The US Government Comparative Toxicogenomics Database associates Fluoride with Behçet's Disease, (closely matching Kawasaki Disease in symptoms), and specifically with APOA1, APOB, CAT, CXCL8 and ICAM1 genes. The database also associates Fluoride with Hemorrhagic Shock through ICAM1, IL6 and TNF genes, Cardiogenic Shock through SOD2, and Septic Shock through NOS2 and TNF genes. Many of these genes have been found to be involved in disease progression in Covid-19.
Previous research has linked Coronavirus with Kawasaki Disease, although this remains controversial. Esper F et al. 2005. The Journal of Infectious Diseases, Volume 191, Issue 4, 15 February Pages 499–502
https://academic.oup.com/jid/article/191/4/499/937208
Will the current surge in "Kawasaki-like" disease since the Covid-19 pandemic outbreak be seen through new light given advances in RNA detection?
As outlined by Roger Seheult on MedCram 67 SARS-CoV-2 reduces ACE2 which leads to increased AT-II and decreased AT1,7 leading to superoxide formation which leads to endothelial cell dysfunction via a NO pathway and increased Von Willibrand Factor release from Weibel-Palade bodies in platelets leading to thrombosis formation in vessels, a feature of Kawasaki disease. The pathogenesis of Covid -19 appears to involve increased oxidative stress. The use of N acetyl cysteine appears promising for reducing the oxidative stress by replenishing reduced glutathione G-SH.
well said - but why did this all start? It seems new.
Best.
Jerry
I understand that Roger Seheult, California, has been trying to understand the pathophysiology of Covid -19 based on his reading of the literature, including papers sent to him by others. There are a number of papers that address the value of NAC in treating respiratory illness and the effects of oxidative stress on von Willebrand factor. Roger came up with the idea of treating Covid19 with NAC but in MedCram 70 he notes that Alexey Polonikov, Kursk State Medical University has also reported a series of patients with Covid-19 and sees endogenous deficiency of glutathione as the most likely cause of serious manifestations and death. Polonikov sees oxidative stress as contributing to the hyperinflammation of the lung and poor antioxidant defences as being due to glutathione deficiency. He recommends treatment with N-acetylcysteine and reduced glutathione. Seheult notes that it appears that the impaired lung oxygenation is related in part to thromobosis of pulmonary arterioles because of the von Willibrand factor molecules from platelets adhering to one another. The clots consist of long strands bound to one another by disulphide bonds. The NAC or reduced glutathione break the linked chains apart by breaking up the SS bonds through reducing them by changing them to SH SH so that the chains are no longer linked together. When the clots are lysed with NAC the hypoxaemia may be relieved. Seheult notes that there are different VWF levels in Group O patients and some racial groups (higher in Americans of African heritage). SARSCoV2 can cause a550% increases in VWF levels and the NAC can reduce this. Polonikov measured the Reactive Oxygen Species/Glutathione ratio. Patients with ratios of 2.9 and 1.2 did better (recovered without treatment) than those with rations of 34.6 (unwell 13 days) and 6.9 (still unwell after 11 days). Clinical trials of NAC for prevention and treatment awaited.