#autoimmune hepatitis
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cancer-researcher · 6 days ago
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pharmanucleus1 · 7 months ago
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Autoimmune Hepatitis Market: Transformative Treatments Await
Global Autoimmune Hepatitis Market, By Type (Type 1, Type 2), Treatment (Medications, Liver Transplant, Others), Diagnosis (Liver Biopsy, Blood Tests, Imaging Tests, Others), Route of Administration (Oral, Parenteral, Others), End-Users (Hospitals, Specialty Clinics, Homecare, Others), Distribution Channel (Hospital Pharmacy, Retail Pharmacy, Online Pharmacy, Others) – Industry Trends and Forecast to 2030
Market Overview
In recent years, the autoimmune hepatitis market is anticipated to grow rapidly during the forecast period. According to the 2019 study "Burden of Liver Diseases in the World," liver illness causes roughly 2 million fatalities worldwide, with 1 million deaths due to cirrhosis complications and 1 million deaths due to viral hepatitis and hepatocellular cancer. Cirrhosis is the 11th most prevalent cause of mortality globally, while liver cancer is the 16th most common cause of death. They are responsible for 3.5 percent of all deaths worldwide.
According to Pharmanucleus, the autoimmune hepatitis market was valued at USD 156.76 million in 2021 and is predicted to reach USD 210.61 million by 2030, showing a CAGR of 3.70% from 2023 to 2030. The Pharmanucleus team curated the market study, which contains extensive expert analysis, patient epidemiology, pipeline analysis, price analysis, and regulatory framework.
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Market Definition
Autoimmune hepatitis is an uncommon but fatal liver disease. When the body mistakes healthy tissue and cells for infectious tissue and cells, antibodies are created to target the healthy liver cells. Autoimmune hepatitis can develop quickly or gradually. The condition's aetiology is unknown, however it may be related to other systemic disorders or medication exposure in some situations. Autoimmune Hepatitis Market Dynamics
Drivers
Increased incidence of autoimmune hepatitis
The rising prevalence of autoimmune hepatitis is a major contributor to the market's rapid expansion. Complications of such illnesses include swollen veins in the oesophagus, fluid accumulation in the abdomen, liver failure, and liver cancer.
Increasing healthcare infrastructure investment
Growing healthcare spending, which aids in infrastructure improvement, is another important aspect driving the autoimmune hepatitis market's growth rate.
The greater governmental and private-sector efforts to promote awareness of the would boost the autoimmune hepatitis market. Furthermore, people's changing lifestyles and high disposable income will drive the autoimmune hepatitis market upward. Furthermore, the expanding older population and an increase in medical tourism will accelerate the market's development pace.
Opportunities
Increase in the number of R&D activities      
Moreover, when R&D activity increases, so does the market. This will create new prospects for the autoimmune hepatitis industry to expand. Additionally, higher medication approvals and launches will drive market growth.
Furthermore, rising investments in the development of innovative technologies, as well as an increase in the number of emerging markets, will create further chances for the autoimmune hepatitis market to expand throughout the projected period..
Restraints/Challenges
On the other hand, the high cost of treatment will hamper the growth rate of the market. Lack of healthcare infrastructure in developing economies and low awareness of autoimmune hepatitis will pose major challenges to the market growth rate. Additionally, shortage of skilled professionals and missed diagnoses will further limit and hamper the growth rate of the market over the forecast period 2023-2030.
This report on the Autoimmune Hepatitis Market discusses recent new developments, trade regulations, import-export analysis, production analysis, value chain optimisation, share market analysis, the impact of national and localised market players, analyses opportunities in terms of emerging revenue pockets, market changes regulations, strategic analysis of market growth, market size, category market growth, niches and dominance of applications, product approvals, and p Contact Pharmanucleus for an Analyst Brief for more information on the Autoimmune Hepatitis industry; our experts will assist you in making an informed market choice to achieve market growth.
Please click here for full report:
https://www.pharmanucleus.com/reports/autoimmune-hepatitis-market
Patient Epidemiology Analysis
Autoimmune hepatitis is an uncommon condition that affects four times as many women as males. Type 1 diabetes is the most common and affects most individuals. Type 2 diabetes is more frequent in young individuals and progresses faster. Every year, 1 to 2 new cases per 100,000 people are expected, for a total of around 24 cases per 100,000 people.
Furthermore, the Autoimmune Hepatitis Market offers in-depth market data for patient analysis, prognosis, and therapy. Prevalence, incidence, mortality, and adherence rates are among the statistical aspects evaluated in the study. Analyses of the direct or indirect influence of epidemiology on market growth are performed in order to develop a more robust cohort multivariate statistical model to forecast market growth during the boom era.
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Post COVID Impact
Since its emergence in December 2019, the COVID-19 virus has indeed had a profound impact on healthcare systems worldwide, which has affected various medical conditions, including autoimmune hepatitis. The declaration of the virus as a public health emergency by the World Health Organization (WHO) prompted healthcare systems to prioritize COVID-19-related treatments and control measures. As a result, specialist healthcare services for other conditions, including autoimmune hepatitis, have faced delays and disruptions.
The financial crisis caused by the pandemic has further compounded the challenges in healthcare systems, leading to resource constraints and reduced access to medical services. Patients with autoimmune hepatitis have faced difficulties in seeing their healthcare providers for various reasons. Some individuals have struggled to access doctors due to overwhelmed healthcare facilities or limited availability of appointments. Fear of contracting the virus has also deterred patients from seeking in-person consultations. Moreover, pandemic-related restrictions, such as lockdowns and travel limitations, have hindered the continuity of essential therapies and procedures for autoimmune hepatitis patients.
These circumstances have the potential to negatively impact the autoimmune hepatitis market in recent months. Reduced access to care, delayed diagnoses, and interruptions in treatment may result in suboptimal disease management, increased disease progression, and worsened patient outcomes. Additionally, the economic consequences of the pandemic may limit patients' ability to afford necessary medications and therapies, affecting market demand.
However, as the global healthcare system adapts and recovers from the pandemic, efforts are being made to address these challenges. Telemedicine and remote healthcare services have gained prominence, allowing patients to connect with their healthcare providers virtually. Gradual easing of pandemic restrictions and resumption of regular healthcare services are expected to alleviate some of the barriers faced by autoimmune hepatitis patients, helping to stabilize the market over time.
Global Autoimmune Hepatitis Market Scope
The market for autoimmune hepatitis is classified by type, therapy, diagnosis, method of administration, end-users, and distribution channel. The growth in these segments will assist you in analysing the growth sectors in industries and providing users with a beneficial market overview and industry insights to assist them in making strategic decisions for finding key market applications.
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munaeem · 1 year ago
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How to live with autoimmune hepatitis?
Autoimmune hepatitis is a chronic liver inflammation caused by an abnormal immune response. The immune system attacks the liver cells as if they were foreign substances, causing inflammation and liver damage.Learn more : Autoimmune hepatitis – symptoms, treatment, prognosis What are the types of autoimmune hepatitis? There are two main types of autoimmune hepatitis: type 1 and type 2. Type 1 is…
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russianreader · 2 years ago
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"Our Family Is Dead": The Story of Yegor Balazeikin, Suspected of Torching a Military Enlistment Office
Yegor Balazeikin. Photo courtesy of RFE/RL Yegor Balazeikin is sixteen years old. In late February, he was detained in Kirovsk, a town in the Leningrad Region: according to police investigators, he wanted to set fire to a military enlistment office, and now he stands accused of “attempted terrorism.” Later, a second criminal case was launched against the schoolboy, also for allegedly attempting…
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punishthemplease · 6 months ago
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bloodwork came back looking waaaay better today :’)
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sleepyfemme24 · 1 year ago
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my symptoms: ibs, joint pain, muscle pain, no period, dry skin, anxiety and depression
every disease ever apparently: oh hey that could be me!
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justkidneying · 3 months ago
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Why the Spleen Sucks
The spleen is a really shittily placed organ, making it prone to injury. This injury is usually severe and can lead to death if not properly managed. We're going to look at the function of the spleen, what happens when it is damaged, and how to write about.
Where is the spleen? It's in the upper left quadrant of the abdominal cavity, nestled right against the ribs (typically 9-11) at the midaxillary line. It's behind the stomach and is considered intraperitoneal. The main thing is that the spleen is very vulnerable. It is literally right up against the ribs without much protecting it. It's shaped like a little bean and is purple in humans. It is fed by the splenic artery, which comes off of the celiac trunk (which sticks off of the abdominal aorta).
What does the spleen do? Its main job is to filter out old and malformed red blood cells. It also holds immune cells. Certain diseases can cause the spleen to enlarge, including cirrhosis of the liver (it's connected to the hepatic portal system), sickle cell anemia (RBCs are stuck in it), and autoimmune disorders. The spleen also holds about 250 mL of RBCs in reserve in case you need them.
What happens when it is injured? The spleen can be ruptured and lacerated kinda easily. Blunt trauma to the ribs can cause it to rupture, and this is seen in contact sports and car accidents mostly. Because of those giant gaps between the ribs, it's also prone to injury from knife attacks. Gunshot wounds are another common cause, as well as broken ribs penetrating it (broken ribs are very sharp, like way sharper than you imagine). Rupture is more likely when someone has splenomegaly.
When the spleen is damaged, you're going to get a lot of intraperitoneal hemorrhaging. The spleen filters a lot of blood and has blood in it, so there's going to be a lot of blood in the abdomen (obviously). This will lead to distention, guarding (abs are tense), and hypovolemia. The left upper quadrant will be painful, and there can also be referred pain to the left shoulder (Kehr's sign).
If the patient has a small laceration, the symptoms aren't always as dramatic. Sometimes they'll just have low hemoglobin (which is on RBCs), maybe some thrombocytopenia (lots of platelets in the blood).
How do you fix this? If the injury is small and the patient is hemodynamically stable, they can usually be given a blood transfusion and the spleen can heal itself. Sometimes surgery is also performed to clamp a vessel or repair the outer layer of the spleen.
If the injury is major, then surgery will be performed. If the patient is less critical, they may go in and try to fix the problem. If it can't be fixed, they may do a splenectomy (remove the spleen). In a critical patient, they might forgo the nice pretty incision on the left side, and instead just split the patient down the middle. In these situations (in my experience), there isn't a lot of time to waste. One thing that we aren't going to waste time on is anesthesia, for example. This is with a lot of very critical surgeries, at least from what I have seen. Like the surgeon will start cutting as they are working on knocking out the patient, but usually they are in so much pain that they don't even register it.
If you remove the spleen, the patient is more at risk for infections, but with modern medicine and vaccinations, it's not as much of a big deal as it used to be. The patient will probably be fine.
Writing tips: (new section idea, hope you guys like it, lol) As with any injury, you have to make sure that you are giving them an acceptable mechanism of injury. With the spleen, this is either blunt trauma or penetration/laceration. Getting tackled, getting stabbed, getting shot, all great MOIs.
Second thing, present the appropriate signs and symptoms. A sign would be like bruising, hypotension, tachycardia, etc. A symptom would be LUQ pain, Kehr's sign, etc.
Next, figure out what you're going to do and where you're going to do it. In the field, there probably isn't much you can do. The most would probably be a laparotomy and clamping the splenic artery, but I mean, when I was an EMT, we were not doing this. There's a lot of stuff you can theoretically do, but never gets done. But I mean you can write it. If the patient makes it to the hospital, I think it would be more fun to do emergency surgery and just split them right down the middle. There's going to be a lot of blood in the greater omentum, very high stakes and exciting.
Anyways, hope you guys liked this, please let me know if I got anything wrong. I wrote this off of my personal experience and a few good textbooks, but there can always been mistakes in things.
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does-truth-matter · 7 months ago
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The CDC has quietly changed who should AVOID the MMR vaccine.
https://www.cdc.gov/vaccines/vpd/mmr/public/index.html
They now state that ANYONE that “Has a parent, brother or sister with a history of immune system problems” should AVOID THE MMR VACCINE!
What exactly is an 'immune system problem?" Every autoimmune disorder.
* Achalasia
* Addison’s disease
* Adult Still's disease
* Agammaglobulinemia
* Alopecia areata
* Amyloidosis
* Amyotrophic lateral sclerosis (Lou Gehrigs)
* Ankylosing spondylitis
* Anti-GBM/Anti-TBM nephritis
* Antiphospholipid syndrome
* Autoimmune angioedema
* Autoimmune dysautonomia
* Autoimmune encephalomyelitis
* Autoimmune hepatitis
* Autoimmune inner ear disease (AIED)
* Autoimmune myocarditis
* Autoimmune oophoritis
* Autoimmune orchitis
* Autoimmune pancreatitis
* Autoimmune retinopathy
* Autoimmune urticaria
* Axonal & neuronal neuropathy (AMAN)
* Baló disease
* Behcet’s disease
* Benign mucosal pemphigoid
* Bullous pemphigoid
* Castleman disease (CD)
* Celiac disease
* Chagas disease
* Chronic inflammatory demyelinating polyneuropathy (CIDP)
* Chronic recurrent multifocal osteomyelitis (CRMO)
* Churg-Strauss Syndrome (CSS) or Eosinophilic Granulomatosis (EGPA)
* Cicatricial pemphigoid
* Cogan’s syndrome
* Cold agglutinin disease
* Congenital heart block
* Coxsackie myocarditis
* CREST syndrome
* Crohn’s disease
* Dermatitis herpetiformis
* Dermatomyositis
* Devic’s disease (neuromyelitis optica)
* Discoid lupus
* Dressler’s syndrome
* Endometriosis
* Eosinophilic esophagitis (EoE)
* Eosinophilic fasciitis
* Erythema nodosum
* Essential mixed cryoglobulinemia
* Evans syndrome
* Fibromyalgia
* Fibrosing alveolitis
* Giant cell arteritis (temporal arteritis)
* Giant cell myocarditis
* Glomerulonephritis
* Goodpasture’s syndrome
* Granulomatosis with Polyangiitis
* Graves’ disease
* Guillain-Barre syndrome
* Hashimoto’s thyroiditis
* Hemolytic anemia
* Henoch-Schonlein purpura (HSP)
* Herpes gestationis or pemphigoid gestationis (PG)
* Hidradenitis Suppurativa (HS) (Acne Inversa)
* Hypogammalglobulinemia
* IgA Nephropathy
* IgG4-related sclerosing disease
* Immune thrombocytopenic purpura (ITP)
* Inclusion body myositis (IBM)
* Interstitial cystitis (IC)
* Juvenile arthritis
* Juvenile diabetes (Type 1 diabetes)
* Juvenile myositis (JM)
* Kawasaki disease
* Lambert-Eaton syndrome
* Leukocytoclastic vasculitis
* Lichen planus
* Lichen sclerosus
* Ligneous conjunctivitis
* Linear IgA disease (LAD)
* Lupus
* Lyme disease chronic
* Meniere’s disease
* Microscopic polyangiitis (MPA)
* Mixed connective tissue disease (MCTD)
* Mooren’s ulcer
* Mucha-Habermann disease
* Multifocal Motor Neuropathy (MMN) or MMNCB
* Multiple sclerosis
* Myasthenia gravis
* Myositis
* Narcolepsy
* Neonatal Lupus
* Neuromyelitis optica
* Neutropenia
* Ocular cicatricial pemphigoid
* Optic neuritis
* Palindromic rheumatism (PR)
* PANDAS
* Parkinson's disease
* Paraneoplastic cerebellar degeneration (PCD)
* Paroxysmal nocturnal hemoglobinuria (PNH)
* Parry Romberg syndrome
* Pars planitis (peripheral uveitis)
* Parsonage-Turner syndrome
* Pemphigus
* Peripheral neuropathy
* Perivenous encephalomyelitis
* Pernicious anemia (PA)
* POEMS syndrome
* Polyarteritis nodosa
* Polyglandular syndromes type I, II, III
* Polymyalgia rheumatica
* Polymyositis
* Postmyocardial infarction syndrome
* Postpericardiotomy syndrome
* Primary biliary cirrhosis
* Primary sclerosing cholangitis
* Progesterone dermatitis
* Psoriasis
* Psoriatic arthritis
* Pure red cell aplasia (PRCA)
* Pyoderma gangrenosum
* Raynaud’s phenomenon
* Reactive Arthritis
* Reflex sympathetic dystrophy
* Relapsing polychondritis
* Restless legs syndrome (RLS)
* Retroperitoneal fibrosis
* Rheumatic fever
* Rheumatoid arthritis
* Sarcoidosis
* Schmidt syndrome
* Scleritis
* Scleroderma
* Sjögren’s syndrome
* Sperm & testicular autoimmunity
* Stiff person syndrome (SPS)
* Subacute bacterial endocarditis (SBE)
* Susac’s syndrome
* Sympathetic ophthalmia (SO)
* Takayasu’s arteritis
* Temporal arteritis/Giant cell arteritis
* Thrombocytopenic purpura (TTP)
* Tolosa-Hunt syndrome (THS)
* Transverse myelitis
* Type 1 diabetes
* Ulcerative colitis (UC)
* Undifferentiated connective tissue disease (UCTD)
* Uveitis
* Vasculitis
* Vitiligo
* Vogt-Koyanagi-Harada Disease
Wonder how many doctors are paying attention?
~shared from Jodi Wilson
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maaarine · 2 years ago
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The Cause of Depression Is Probably Not What You Think (Joanna Thompson, Quanta Magazine, Jan 26 2023)
"A literature review that appeared in Molecular Psychiatry in July was the latest and perhaps loudest death knell for the serotonin hypothesis, at least in its simplest form.
An international team of scientists led by Joanna Moncrieff of University College London screened 361 papers from six areas of research and carefully evaluated 17 of them.
They found no convincing evidence that lower levels of serotonin caused or were even associated with depression.
People with depression didn’t reliably seem to have less serotonin activity than people without the disorder.
Experiments in which researchers artificially lowered the serotonin levels of volunteers didn’t consistently cause depression. (…)
Although serotonin levels don’t seem to be the primary driver of depression, SSRIs show a modest improvement over placebos in clinical trials.
But the mechanism behind that improvement remains elusive.
“Just because aspirin relieves a headache, [it] doesn’t mean that aspirin deficits in the body are causing headaches,” said John Krystal, a neuropharmacologist and chair of the psychiatry department at Yale University.
“Fully understanding how SSRIs produce clinical change is still a work in progress.”
Speculation about the source of that benefit has spawned alternative theories about the origins of depression. (…)
Repple warns, however, that another explanation for the effects his team observed is also possible: Perhaps the depressed patients’ brain connections were impaired by inflammation.
Chronic inflammation impedes the body’s ability to heal, and in neural tissue it can gradually degrade synaptic connections.
The loss of such connections is thought to contribute to mood disorders.
Good evidence supports this theory.
When psychiatrists have evaluated populations of patients who have chronic inflammatory diseases like lupus and rheumatoid arthritis, they’ve found that “all of them have higher-than-average rates of depression,” said Charles Nemeroff, a neuropsychiatrist at the University of Texas, Austin.
Of course, knowing that they have an incurable, degenerative condition may contribute to a patient’s depressed feelings, but the researchers suspect that the inflammation itself is also a factor.
Medical researchers have found that inducing inflammation in certain patients can trigger depression.
Interferon alpha, which is sometimes used to treat chronic hepatitis C and other conditions, causes a major inflammatory response throughout the body by flooding the immune system with proteins known as cytokines — molecules that facilitate reactions ranging from mild swelling to septic shock.
The sudden influx of inflammatory cytokines leads to appetite loss, fatigue and a slowdown in mental and physical activity — all symptoms of major depression.
Patients taking interferon often report feeling suddenly, sometimes severely, depressed.
If overlooked chronic inflammation is causing many people’s depression, researchers still need to determine the source of that inflammation.
Autoimmune disorders, bacterial infections, high stress and certain viruses, including the virus that causes Covid-19, can all induce persistent inflammatory responses.
Viral inflammation can extend directly to tissues in the brain. Devising an effective anti-inflammatory treatment for depression may depend on knowing which of these causes is at work.
It’s also unclear whether simply treating inflammation could be enough to alleviate depression.
Clinicians are still trying to parse whether depression causes inflammation or inflammation leads to depression. “It’s a sort of chicken-and-egg phenomenon,” Nemeroff said.
Increasingly, some scientists are pushing to reframe “depression” as an umbrella term for a suite of related conditions, much as oncologists now think of “cancer” as referring to a legion of distinct but similar malignancies.
"And just as each cancer needs to be prevented or treated in ways relevant to its origin, treatments for depression may need to be tailored to the individual."
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aressida · 4 months ago
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Wrote a long one cos the in law family wanted him to take the flu shot, I said no.
"Dear Family, Friends, and Medical Professionals,
I am writing to share some thoughts and questions about vaccines, particularly in light of recent developments.
Do we believe that vaccines are the ultimate solution in medicine?
It is commonly known that influenza vaccines are reformulated each season due to the virus’s constant mutation, making it challenging to predict and protect against new strains accurately.
Is it true that these vaccines bypass the liver’s natural filtration system, potentially causing a shock to our bodies?
How should we classify these ingredients—as toxic or benign?
Here are just some vaccine ingredients, and these are being injected into your body and into your children’s bodies if you choose to vaccinate:
– Formaldehyde/Formalin – Highly toxic systemic poison and carcinogen.
– Betapropiolactone – Toxic chemical and carcinogen. May cause death or permanent injury after very short exposure to small quantities. Corrosive chemical.
– Hexadecyltrimethylammonium bromide – May cause damage to the liver, cardiovascular system, and central nervous system. May cause reproductive effects and birth defects.
– Aluminum hydroxide, aluminum phosphate, and aluminum salts – Neurotoxin. Carries risk for long-term brain inflammation/swelling, neurological disorders, autoimmune disease, Alzheimer’s, dementia, and autism. It penetrates the brain where it persists indefinitely.
– Thimerosal (mercury) – Neurotoxin. Induces cellular damage, reduces oxidation-reduction activity, cellular degeneration, and cell death. Linked to neurological disorders, Alzheimer’s, dementia, and autism.
– Polysorbate 80 & 20 – Trespasses the blood-brain barrier and carries with it aluminum, thimerosal, and viruses; allowing them to enter the brain.
– Glutaraldehyde – Toxic chemical used as a disinfectant for heat-sensitive medical equipment.
– Fetal Bovine Serum – Harvested from bovine (cow) fetuses taken from pregnant cows before slaughter.
– Human Diploid Fibroblast Cells – Aborted fetal cells. Foreign DNA has the ability to interact with our own.
– African Green Monkey Kidney Cells – Can carry the SV-40 cancer-causing virus that has already tainted about 30 million Americans.
– Acetone – Can cause kidney, liver, and nerve damage.
– E. Coli – Yes, you read that right.
– DNA from porcine (pig) Circovirus type-1
– Human embryonic lung cell cultures (from aborted fetuses)
You can view all of these ingredients on the CDC’s website. I encourage everyone to do their own research. Look up the MSDS on these chemicals. Read the thousands of peer-reviewed studies that have evaluated the biological consequences these chemicals can have on the body, especially when being injected.
Injecting foreign substances directly into the bloodstream—viruses, toxins, and proteins—has been linked to various diseases and disorders. These include conditions like atypical measles, cancer, leukemia, multiple sclerosis, and even SIDS (Sudden Infant Death Syndrome).
Conditions like Addison’s disease, anaphylactic shock, arthritis, asthma, asymptomatic COVID-19, Crohn’s disease, epilepsy, facial paralysis, fibromyalgia, fetal distress syndrome, foreign body embolism, genital herpes, hepatitis, hyperthyroidism, inflammatory bowel disease, jugular vein embolism, lung abscess, lupus, meningitis, MERS-CoV test positive, migraine-triggered seizures, multiple organ dysfunction syndrome, multiple sclerosis, multisystem inflammatory syndrome in children, pneumonia, stiff leg syndrome, stiff person syndrome, stillbirth, sudden heart attack, sudden respiratory failure, type 1 diabetes, uterine rupture, viral bronchitis—and much more.
This does not mean everyone will experience these reactions, but a significant number of test subjects have experienced one or more.
It is more than enough evidence to show that vaccine mandates are completely anti-scientific.
How can you make an informed decision if you do not have all the information?
We have also seen a shift where flu vaccines are now mRNA-based. But does a "vaccine" really prevent a virus or its recurrence as we expect it to?
The annual flu shot is, at best, a partial defense, aimed at last year’s strain. Does it truly help against the ever-mutating new flu, or is it just a temporary fix?
My concern is that this mindset—that a vaccine is a quick fix for everything—is flawed. The immune system may struggle to handle these types of agents, leading to breakthrough infections and potentially higher mortality rates.
For those who are vaccinated, I respect your choice. I simply ask for the same respect in return for my decision not to vaccinate. My reasons are personal and grounded in a belief that the government should not dictate my health choices and my family's.
Have you heard about Pfizer’s side effects?
Have you read the Pfizer documentation? Ask yourself if a drug with 32 pages of side effects is right for you.
The list of potential vaccine side effects released by Pfizer is alarming, ranging from autoimmune disorders to serious conditions like multiple organ dysfunction and sudden respiratory failure. Yet, this information was kept under wraps and only recently made public. Shouldn’t we be informed of the risks?
Do we even know the medium- or long-term effects of these vaccines?
Are they still in clinical trials? Is there a control group? What about Antibody-Dependent Enhancement (ADE) – has it been adequately tested? And why are ingredients like formaldehyde and mercury, known toxins, included in these vaccines?
Do you truly think this vaccine is 100% safe?
Transparency is crucial.
How can we make informed decisions if we are not given all the information?
We must ask ourselves, do we trust the pharmaceutical companies and their relationships with organizations like the CDC and FDA?
The FDA requested 75 years to release data on the Pfizer vaccine—why? Why did it take only 108 days to approve this vaccine, yet it supposedly requires decades to fully understand its effects?
Do you believe that SARS-CoV-2 has been isolated?
How well-informed are you about the CDC, FDA, pharmaceutical companies, and their donors? Do you think their qualifications are reliable?
These are important questions that deserve honest discussions. And, I believe it is crucial to acknowledge the existence of these alternative perspectives and engage in open discussions to gain a more comprehensive understanding.
Our health and freedom are at stake, and I urge everyone to think critically and seek out all the information before making decisions.
Thank you for taking the time to consider these points."
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covid-safer-hotties · 1 month ago
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Also preserved in our archive
By Gavin Giovannoni
Long COVID is defined as a clinical syndrome of persistent symptoms after acute COVID-19 that last longer than 12 weeks. The symptoms associated with long COVID are numerous and include (see NHS website for more information on long COVID):
extreme tiredness (fatigue)
feeling short of breath
problems with your memory and concentration ("brain fog")
heart palpitations
dizziness
joint pain and muscle aches
loss of smell
chest pain or tightness
difficulty sleeping (insomnia)
pins and needles
depression and anxiety
tinnitus, earaches
feeling sick, diarrhoea, stomach aches, loss of appetite
cough, headaches, sore throat, changes to sense of smell or taste
rashes
Many of these symptoms overlap with multiple sclerosis, chronic fatigue syndrome, and post-viral fatigue syndromes, which are common to numerous viruses, including Epstein-Barr virus (EBV). While the exact mechanisms driving long COVID are still unclear, several sources suggest that EBV reactivation could contribute. This is when I became very interested. Could long COVID be the gateway to developing effective antiviral treatments for EBV and MS?
Like long COVID, EBV-associated infectious mononucleosis (IM) is also a post-acute infection syndrome. It features similar symptoms, including fatigue and muscle pain (myalgia), low mood, cog-fog, insomnia and other mental health problems (depression and anxiety). EBV typically enters a latent phase after the initial infection, be it symptomatic (IM) or asymptomatic, but can reactivate under certain conditions, including acute infections, severe illnesses, or immunosuppression. Several studies have shown evidence of EBV reactivation in COVID-19 patients, which includes:
The presence of detectable EBV viraemia during the acute phase of COVID-19 is predictive of persistent symptoms.
An association between increased seroreactivity to EBV early antigen (EA) and viral capsid antigen (VCA) and the development of long COVID.
It is important to stress that the link between EBV and long COVID is currently an association and not necessarily causal. To prove causation, more research will be done, including trials targeting EBV with antivirals as a potential treatment for long COVID. It is important to note that EBV reactivation can occur in various immune dysregulation contexts, not just long COVID, which some would argue that these findings are non-specific. Intermittent reactivation occurs in MS, and it is this intermittent cycling between latent and lytic infection that may be driving MS disease activity.
As a young general medical registrar or trainee, I was always struck by how tired and ill people were with chronic or persistent infections, be it tuberculosis, hepatitis or HIV in the pre-antiretroviral era. I later learnt about sickness behaviour, a complex behavioural syndrome in response to inflammation, be it from infection or another inflammatory stimulus such as that which occurs with autoimmune diseases. What long COVID is, and probably MS, is a form of sickness behaviour, which is why the symptoms of these two diseases overlap so much. If intermittent EBV reactivation drives long COVID and MS, it should respond to EBV antiviral strategies. I am aware that many pwMS have started taking antivirals off-label to manage their MS. It is remarkable how many pwMS have contacted me to tell me how well they are doing on antivirals. This is reassuring and supports our efforts to develop antiviral therapies for MS. Are you taking antivirals? Which ones? Have any of you noted any response?
Please note that I can not sanction the use of off-label antiviral medications to treat MS. Antivirals need to be tested in well-designed, randomised controlled trials. Without class 1 evidence, we will not be able to get antivirals licensed to treat MS, nor will payers pay for these treatments. Prescribing medications off-label comes with many risks to pwMS, the prescriber and the healthcare system the prescriber works in.
For more information on sickness behaviour, I would recommend an earlier MS-Selfie newsletter on this subject: ‘ Do you suffer from cog-fog, fatigue or sickness behaviour?’ (19-Oct-2021).
The review article that triggered me to write this newsletter below discusses the current understanding of long COVID and the persistent symptoms experienced by some individuals following a SARS-CoV-2 infection. You may find this article of interest; it is accessible to download. The authors discuss the various challenges in defining and researching long COVID, including its wide range of symptoms, variability in symptom severity, and potential mechanisms. The review explores multiple possible causes, such as persistent viral reservoirs, dysregulated immune responses, direct viral damage, and vascular endothelium activation. The article also examines the progress of animal models and clinical trials aimed at understanding and treating long COVID, highlighting the need for more extensive human studies to confirm the effectiveness of various therapeutic approaches.
Paper Antar & Cox. Translating insights into therapies for Long Covid. Sci Transl Med. 2024 Nov 13;16(773):eado2106. www.science.org/doi/10.1126/scitranslmed.ado2106?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
Long Covid is defined by a wide range of symptoms that persist after the acute phase of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Commonly reported symptoms include fatigue, weakness, postexertional malaise, and cognitive dysfunction, with many other symptoms reported. Symptom range, duration, and severity are highly variable and partially overlap with symptoms of myalgic encephalomyelitis/chronic fatigue syndrome and other post-acute infectious syndromes, highlighting opportunities to define shared mechanisms of pathogenesis. Potential mechanisms of Long Covid are diverse, including persistence of viral reservoirs, dysregulated immune responses, direct viral damage of tissues targeted by SARS-CoV-2, inflammation driven by reactivation of latent viral infections, vascular endothelium activation or dysfunction, and subsequent thromboinflammation, autoimmunity, metabolic derangements, microglial activation, and microbiota dysbiosis. The heterogeneity of symptoms and baseline characteristics of people with Long Covid, as well as the varying states of immunity and therapies given at the time of acute infection, have made etiologies of Long Covid difficult to determine. Here, we examine progress on preclinical models for Long Covid and review progress being made in clinical trials, highlighting the need for large human studies and further development of models to better understand Long Covid. Such studies will inform clinical trials that will define treatments to benefit those living with this condition.
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darkmaga-returns · 2 days ago
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A group of leading scientists in Europe have found that Covid mRNA “vaccines” have caused a surge in once-rare liver failure.
The peer-reviewed study critically examined cases of autoimmune-like hepatitis that emerged in patients who had received Covid mRNA injections.
The researchers discovered that the mRNA “vaccines” had triggered deadly liver failure in the patients.
Following the study’s bombshell findings, the group of scientists has now introduced the term “SARS-CoV-2 vaccine-associated liver injury” (SVALI) to describe this phenomenon.
The findings of the study were published in the journal Liver International.
The study was led by renowned Swiss pathologist Dr. Benedetta Terziroli Beretta-Piccoli.
The researchers worked in collaboration with leading gastroenterology and pathology experts in Switzerland, the United Kingdom, and Turkey.
Researchers reviewed global data and analyzed potential mechanisms.
They focused on the role of the vaccine-encoded spike protein in provoking an aberrant immune response.
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read-watch-sleep · 5 months ago
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I am being so silly in your inbox (+ Discord) I have managed to convert you to the ScarVi verse and Im cackling like an evil villian about it
Well, my dear Kai, you're not the only one with the capacity for evil. (It is a delight to hear from you always). I'm using your ask as an opportunity to spread propaganda featuring my Pokémon conspiracy theory about a game I've never played (I only play pkmn Emerald on an emulator and Diamond on my jalbroken 3DS). You already know about this, of course. But I digress,
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^ This Guy Is a Reference to the Toxic Oil Syndrome Outbreak of 1981 
(gifs by @/ianime0 and rant under the cut)
His name in the Japanese game is Colza, and in the English translation is Brassius, both names for the plant known as Rapeseed, and the plant that makes Canola Oil. We also know that he looks sickly, and at one point, he was deathly ill with something unknown, which is part of what inspired his work Surrendering Sunflora.
In the 80s, canola/colza oil was illegal to sell for cooking in Spain (mostly for economic reasons) and had to be denatured for industrial use to be imported in as lubricant or biodiesel.
Now, in 1981, some 20,000+ people developed a strange musculoskeletal disease, that resulted in pulmonary edema (fluid in the lungs), muscle pain and failure, fever, and eosinophilia (too many eosinophil white blood cells), scleroderma (autoimmune rash) ect. The progression was brutal. Patients would go from a cough and a fever to strange rashes and rapidly losing weight, to having their muscles seize permanently and lifelong hepatitis. Thousands of people were permanently disabled, and more than 400 people died.
The cause?
Colza/Rapeseed oil, having been denatured with the chemical aniline, then filtered and mixed with olive oil to sell as edible cooking oil (which wasn't at all safe to eat).
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It's just a bit of a coincidence that one of the few canonically ill characters in the Pokémon universe just happens to be named after a plant that caused an epidemic in the place where he's meant to be from, especially when he always battles with Pokémon from the Arboliva line.
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So yeah, my theory is that he's got Toxic Oil Syndrome.
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loderlied · 3 months ago
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negative for the autoimmune hepatitis antibodies. what the fuck is going on with my liver seriously. she lives for mystery and the drama tm i guess
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The Physiology Of The Liver
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The liver is a vital organ responsible for numerous functions including metabolism, immunity, digestion, detoxification, and vitamin storage. It weighs around 2% of an adult’s body weight and is unique due to its dual blood supply from the portal vein (75%) and the hepatic artery (25%).
Cellular Structure
The liver’s functional unit is the lobule, which is hexagonal in shape. Each corner of the hexagon has a portal triad consisting of the portal vein, hepatic artery, and bile duct. The lobule is composed mainly of hepatocytes, which have distinct apical and basolateral membranes. Hepatocytes are categorized into three zones based on their function and blood supply:
Zone I (periportal region): Closest to the blood supply, involved in oxidative metabolism (e.g., gluconeogenesis, bile formation).
Zone II (pericentral region): Sits between Zones I and III.
Zone III: Farthest from the blood supply, primarily involved in detoxification and biotransformation.
Blood and bile flow in opposite directions within the liver. The space of Disse, between the hepatocytes and the sinusoidal lumen, contains Kupffer cells (macrophages) and Ito cells (fat-storing stellate cells).
Development
The liver develops from endodermal cells of the foregut as the hepatic diverticulum around the fourth week of embryonic development. It undergoes complex differentiation influenced by various pathways (e.g., Wnt/β-catenin, FGF). By the sixth week, the liver participates in hematopoiesis, and hepatocytes begin bile production by the 12th week.
Organ Systems and Functions
The liver interacts with multiple body systems:
Digestive and Metabolic Roles: Aids in digestion, stores fat-soluble vitamins, and handles cholesterol.
Hematological Functions: Produces clotting factors and proteins.
Detoxification: Metabolizes drugs and other xenobiotics through phase I (oxidation, reduction, hydrolysis) and phase II (conjugation) reactions.
Bilirubin Metabolism: Converts heme to unconjugated bilirubin, then conjugates it for excretion.
Hormonal and Protein Synthesis: Involved in thyroid hormone activation and synthesis of nearly all plasma proteins.
Related Testing
Liver function tests (LFTs), including ALT, AST, bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase (GGT), help assess liver health. Imaging techniques like ultrasound, CT, and MRI are also employed to identify liver abnormalities.
Pathophysiology
Cirrhosis results from chronic liver injury (e.g., due to alcoholism, hepatitis B and C), leading to fibrosis and necrosis. It causes symptoms like portal hypertension, coagulopathy, and jaundice. Hepatitis viruses (A, B, C, D, E), autoimmune diseases (e.g., primary biliary cholangitis), and metabolic conditions (e.g., non-alcoholic fatty liver disease) also contribute to liver pathology.
Clinical Significance
Understanding liver physiology helps manage conditions like viral hepatitis, alcoholic liver disease, benign liver lesions, and liver cancers. Early detection through appropriate testing and management strategies is essential for preventing end-stage liver disease and improving patient outcomes
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saltiecattoz · 1 year ago
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me trying to explain to my doctor that i have AUTOIMMUNE hepatitis and not the std kind of hepatitis
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