of severe COVID-19 cases.
The capillaries were congested, which happens when blood clots in larger vessels prevent blood from moving smoothly out of them.
In the elderberry issue, I suggested based on findings in SARS that macrophages accumulate in the lungs and drive the inflammation. Indeed, they found “a large number” of macrophages in the alveolar lumens, which are the open spaces within tiny sacs where gas exchange takes place.
The macrophages may be generating cytokines such as interleukin-6 (IL-6) that increase the formation of blood clots. In the April 6 issue of this newsletter, I reviewed a paper showing that blood levels of IL-6 could predict who would go on to require ventilation with stunning accuracy. In that same paper, the level of D-dimer, a protein formed from the breakdown of blood clots, was nearly twice as high in the patients who required mechanical ventilation than in other severe cases.
Together these data support an emerging picture wherein inflammatory macrophages accumulate in the lung in response to the viral infection; they make cytokines such as IL-6 that increase the formation of blood clots; clotting in the small arteries of the lungs blocks the flow of blood, backing up blood in the capillaries, and preventing adequate oxygen from reaching the systemic circulation.
Theoretically drugs that block the actions of IL-6 or that reduce clotting could be useful.
Another preprint released today looked retrospectively at people who were and weren't treated with IL-6 blockers. It wasn't randomized and it is possible that randomized controlled trials (RCTs) will wind up undermining its conclusions, but patients who took the IL-6-blocking drugs had a 58% lower risk of going on to need mechanical ventilation and a 75% lower risk of dying. 3 out of the 30 patients had adverse outcomes that might have been related to treatment, two with mild damage to liver cells and one who acquired pneumonia from ventilation. There are three RCTs of IL-6 blockers underway, and we should have far more reliable results soon.
There currently are no evaluations of the safety or efficacy of anticoagulants in COVID-19.
It is important not to jump to conclusions here and use drugs with anti-clotting activity, such as NSAIDs, to treat COVID-19 before we have more data. Such drugs can alter levels of PGE2, a substance that is involved in blood clotting, but which also can promote or inhibit viral growth, depending on the virus.
Many nutrients and natural remedies impact blood clotting. I will be keeping a special lookout for evidence that any nutritional or herbal substances that affect clotting could impact the severity of COVID-19 and report what I find in this newsletter.
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* The term “preprint” is often used in these updates. Preprints are studies destined for peer-reviewed journals that have yet to be peer-reviewed. Because COVID-19 is such a rapidly evolving disease and peer-review takes so long, most of the information circulating about the disease comes from preprints.