Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study.Goshua G, Pine AB, Meizlish ML et al. :ancet Haematology
What has this got to do with MS and MS-drugs….very little. I think and this is one of the reasons why MS drugs are not influencing COVID-19 in a negative way.
It says that a problem for COVID-19 is that there is damage to the blood vessels and this results in blood clots as a central problem in COVID-19. The clot blocks the vessels making it hard to breathe, but they are also causing all sorts of organ failure. If you have been reading our reviews, we brought this concept to you about two months ago.
This is thought to be in part due to the damage to the vessels facilitating the release something called von Willebrand factor (VWF), which is a pro-blood clotting factor. In more severe COVID-19 you can see it is much higher in the blood (see below) in people in red (intensive care unit = ICU). However you can see it also occurs in people that are not in intensive care….that’s because it probably central to a real problem with the SARS-CoV-2 virus
We had got this in our first paper just but it it is in the latest paper on COVID-19.
David Baker, Charles Roberts, Gareth Pryce, et al. COVID-19 vaccine-readiness for ocrelizumab and other anti-CD20-depleting therapies in multiple sclerosis and other autoimmune diseases. Authorea. June 23, 2020.
We have been given assistance to drawn a figure so figure 1 got a make over
Please note I said limited influence, I won’t say no influence.
However, this is an opinion, there are other views that don’t even consider co-aggulation as a problem
Endotheliopathy in COVID-19-associated coagulopathy: evidence from a single-centre, cross-sectional study.Goshua G, Pine AB, Meizlish ML et al. :ancet Haematology. Lancet Haematol DOI:https://doi.org/10.1016/S2352-3026(20)30216-7
Summary Background An important feature of severe acute respiratory syndrome coronavirus 2 pathogenesis is COVID-19- associated coagulopathy (clotting) , characterised by increased thrombotic and microvascular complications. Previous studies have suggested a role for endothelial cell (Blood vessel cell) injury in COVID-19-associated coagulopathy. To determine whether endotheliopathy is involved in COVID-19-associated coagulopathy pathogenesis, we assessed markers of endothelial cell and platelet activation in critically and non-critically ill patients admitted to the hospital with COVID-19.
Methods In this single-centre cross-sectional study, hospitalised adult (≥18 years) patients with laboratory-confirmed COVID-19 were identified in the medical intensive care unit (ICU) or a specialised non-ICU COVID-19 floor in our hospital. Asymptomatic, non-hospitalised controls were recruited as a comparator group for biomarkers that did not have a reference range. We assessed markers of endothelial cell and platelet activation, including von Willebrand Factor (VWF) antigen, soluble thrombomodulin, soluble P-selectin, and soluble CD40 ligand, as well as coagulation factors, endogenous anti-coagulants, and fibrinolytic enzymes. We compared the level of each marker in ICU patients, non-ICU patients, and controls, where applicable. We assessed correlations between these laboratory results with clinical outcomes, including hospital discharge and mortality. Kaplan–Meier analysis was used to further explore the association between biochemical markers and survival.
Findings 68 patients with COVID-19 were included in the study from April 13 to April 24, 2020, including 48 ICU and 20 non-ICU patients, as well as 13 non-hospitalised, asymptomatic controls. Markers of endothelial cell and platelet activation were significantly elevated in ICU patients compared with non-ICU patients, including VWF antigen (mean 565% [SD 199] in ICU patients vs 278%  in non-ICU patients; p<0·0001) and soluble P-selectin (15·9 ng/mL [4·8] vs 11·2 ng/mL [3·1]; p=0·0014). VWF antigen concentrations were also elevated above the normal range in 16 (80%) of 20 non-ICU patients. We found mortality to be significantly correlated with VWF antigen (r = 0·38; p=0·0022) and soluble thrombomodulin (r = 0·38; p=0·0078) among all patients. In all patients, soluble thrombomodulin concentrations greater than 3·26 ng/mL were associated with lower rates of hospital discharge (22 [88%] of 25 patients with low concentrations vs 13 [52%] of 25 patients with high concentrations; p=0·0050) and lower likelihood of survival on Kaplan–Meier analysis (hazard ratio 5·9, 95% CI 1·9–18·4; p=0·0087).
Interpretation Our findings show that endotheliopathy is present in COVID-19 and is likely to be associated with critical illness and death. Early identification of endotheliopathy and strategies to mitigate its progression might improve outcomes in COVID-19.
We have been saying this for weeks. It is in their in our review