Signed in as:
filler@godaddy.com
Signed in as:
filler@godaddy.com
The term “auto inflammatory” appeared on Cell in the spring of 1999 to describe an emerging family of clinical disorders, different from autoimmune syndromes. These were in fact characterized by episodes of apparently unprovoked inflammation, due to dis-regulation of the innate immune system, without auto reactive T lymphocytes and auto antibodies and therefore different from classical autoimmune diseases [1].
Although initially auto inflammatory diseases represented a clinical niche sector in the field of medicine, the last decade has witnessed a growing interest in the field of auto inflammation. This interest is related to an increase of the knowledge about the immunopathogenesis of a broad spectrum of diseases not only of immunological and allergic nature, but also of metabolic, chronic degenerative, neoplastic and inflammatory nature. Atherosclerosis, diabetes, neurodegenerative syndrome and osteoporosis [2] are significant examples of common diseases in which the well known inflammatory substrate shares many similarities with the typical auto inflammatory state. From a therapeutic point of view, it is now common experience that shared immunological targets are often used for the treatment of these conditions apparently distant from each other. Also aging, characterized by chronic inflammatory status which supports its progression as well as the onset of age-related diseases, could be considered an auto inflammatory para physiological condition.
In the light of these considerations, a new interpretation of auto inflammation emerges with both theoretical and clinical implications. The current increase in the prevalence of chronic inflammatory diseases makes this subject of topical interest.
(Department of Life, Health and Environmental Sciences, University of L’Aquila, Italy)
Your immune system is made up of organs and cells meant to protect your body from bacteria, parasites, viruses and cancer cells. An autoimmune disease is the result of the immune system accidentally attacking your body instead of protecting it. It's unclear why your immune system does this.
There are over 100 known autoimmune diseases. Common ones include lupus, rheumatoid arthritis, Crohn’s disease and ulcerative colitis.
Autoimmune diseases can affect many types of tissues and nearly any organ in your body. They may cause a variety of symptoms including pain, tiredness (fatigue), rashes, nausea, headaches, dizziness and more. Specific symptoms depend on the exact disease.
Experts don’t know why your immune system turns on you. It’s like it can no longer tell the difference between what’s healthy and what’s not — between what’s you and what’s an invader. There are some theories about why this happens, but experts aren’t completely sure.
Many autoimmune diseases are more common in women than in men. The diseases are common — 1 in 15 people in the U.S. have an autoimmune disease. One million people in the U.S. have lupus and 1.4 million have Crohn’s disease or ulcerative colitis
The precise cause of autoimmune diseases is unknown. However, there are risk factors that may increase your chances of getting an autoimmune disease. Risk factors include:
(Cleveland Clinic Org)
Myocarditis (with overall rate around 1.62%) was shown to be the most common post-COVID19 immunization cardiac event. More than 90% of post-COVID19 vaccination myocarditis occurred after receiving mRNA vaccines (Moderna & Pfizer-BioNTech), but the report of this event was less in the case of vector-based vaccinations and/or inactivated vaccines. Myocarditis was reported more commonly in men and following the second dose of the immunization. Takotsubo cardiomyopathy (TTC) was reported after mRNA (more commonly) and vector-based vaccinations, with no case report after inactivated vaccines. When mRNA and vector-based vaccinations were used instead of inactivated vaccines, a greater frequency of vaccine-induced thrombotic thrombocytopenia (VITT) and pulmonary emboli (PE) was reported. Myocardial infarction/cardiac arrest was recorded in those beyond the age of 75 years.
(Cardiologist, Cardiology Department, Chamran Cardiovascular Medical and Research Hospital, Isfahan University of Medical Sciences, Isfahan, Iran
bAssociate Professor of Cardiology, Echocardiologist, Cardiac Rehabilitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran
cEchocardiography Department, Chamran Cardiovascular Medical and Research Hospital, Isfahan University of Medical Sciences, Isfahan, Iran
⁎Corresponding author at: Associate Professor of Cardiology, Cardiac Rehabilitation Research Center, Isfahan Cardiovascular Research Institute, Isfahan University of Medical Sciences, Isfahan, Iran)
In a Mexican study, 6536 adverse events were recorded after Pfizer-BioNTech vaccination among 704,003 subjects. Sixty-five percent of these had at least one neurologic complication, 99% were mild and transient. The most commonly reported events included headache, transient sensory symptoms, and generalized weakness. The only severe adverse events recorded were seizures in 7, Guillain-Barré syndrome in 3 patients, and transverse myelitis in 2 patients [19••]. Similar rates were seen in a South Korean study by Kim et al. looking at adverse effects after the first dose of ChAdOx1 nCoV-19 and BNT162b2 vaccines [20]. In another study conducted amongst healthcare workers in the UK after two doses of the BNT162b2 mRNA vaccine, the most common adverse effects were myalgia, headache, chills, fatigue, and fever. These complications were higher after the second dose than with the first dose [21].
(Department of Neurology, Fortis Hospital, Kolkata, India)
.
COVID-19 can cause long-term problems with thinking, concentrating, and remembering. This condition is commonly known as “brain fog.” Brain fog after COVID-19 has been studied mostly by observing previously healthy people.
In a small study supported by the National Institute of Neurological Disorders and Stroke (NINDS), researchers examined the cognitive impact of COVID-19 on people with dementia. The researchers found that having COVID-19 rapidly accelerated the structural and functional brain deterioration of patients with dementia, regardless of the type of dementia being experienced.
Researchers followed 14 patients with preexisting dementia who were already enrolled in an ongoing dementia study and who had COVID-19 while participating in the study. Among these patients, four had Alzheimer’s disease, five had vascular dementia, three had Parkinson’s disease dementia, and two had the behavioural variant of frontotemporal dementia.
The researchers tested various cognitive functions and conducted brain imaging, comparing results from assessments within three months before their cases of COVID-19 and then one year after infection.
A year after contracting COVID-19, all of the patients with dementia had experienced a significant increase in fatigue and depression, as well as worsening attention, memory, speech, visuospatial capabilities, and executive functions. All the patients also had cerebral atrophy, which is the loss of neurons and connections between neurons, and lesions deep in the white matter of their brains.
Despite having different types of dementia, these patients developed similar dementia symptoms after having COVID-19. Overall, these patients experienced rapid structural and functional brain deterioration after COVID-19 infection.
Based on the unique brain changes seen in these patients, the researchers proposed a new term to describe the brain complications associated with COVID-19 in people with dementia: FADE-IN MEMORY (Fatigue, decreased Fluency, Attention deficit, Depression, Executive dysfunction, slowed Information processing speed, and subcortical MEMORY impairment).
The onset of chronic, debilitating symptoms following SARS-CoV-2 vaccination is thought to constitute a novel disease entity, for which the term post-acute COVID-19 vaccination syndrome (PACVS) has recently been suggested [1]. The symptoms reported by PACVS-affected persons start shortly after SARS-CoV-2 vaccination, continue in episodes over several months, and severely compromise the quality of life. A systematic survey of the clinical features of PACVS has yet to be carried out. However, published case reports [1] indicate that PACVS differs from the usual adverse effects of SARS-CoV-2 vaccination [2,3,4,5]. The symptoms most frequently reported in the context of PACVS encompass impaired well-being (exhaustion, malaise, chronic fatigue), cardiovascular disturbances (orthostatic intolerance, tachycardia, palpitations), peripheral neuropathy (dysesthesia, hypesthesia), central nervous system dysfunction (lack of concentration, brain fog, cognitive deficits, sleep disorders), muscular dysfunction (myalgia, weakness, fibrillations), and gastro-intestinal afflictions (nausea, strong weight changes). In summary, PACVS presents a phenotype of acquired autonomous dysfunction that overlaps with various established multisystemic dysautonomia syndromes such as myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) [6,7], postural orthostatic tachycardia syndrome (POTS) [8], fibromyalgia/chronic pain syndrome [9], small fibre neuropathy (SFN) [10] and mast cell activation syndrome (MCAS) [11]. Interestingly, symptoms similarly conforming to ME/CFS and POTS have been observed following vaccinations against human papillomavirus [12,13,14,15,16] and hepatitis B virus [17].
(Vaccines (Basel). 2023 Nov; 11(11): 1642)
Vaccine Injury Support
Copyright © 2024 Vaccine Injury Support - All Rights Reserved.
Powered by GoDaddy
We use cookies to analyze website traffic and optimize your website experience. By accepting our use of cookies, your data will be aggregated with all other user data.