” . . .As the medical community does not recognize this serious humanitarian disaster, these patients have unfortunately been shunned and denied access to the medical care they need and deserve. Furthermore, there is limited clinical, molecular, and pathological data on these patients to inform an approach to treating the condition.
Consequently, our approach to the management of vaccine-injured patients is based on the presumed pathogenetic mechanism, as well as the clinical observations of physicians and patients themselves.
-PATHOGENSIS
The spike protein, notably the S1 segment, is likely the major pathogenetic factor leading to post-vaccine syndrome. [4,5] The S1 protein is profoundly toxic. Multiple intersecting and overlapping pathophysiologic processes likely contribute to the vast spectrum of vaccine injuries: [1,6]
A prospective study on 64,900 medical employees, in which reactions to their first mRNA vaccination were carefully monitored, found that 2.1% of subjects reported acute allergic reactions.[11]
The acute myocarditis/sudden cardiac death syndrome that occurs post vaccination(within hours to 48 hours), noted particularly in young athletes, may be caused by a “stress cardiomyopathy” due to excessive catecholamines produced by the adrenal medulla in response to spike protein-induced metabolic aberrations.[12]
The inflammatory response is mediated by spike protein-induced mononuclear cell activation in almost every organ in the body but most notably involving the brain, heart and endocrine organs.
The lipid nanoparticles (LNP) themselves are highly proinflammatory Neuro-COVID, the neurological manifestations related to the spike protein, are related to the complex interplay of neuroinflammation,[18] production of amyloid and prion protein,[19-23] autoantibodies, microvascular thrombosis, and mitochondrial dysfunction. [24]
As the medical community does not recognize this serious humanitarian disaster, these patients have unfortunately been shunned and denied access to the medical care they need and deserve. Furthermore, there is limited clinical, molecular, and pathological data on these patients to inform an approach to treating the condition.
The spike protein is highly thrombogenic, directly activating the clotting cascade; in addition, the clotting pathway is initiated via inflammatory mediators produced by mononuclear cells and platelets. [5] Activation of the clotting cascade leads to both large clots (causing strokes and pulmonary emboli) as well as micro clots (causing microinfarcts in many organs, but most notably the brain)
And finally, due to altered immune function, the activation of dormant viruses and bacterial pathogens may occur, resulting in reactivated Herpes Simplex, Herpes Zoster, Epstein Barr Virus (EBV) and cytomegalovirus (CMV)infection, as well as reactivation of Lyme disease and mycoplasma. [45-47]
The common factor underlying the pathogenic mechanism in the vaccine-injured patient is “immune dysregulation.” . . .
” . . .It appears that about 80 percent of vaccine-injured patients are female. Women are known to be at a much higher risk of autoimmune diseases (especially SLE) and this likely explains this finding.
-TREATMENT APPROACH
Our treatment approach is, therefore, based on the postulated pathogenetic mechanism, clinical observation, and patient anecdotes.
The core problem in post-vaccine syndrome is chronic “immune dysregulation.” The primary treatment goal is to help the body to restore and normalize the immune system—in other words to let the body heal itself.
Early treatment is essential; it is likely that the response to treatment will be attenuated when treatment is delayed.
It is likely that COVID-19 will exacerbate the symptoms of vaccine injury.
Hyperbaric oxygen therapy (HBOT)should be considered in cases of severe neurological injury and in patients showing a rapid downhill course
-BASELINE TESTING
We recommend a number of simple, basic screening tests that should be repeated, as clinically indicated, every 4 to 6 months
CBC with differential and platelet count
Standard blood chemistries, including liver function tests
D-Dimer—as a marker of clotting activation
CRP—as a marker of ongoing inflammation (A comprehensive extensive
cytokine/chemokine panel is unnecessary and very costly, and the results will not change the treatment approach.
Early morning cortisol—some patients develop autoimmune adrenal failure)
TSH—to exclude thyroid disease
HbA1C—Vaccine-injured patients are at an increased risk of developing diabetes
Troponin and pro-BNP to exclude cardiac disease.
CMV, EBV, Herpes simplex, HHV6and mycoplasma serology/PCR
Vitamin D level(25OH Vitamin D) . . .’’ (continued next post)