Not exactly a CLL post but an interesting article that poses the question that COVID19 is a vascular infection instead of a purely respiratory one.
There is now a growing body of evidence to support the theory that the novel coronavirus can infect blood vessels, which could explain not only the high prevalence of blood clots, strokes, and heart attacks, but also provide an answer for the diverse set of head-to-toe symptoms that have emerged and that 40% of deaths from Covid-19 are related to cardiovascular complications.
However, a respiratory virus infecting blood cells and lining of the blood vessesl circulating through the body is virtually unheard of. The difference between the orginal SARS and COVID19 likely stems from an extra protein each of the viruses requires to activate and spread. Although both viruses dock onto cells through ACE2 receptors, another protein is needed to crack open the virus so its genetic material can get into the infected cell. The additional protein the original SARS virus requires is only present in lung tissue, but the protein for SARS-CoV-2 to activate is present in all cells, especially endothelial cells. The theory could even explain why ventilation often isn’t enough to help many Covid-19 patients breathe better because if the lung blood vessels are blocked with clots, the full benefits of mechanical ventilatory support are somewhat thwarted.
We have seen reports of COVID19 patients on Ibruinib faring better than others and thought it was connected to prevention of the cytokine storm. Ibrutinib treatment carries an increased bleeding risk because of the effects of ibrutinib on several distinct platelet signaling pathways and the endothelium or lining of the blood vessels - a 'von willibrand' like effect. Perhaps this slight anticoagulant off target activity of Ibrutinib is the real reason and not the prevention of the cytokine storm.
This is very interesting and makes sense to me Jackie. Might actually be an advantage having slight thrombocytopenia and be on Ibrutinib at the moment!
I read about that about 3 weeks ago. The Ace receptors are the doorway to the virus into your body and they are in multiple locations depending on the person. Mainly in the lungs but also in the gut, nose, heart and blood vessels.
Hence the clots but also explains why some people get abdominal pain or loss of smell and taste. It depends on where the ace receptors are.
The side effects of ibrutinib are looking better 🤪
The Ace receptors are made by the body in people with the reported comorbitities in large numbers and not in young people and children.
So interesting. I almost love my Ibrutinib now, side effects and all. The picture at the top, yes the corona like Covid one made me wonder yet again how much like that my RBC spur cells look.
Wow! Thank you! Interesting indeed. Came home yesterday after two weeks in coronaward. Was admitted there after five days of climbing fever. Lung changes on CTscan but several negative covid-tests. Lost my smell. Been on a trombocytopenic rollercoaster since five years. They stopped my Revolade ( trombocyte boosting pills) when I was hospitalized and yet my platelets increased from 190 (optimal on Revolade is 50-100) to 419 within five days! They treated me as Covid and gave Fragmin shots quite early....And platelets started to slowly decline.
I am happy that I didnt know all this at that time!!! Worrying was enough, although I was often too weak to bother, and they seem to have treated me right.
Yesterday home with no fever, platelets 130, starting Revolade plus Fragmin shots.
New blood test on Thursday.
Pray trombocyte balance is right!
Warm greetings Christina
PS. I shall from now on take my morning Fragmin shots with joy!
And thank myself for the extra fat I have left since ages on my lower stomach, making it easier for me to inject....
If you want to understand how the virus goes about its evil work, I recommend this presentation - for medical students, so it's on the techy side.
He covers everything from epidemiology to pathology of the disease, only gets inside the lungs around 28 minutes in, and covers how the virus can damage blood vessels and cause blood clots.
Venous Thrombosis Among Critically Ill Patients With Coronavirus Disease 2019 (COVID-19)
A total of 34 consecutive patients were included in this study.
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Deep vein thrombosis was found in 22 patients (65%) at admission and in 27 patients (79%) when the venous ultrasonograms performed 48 hours after ICU admission were included (Table 2). Eighteen patients (53%) had bilateral thrombosis, and 9 patients (26%) had proximal thrombosis. Comparable with previously published data,2,3 our population had high levels of D-dimer (mean [SD], 5.1 μg/mL [to convert to nanomoles per liter, multiply by 5.476]), fibrinogen (mean [SD], 760 [170] mg/dL [to convert to grams per liter, multiply by 0.01]) and C-reactive protein (mean [SD], 22.8 [12.9] mg/dL [to convert to milligrams per liter, multiply by 10]). Prothrombin activity (mean [SD], 85% [11.4%]) and platelet count (mean [SD], 256 [107] × 103/μL) were normal.
Discussion
Mortality of patients with COVID-19 admitted to ICUs has been reported to be high, at 50%. Frequent venous and arterial thrombotic events have been reported, with rates from 27% to 69% of peripheral venous thromboembolism and up to 23% of pulmonary embolism. The occurrence of pulmonary embolism might be favored by deep vein thrombosis. The main limitations of this study were its monocentric nature and the relatively small size of our cohort. In view of the high rate (ie, 79%) of deep vein thrombosis reported in this study, prognosis might be improved with early detection and a prompt start of anticoagulant therapy. Despite anticoagulant prophylaxis, 15% of our patients developed deep vein thrombosis only 2 days after ICU admission. Systematic anticoagulant therapy for all ICU patients with COVID-19 should be assessed.
Looking at the information in this post and the additional report by AussieNeil , the message should be clear that if you suspect you have COVID get tested asap.
If you test positive get support and possible treatment (might be a trial) much sooner rather than later, don't try to recover without medical help.
I hope the COVID medical teams start to anticoagulate patients before they get to ICU, perhaps when they are receiving CPAP oxygen in order to prevent these thrombotic complications and further deterioration of the patient which might result in intubation.
Pulmonary Complications Common in Surgery Patients With COVID-19
— Half had pneumonia, ARDS, or other complications in study
Pneumonia and other pulmonary complications occurred in half of postsurgical patients with perioperative COVID-19 in an international study, and these complications were associated with a higher risk for early death.
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The study by Bhangu and colleagues included 835 patients who had emergency surgeries and 280 who had elective surgeries. Reasons for surgery included benign disease (54.4%), cancer (24.7%), and trauma (20.1%), and the main study outcomes were 30-day post-surgical mortality and pulmonary complications.
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CLL Meets COVID Vaccines/ Dr. Brian Koffman's take
What causes neutrophils to go so low after Obinutuzumab?
