New: Hypocortisolemic ASIA: a vaccine- and chronic infection-induced syndrome behind the origin of long COVID and myalgic encephalomyelitis

[Violeta]

The important thing is the doses and to maintain as much as possible the stable levels in the blood.

How often do you take them to keep the blood levels stable?

I am going to find out tonight if ginseng in the evening affects sleep.

 

[Manuel]

How often do you take them to keep the blood levels stable?

I am going to find out tonight if ginseng in the evening affects sleep.

Be careful with ginseng at night. It is the only one to be taken simulating the circadian rhythm of cortisol. That is to say, with less doses at night and more doses in the morning and at mealtime.
As for the doses and times of intake I am looking for a way to communicate it and do it through clinical trials. If I say it through social networks and someone gets sicker or has to go to the hospital because he/she has taken more doses in relation to his/her weight, I would get into legal and moral problems. That is why we are looking for a way to start clinical trials as soon as possible but we are still without funding.

 

[Violeta]

Be careful with ginseng at night. It is the only one to be taken simulating the circadian rhythm of cortisol. That is to say, with less doses at night and more doses in the morning and at mealtime.
As for the doses and times of intake I am looking for a way to communicate it and do it through clinical trials. If I say it through social networks and someone gets sicker or has to go to the hospital because he/she has taken more doses in relation to his/her weight, I would get into legal and moral problems. That is why we are looking for a way to start clinical trials as soon as possible but we are still without funding.

Okay, thank you, and I do underestand about not communicating doses on social media.

I did take ginseng last night, and I slept okay. As you indicate, it will be an individual thing. I have had ME/CFS since 1982, so I may need some even to be able to sleep, at least for now.

I will try to be consistent with taking both every 6 hours. I'll see how that goes.

 

[civicko]

I have not yet introduced replacement doses of hydrocortisone because I wanted to see if the damage to my ACTH secretion was irreparable. I am not fully recovered with these treatments but I can do anaerobic exercise, study, go outside and have an almost normal life (but with some limitations). I still have some symptoms in the mornings and improve throughout the day with the treatments.
All these treatments influence and help the deficiencies caused by the infection so they should be combined. The ones I noticed the most in my symptomatic improvement were the antivirals, antihistamines, astragalus, NAC and ginseng. The important thing is the doses and to maintain as much as possible the stable levels in the blood.

Aren't you concerned about the antivirals long term use? You are taking valtrex and desloratadine? Did you introduced all at once or slowly one by one?

 

[Manuel]

𝐎𝐥𝐝 𝐀𝐫𝐭𝐢𝐜𝐥𝐞𝐬 𝐭𝐡𝐚𝐭, 𝐢𝐟 𝐏𝐮𝐛𝐥𝐢𝐬𝐡𝐞𝐝 𝐓𝐨𝐝𝐚𝐲, 𝐖𝐨𝐮𝐥𝐝 𝐁𝐞 𝐭𝐡𝐞 𝐊𝐞𝐲 𝐭𝐨 𝐭𝐡𝐞 𝐃𝐞𝐯𝐞𝐥𝐨𝐩𝐦𝐞𝐧𝐭 𝐨𝐟 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃, 𝐌𝐲𝐚𝐥𝐠𝐢𝐜 𝐄𝐧𝐜𝐞𝐩𝐡𝐚𝐥𝐨𝐦𝐲𝐞𝐥𝐢𝐭𝐢𝐬 𝐚𝐧𝐝 𝐏𝐨𝐬𝐭 𝐕𝐚𝐜𝐜𝐢𝐧𝐚𝐥 𝐒𝐲𝐧𝐝𝐫𝐨𝐦𝐞𝐬



𝐒𝐭𝐮𝐝𝐲 𝐨𝐧 𝐇𝐲𝐩𝐨𝐭𝐡𝐚𝐥𝐚𝐦𝐢𝐜-𝐏𝐢𝐭𝐮𝐢𝐭𝐚𝐫𝐲-𝐀𝐝𝐫𝐞𝐧𝐚𝐥 𝐀𝐱𝐢𝐬 (𝐇𝐏𝐀) 𝐢𝐧 𝐒𝐀𝐑𝐒 𝐒𝐮𝐫𝐯𝐢𝐯𝐨𝐫𝐬

An article in 𝐶𝑙𝑖𝑛𝑖𝑐𝑎𝑙 𝐸𝑛𝑑𝑜𝑐𝑟𝑖𝑛𝑜𝑙𝑜𝑔𝑦 (2005) investigated endocrine sequelae in SARS survivors, revealing that 39.3% of patients had hypocortisolism. The low-dose Synacthen test (1 μg) was crucial in detecting subtle HPA axis dysfunctions, showing that many patients recovered HPA axis function within 1 year after treatment. In addition, transient thyroid dysfunction was observed in some patients, resolving between 3 and 9 months. These findings suggest that SARS-CoV can cause long-lasting endocrine dysfunction, which is relevant to understanding Long COVID, Myalgic Encephalomyelitis and post-vaccinal complications. The improvement in serum cortisol levels and resolution of symptoms such as fatigue and postural dizziness suggest that cortisol replacement was effective in most cases.

: https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2005.02325.x



𝐒𝐭𝐮𝐝𝐲 𝐨𝐧 𝐌𝐨𝐥𝐞𝐜𝐮𝐥𝐚𝐫 𝐌𝐢𝐦𝐢𝐜𝐫𝐲 𝐨𝐟 𝐀𝐂𝐓𝐇 𝐢𝐧 𝐒𝐀𝐑𝐒 𝐚𝐧𝐝 𝐢𝐭𝐬 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐰𝐢𝐭𝐡 𝐂𝐨𝐫𝐭𝐢𝐜𝐨𝐬𝐭𝐞𝐫𝐨𝐢𝐝𝐬.

Another study, published in 𝑀𝑒𝑑𝑖𝑐𝑎𝑙 𝐻𝑦𝑝𝑜𝑡ℎ𝑒𝑠𝑒𝑠 (2004), proposes that SARS and other coronaviruses employ molecular mimetic strategies to evade the host immune response. The SARS virus expresses amino acid sequences that mimic host adrenocorticotropic hormone (ACTH). This induces the production of autoantibodies against ACTH, limiting the host stress response and leading to relative adrenocortical insufficiency.

Corticosteroid treatment can mitigate these effects by providing the corticosteroid levels needed to fight infection. According to the study, initiating corticosteroid treatment as early as possible allows the use of lower doses, whereas a delay in treatment requires higher doses to suppress virus-induced inflammatory cytokine dysfunction. In addition, prophylactic use of moderate doses of corticosteroids could prevent clinical infection with SARS by preventing the ACTH mimetic strategy of the virus from becoming active.

The results show that SARS patients treated with corticosteroids experienced clinical improvements, supporting the hypothesis that autoantibodies against ACTH play a crucial role in the pathogenesis of SARS. Also, these findings could be applicable to the treatment and prevention of complications in Long COVID, post-vaccinal syndromes and Myalgic Encephalomyelitis, given that SARS-CoV-2 and other viruses may employ similar immune evasion mechanisms.

: https://www.sciencedirect.com/science/article/pii/S0306987704002828?via=ihub



𝐒𝐭𝐮𝐝𝐲 𝐨𝐧 𝐀𝐧𝐭𝐢-𝐀𝐂𝐓𝐇 𝐀𝐧𝐭𝐢𝐛𝐨𝐝𝐢𝐞𝐬 𝐢𝐧 𝐂𝐫𝐢𝐭𝐢𝐜𝐚𝐥𝐥𝐲 𝐈𝐥𝐥 𝐏𝐚𝐭𝐢𝐞𝐧𝐭𝐬 𝐰𝐢𝐭𝐡 𝐂𝐎𝐕𝐈𝐃-𝟏𝟗.

A recent study published in 𝑀𝑒𝑑𝑖𝑐𝑖𝑛𝑎 𝐼𝑛𝑡𝑒𝑛𝑠𝑖𝑣𝑎 (2021) evaluated the presence of anti-ACTH antibodies in critically ill patients with COVID-19. The authors, D. Pérez-Torres, C. Díaz-Rodríguez, and A. Armentia-Medina, investigated whether anti-ACTH antibodies were detectable in these patients and measured plasma cortisol and ACTH levels.

The study found that 60% of critically ill COVID-19 patients had anti-ACTH antibodies, and half of these patients showed low cortisol and ACTH levels. These findings support the theory that SARS-CoV-2 may use molecular mimetic strategies to evade the host immune response. The presence of these antibodies may block the immune response and attenuate the natural HPA axis response to stress, leading to relative adrenal insufficiency.

: https://www.sciencedirect.com/science/article/pii/S0210569121001960?via=ihub



𝐈𝐦𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬 𝐟𝐨𝐫 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃, 𝐌𝐲𝐚𝐥𝐠𝐢𝐜 𝐄𝐧𝐜𝐞𝐩𝐡𝐚𝐥𝐨𝐦𝐲𝐞𝐥𝐢𝐭𝐢𝐬 𝐚𝐧𝐝 𝐏𝐨𝐬𝐭-𝐕𝐚𝐜𝐜𝐢𝐧𝐚𝐥 𝐒𝐲𝐧𝐝𝐫𝐨𝐦𝐞𝐬.

The findings of these studies are highly relevant to understanding the complications of Long COVID, Myalgic Encephalomyelitis, and post-vaccinal syndromes. HPA axis dysfunction and the production of autoantibodies against ACTH could explain some of the persistent symptoms observed in these patients. The use of stimulation testing and early treatment with corticosteroids could be useful strategies to diagnose and treat these complications.



All of this is detailed in our 𝐫𝐞𝐯𝐢𝐞𝐰 𝐚𝐫𝐭𝐢𝐜𝐥𝐞: https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1422940/full



And you can see it summarized in 𝐭𝐡𝐢𝐬 𝐯𝐢𝐝𝐞𝐨:

𝐒𝐡𝐚𝐫𝐞 this information with your doctors and other patients to explore treatment options! Together we can work toward a better quality of life.

Link X:https://x.com/manruipa/status/1818652670887931945?s=46&t=m4Zmq5Ji7bf6LgmUbeK4pA

 

[SWAlexander]

Some remember when I pointed out very early how vaccine impacts hormones.

If anybody is still in doubt read this thread: https://x.com/HouseLyndseyRN/status/1820233070424866833

 

[Manuel]

ICI-treated individuals who develop hypophysitis may hold the key to the development of ME/CFS, Long COVID and post-vaccinal syndromes


In the field of immunology and cancer treatment, Immune Checkpoint Inhibitors (ICIs) have revolutionized cancer therapy by activating the immune system to attack cancer cells. However, this immune hyperactivation can have significant side effects, known as immune-related adverse events (irAEs), including hypophysitis, an inflammation of the pituitary gland.


Immune Hyperactivation and Hypophysitis.
ICIs work by blocking immune regulatory proteins, such as CTLA-4 and PD-1, which boosts the immune response against cancer. This dysregulation can, however, lead to immune hyperactivation that not only attacks cancer cells, but also healthy tissues. A clear example is hypophysitis, where the pituitary gland becomes inflamed due to the uncontrolled action of the immune system. Inflammation and damage of the pituitary gland affects the production and secretion of pituitary hormones, which can lead to a variety of clinical symptoms depending on the hormones affected (such as ACTH, TSH, GH, among others).


Similarity with Long COVID, ME/CFS and Post-Vacunal Syndromes.
Current research suggests that similar immune hyperactivation may be involved in conditions such as Long COVID, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and post-vacunal syndromes. These conditions share features such as chronic inflammation, autoimmunity and immune depletion.


Long COVID
Long COVID, a condition that persists in some individuals after acute SARS-CoV-2 infection, shows signs of a dysregulated immune response similar to that seen in patients treated with ICI. Prolonged inflammation and possible reactivation of latent viruses, such as Epstein-Barr, may contribute to persistent symptomatology, including chronic fatigue, cognitive dysfunction, and hormonal imbalances.


ME/CFS
ME/CFS is a debilitating disease characterized by extreme fatigue following infection that is not relieved by rest and worsens with physical or mental activity. As in ICI-induced hypophysitis, it has been proposed that a chronic dysregulated immune response may play a crucial role in the development of ME/CFS. This immune response may be directed not only against infectious agents, but also against the body's own tissues, resulting in a state of persistent inflammation and dysfunction.


Post-vaccinal syndromes
Post-vaccinal syndromes, although rare, have been reported in some individuals after receiving certain vaccines, including COVID-19 vaccines. These syndromes can include symptoms similar to those of ME/CFS and Long COVID, such as chronic fatigue, muscle aches, and neurological problems. It is believed that in these cases, a vaccine-induced hyperactivation of the immune system could trigger autoimmune and inflammatory responses that contribute to these symptoms.


Hypophysitis as a Study Model
ICI-induced hypophysitis provides a useful model for understanding how a dysregulated immune response can lead to systemic disease. The study of this condition may offer crucial clues to the mechanisms underlying ME/CFS, Long COVID and post-vaccinal syndromes. For example:

• Chronic Inflammation: persistence of inflammation in hypophysitis may mirror the chronic inflammation seen in ME/CFS and Long COVID.
• Hormonal Dysregulation: hypophysitis may cause hormonal deficiencies, similar to the imbalances observed in ME/CFS and Long COVID.
• Autoimmunity: The autoimmune nature of hypophysitis may parallel the autoimmune responses suspected in ME/CFS, Long COVID and post-vaccine syndromes.
• HLA-DRB1 allele: Both hypophysitis in ICI-treated patients and ME/CFS conditions, Long COVID and post-vaccinal syndromes, could be associated with susceptible HLA-DRB1 alleles. In patients treated with ICI, the immune hyperactivation is due to the therapy itself, and upon termination of ICI treatment, the problem usually resolves. In contrast, in ME/CFS, Long COVID and post-vaccinal syndromes, persistence of viral antigen perpetuates hyperactivation and autoimmune damage.

Conclusion
Hyperactivation of the immune system, whether induced by ICI treatments, viral infections such as SARS-CoV-2 or herpesviruses, or even vaccines, can result in a variety of immune-related adverse events (irAEs) and chronic conditions such as hypophysitis, ME/CFS, Long COVID, and post-vaccinal syndromes. Understanding these shared mechanisms, especially in individuals with susceptible HLA-DRB1 alleles, may be the key to developing effective treatments and improving the quality of life for patients affected by these debilitating diseases.


More information in this thread :

https://x.com/manruipa/status/1810664159354192253?s=46&t=m4Zmq5Ji7bf6LgmUbeK4pA

 

[SWAlexander]

Finally, I have been discussing hormonal deficiency in relation to ME/CFS and COVID-19 since mid-2020.
how many people ever had an MRI for hypophysitis?
Hypophysitis causes are autoimmune, but other etiologies include inflammation secondary to sellar tumors or cysts, systemic diseases, and infection or drug-induced causes.

 

[SWAlexander]

STORM in the Lungs: Lessons from COVID-19 and Implications for Future Pandemics:

Excerpt:
" How STORM Affects the Lungs​

The immune system’s overreaction in STORM can lead to several serious lung disorders:

• Acute Respiratory Distress Syndrome (ARDS): This condition causes severe breathing difficulties and low oxygen levels in the blood. This was observed in patients who suddenly struggled to breathe on the eighth day of illness.
• Pulmonary Fibrosis: Over time, the damage from inflammation can lead to scarring in the lungs, making it harder to breathe normally.
• Pulmonary Hypertension: The damage to blood vessels in the lungs can increase pressure in these vessels, straining the heart.
• Persistent Cough: Ongoing inflammation with bronchitis can irritate the airways, causing a long-lasting cough.
• Reduced Lung Function: The lungs may become less efficient at transferring oxygen to the blood, leading to fatigue and difficulty with physical activities."

 

[sunshine44]

Wow, thank you for sharing this.

 

[hapl808]

Finally, I have been discussing hormonal deficiency in relation to ME/CFS and COVID-19 since mid-2020.
how many people ever had an MRI for hypophysitis?
Hypophysitis causes are autoimmune, but other etiologies include inflammation secondary to sellar tumors or cysts, systemic diseases, and infection or drug-induced causes.

I have a friend with some ME/CFS symptoms (among some other autoimmune issues) who had a MRI that found a pituitary cyst if I recall correctly. However, the physician who requests the diagnostic didn't have any suggestions for treatment. I'm always amazed that even when labs sometimes turn up abnormalities, doctors are like, "Nah, we don't need to do anything." Ok, then why run the labs?

 

[sunshine44]

I have a friend with some ME/CFS symptoms (among some other autoimmune issues) who had a MRI that found a pituitary cyst if I recall correctly. However, the physician who requests the diagnostic didn't have any suggestions for treatment. I'm always amazed that even when labs sometimes turn up abnormalities, doctors are like, "Nah, we don't need to do anything." Ok, then why run the labs?

Right?!

It’s why I’ve not pushed to even get the testing I deserve for so long after 7 years in this room because it’s often insane how little they care when they do find something in me. Like the lesions on my brain.

Sigh.

 

[Wishful]

Ok, then why run the labs?

Maybe in case they find something that does need to be corrected? I read that most men die with prostate tumors, but few die from those tumors. Our bodies accumulate defects, but those defects may not be worth the risk or effort of correcting.

 

[Manuel]

𝐍𝐞𝐰 𝐀𝐫𝐭𝐢𝐜𝐥𝐞 𝐂𝐨𝐮𝐥𝐝 𝐑𝐞𝐯𝐞𝐚𝐥 𝐭𝐡𝐞 𝐎𝐫𝐢𝐠𝐢𝐧 𝐨𝐟 𝐭𝐡𝐞 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃!

𝐌𝐨𝐝𝐞𝐥 𝐨𝐟 𝐭𝐡𝐞 𝐧𝐞𝐰 𝐚𝐫𝐭𝐢𝐜𝐥𝐞.

1. 𝐈𝐦𝐦𝐮𝐧𝐞 𝐒𝐞𝐧𝐬𝐢𝐭𝐢𝐳𝐚𝐭𝐢𝐨𝐧 𝐚𝐧𝐝 𝐈𝐧𝐟𝐥𝐚𝐦𝐦𝐚𝐭𝐨𝐫𝐲 𝐑𝐞𝐬𝐩𝐨𝐧𝐬𝐞:

𝐏𝐫𝐨𝐩𝐨𝐬𝐢𝐭𝐢𝐨𝐧: the S1 subunit of SARS-CoV-2 can induce a form of “sensitization” in the immune system. This means that, following exposure to the S1 protein, the immune system becomes more reactive to future inflammatory stimuli. This sensitization leads to a more intense and longer lasting inflammatory response compared to a normal response to an inflammatory stimulus.

𝐌𝐞𝐜𝐡𝐚𝐧𝐢𝐬𝐦: Sensitization is associated with an increase in the expression of antigen-presenting molecules such as MHC-II in brain microglial cells. This suggests that the S1 protein alters the activation threshold of immune cells, making them more likely to respond in an exaggerated manner to future exposures to pathogens or inflammatory stimuli.


2. 𝐈𝐦𝐩𝐚𝐜𝐭 𝐨𝐧 𝐇𝐏𝐀 𝐀𝐱𝐢𝐬 𝐚𝐧𝐝 𝐂𝐨𝐫𝐭𝐢𝐬𝐨𝐥 𝐏𝐫𝐨𝐝𝐮𝐜𝐭𝐢𝐨𝐧:

𝐇𝐏𝐀 𝐀𝐱𝐢𝐬: Unlike pathogen antigens, such as LPS, which stimulate the HPA axis to increase cortisol production, the S1 subunit does not follow this pattern. Instead of increasing cortisol levels, exposure to S1 causes a decrease in basal cortisol levels in the brain and does not activate the HPA axis in the expected manner. This may contribute to down-regulation of inflammation and an uncontrolled immune response.

𝐂𝐨𝐫𝐭𝐢𝐬𝐨𝐥: The decrease in cortisol observed after S1 exposure suggests that the immune system becomes less regulated, which may lead to exacerbated inflammation and increased sensitivity to future inflammatory stimuli.


3. 𝐂𝐨𝐧𝐬𝐞𝐪𝐮𝐞𝐧𝐜𝐞𝐬:

Symptoms and Behavior: S1-triggered sensitization manifests in symptoms such as changes in physical activity, eating behavior, and fever response. These effects are related to alterations in the functioning of the hypothalamus, which regulates multiple physiological and behavioral functions.

Disease Model: Results suggest that exposure to S1 may induce long-lasting changes in the immune system and hormonal regulation, contributing to increased vulnerability to inflammation and symptoms similar to those seen in disorders such as Long COVID.

: https://www.sciencedirect.com/science/article/pii/S0889159124005105?via=ihub


𝐌𝐨𝐝𝐞𝐥 𝐏𝐫𝐨𝐩𝐨𝐬𝐞𝐝 𝐢𝐧 𝐎𝐮𝐫 𝐑𝐞𝐯𝐢𝐞𝐰 𝐀𝐫𝐭𝐢𝐜𝐥𝐞.

1. 𝐌𝐨𝐥𝐞𝐜𝐮𝐥𝐚𝐫 𝐌𝐢𝐦𝐢𝐜𝐫𝐲 𝐚𝐧𝐝 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐢𝐭𝐲:

𝐏𝐫𝐨𝐩𝐨𝐬𝐞𝐝: SARS-CoV-2 protein S induces molecular mimicry with ACTH, generating an autoimmune response against ACTH. This results in hypophysitis and cortisol depletion.

𝐌𝐞𝐜𝐡𝐚𝐧𝐢𝐬𝐦: HLA-DRB1 alleles, such as DR15, can promote immune hyperactivation against the SARS-CoV-2 S protein. This hyperactivation may lead to an autoimmune response due to molecular mimicry with ACTH. In individuals with these susceptible alleles, the exacerbated immune response can result in pituitary damage and reduced ACTH production.

2. 𝐇𝐏𝐀 𝐀𝐱𝐢𝐬 𝐚𝐧𝐝 𝐇𝐨𝐫𝐦𝐨𝐧𝐚𝐥 𝐃𝐲𝐬𝐟𝐮𝐧𝐜𝐭𝐢𝐨𝐧:

* 𝐇𝐏𝐀 𝐀𝐱𝐢𝐬: Autoimmune hypophysitis and decreased ACTH lead to reduced cortisol production. Prolonged exposure to these viral antigens causes pituitary dysfunction and contributes to symptoms such as chronic fatigue and hormonal disturbances. Decreased cortisol levels lead to immune exhaustion by not decreasing T-lymphocyte activation.

: https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1422940/full


𝐌𝐨𝐝𝐞𝐥 𝐂𝐨𝐦𝐩𝐚𝐫𝐢𝐬𝐨𝐧 𝐚𝐧𝐝 𝐒𝐮𝐩𝐩𝐨𝐫𝐭 𝐟𝐨𝐫 𝐭𝐡𝐞 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐞 𝐇𝐲𝐩𝐨𝐭𝐡𝐞𝐬𝐢𝐬.
The new article indirectly supports our hypothesis by demonstrating that the S1 subunit of SARS-CoV-2 protein S induces a neuroinflammatory priming and increases MHC-II expression in microglial cells. This priming elevates S1 protein presentation through MHC-II, which may lead to prolonged hyperactivation of the immune system. This sensitization could increase the propensity of the immune system to respond in an exaggerated manner to future exposures to pathogens or inflammatory stimuli and to attack self-antigens with molecular mimicry, such as ACTH, particularly in individuals genetically predisposed via HLA-II alleles.

Furthermore, the reduction in brain corticosterone following S1 exposure, together with dysfunction in the HPA axis, supports the idea that neuroinflammatory priming contributes to a dysregulated immune response and increased activation of autoimmune processes.


𝐏𝐚𝐫𝐚𝐥𝐥𝐞𝐥𝐢𝐬𝐦 𝐰𝐢𝐭𝐡 𝐀𝐮𝐭𝐨𝐢𝐦𝐦𝐮𝐧𝐞 𝐇𝐲𝐩𝐨𝐩𝐡𝐲𝐬𝐢𝐭𝐢𝐬 𝐈𝐧𝐝𝐮𝐜𝐞𝐝 𝐛𝐲 𝐈𝐦𝐦𝐮𝐧𝐞 𝐂𝐡𝐞𝐜𝐤𝐩𝐨𝐢𝐧𝐭 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬 (𝐈𝐂𝐈𝐬)
Immune Checkpoint Inhibitors (ICIs) provide a relevant example of how immune hyperactivation can induce autoimmune hypophysitis in genetically susceptible individuals (HLA-II alleles). ICIs, by blocking immune regulatory proteins, can cause uncontrolled inflammation of the pituitary gland. This phenomenon is particularly notable in patients with susceptible HLA-II alleles, who may experience an autoimmune response directed against the pituitary gland. ICI-induced autoimmune hypophysitis illustrates how immune hyperactivation can result in significant pituitary damage, similar to that seen in conditions such as ME/CFS, Long COVID and post-vaccinal syndromes.

𝐂𝐨𝐦𝐩𝐚𝐫𝐢𝐬𝐨𝐧 𝐰𝐢𝐭𝐡 𝐋𝐨𝐧𝐠 𝐂𝐎𝐕𝐈𝐃 𝐏𝐨𝐬𝐭-𝐕𝐚𝐜𝐜𝐢𝐧𝐚𝐭𝐢𝐨𝐧 𝐂𝐚𝐬𝐞𝐬.
The immune hyperactivation observed in ICI-induced autoimmune hypophysitis and in the SARS-CoV-2 model in individuals with susceptible HLA-II alleles may provide an explanation for Long COVID cases developed after vaccination. In these cases, exposure to SARS-CoV-2 protein S by vaccination may induce the same immune hyperactivation. This hyperactivation may result in persistent inflammation and autoimmune responses similar to those seen in viral infection-induced hypophysitis, due to molecular mimicry with ACTH and altered regulation of the HPA axis.


𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭.
1. 𝐄𝐥𝐢𝐦𝐢𝐧𝐚𝐭𝐞 𝐕𝐢𝐫𝐚𝐥 𝐀𝐧𝐭𝐢𝐠𝐞𝐧: Use antivirals or strategies to eliminate SARS-CoV-2 protein S and reduce immune hyperactivation.

2. 𝐂𝐨𝐫𝐭𝐢𝐜𝐨𝐬𝐭𝐞𝐫𝐨𝐢𝐝𝐬: Apply corticosteroids to reduce inflammation and, if pituitary damage is present, consider corticosteroids in replacement doses for hormone deficiency.

3. 𝐀𝐬𝐬𝐞𝐬𝐬 𝐂𝐨𝐫𝐭𝐢𝐬𝐨𝐥: Morning cortisol tests may not be reliable for detecting hypocortisolism. Perform saliva cortisol testing in several shots throughout the day for accurate assessment of hypocortisolism.

4. 𝐒𝐮𝐩𝐩𝐥𝐞𝐦𝐞𝐧𝐭𝐬 𝐚𝐧𝐝 𝐀𝐝𝐝𝐢𝐭𝐢𝐨𝐧𝐚𝐥 𝐒𝐮𝐩𝐩𝐨𝐫𝐭: Use anti-inflammatory and antioxidant supplements to support treatment and reduce residual inflammation.

𝐒𝐡𝐚𝐫𝐞 with other patients so they can understand their disease.

𝐌𝐨𝐫𝐞 𝐢𝐧𝐟𝐨𝐫𝐦𝐚𝐭𝐢𝐨𝐧: https://x.com/manruipa/status/1810664159354192253

 

[Wishful]

The S1 hypothesis is interesting, but according to that, wouldn't supplemental cortisol reduce symptoms continually? With ME, it seems that many people report a reduction--even temporary full remission--when first taking it, but then it stops working and doesn't ever work again.

 

[Manuel]

The S1 hypothesis is interesting, but according to that, wouldn't supplemental cortisol reduce symptoms continually? With ME, it seems that many people report a reduction--even temporary full remission--when first taking it, but then it stops working and doesn't ever work again.

It should be noted that there is currently no treatment that perfectly simulates the demand for cortisol. Hydrocortisone is given in substitute doses but it is up to you to increase the dose if you have an infection, reactivation, if you have a long period of stress, if you do sports, etc. In addition, since there are viral reservoirs that constantly maintain inflammation, it would be necessary to give doses that simulate cortisol levels during infections. In other words, it is very difficult to regulate this. Therefore, in addition to taking hydrocortisone replacement doses, you also have to control anything that increases inflammation. That is, it is no use giving you cortisol replacement doses if I don't treat the viral infection with antivirals, for example. It would only help keep you from getting worse.

 

[Manuel]

𝐃𝐢𝐬𝐜𝐨𝐯𝐞𝐫 𝐭𝐡𝐞 𝐒𝐄𝐂𝐑𝐄𝐓 𝐡𝐢𝐝𝐝𝐞𝐧 𝐢𝐧 𝐯𝐚𝐜𝐜𝐢𝐧𝐞𝐬: 𝐀𝐫𝐞 𝐰𝐞 𝐢𝐧 𝐃𝐀𝐍𝐆𝐄𝐑?

Have you ever wondered if vaccines are really safe? Are you worried that they may trigger autoimmune diseases? In our new video on @Foropacientes , we unravel the truth behind vaccines, their importance and how they might affect some people with certain genetic predispositions. you can't miss it!


𝐄𝐱𝐩𝐥𝐨𝐫𝐞 𝐰𝐢𝐭𝐡 𝐮𝐬:

* Are vaccines dangerous or a modern miracle?
* How do they really work in your body?
* The hidden impact on people with genetic predispositions

Click now, stay to the end and 𝐬𝐡𝐚𝐫𝐞 this video with those who matter most to you! Don't forget to subscribe to ForoPatients for more vital content about your health.

𝐖𝐞 𝐡𝐚𝐯𝐞 𝐚𝐝𝐝𝐞𝐝 𝐄𝐧𝐠𝐥𝐢𝐬𝐡 𝐬𝐮𝐛𝐭𝐢𝐭𝐥𝐞𝐬. 𝐘𝐨𝐮 𝐜𝐚𝐧 𝐠𝐨 𝐭𝐨 𝐬𝐞𝐭𝐭𝐢𝐧𝐠𝐬 𝐚𝐧𝐝 𝐬𝐞𝐥𝐞𝐜𝐭 𝐭𝐡𝐞𝐦 (𝐧𝐨𝐭 𝐭𝐡𝐞 𝐚𝐮𝐭𝐨𝐦𝐚𝐭𝐢𝐜 𝐭𝐫𝐚𝐧𝐬𝐥𝐚𝐭𝐢𝐨𝐧).

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[beingsamiracle]

It should be noted that there is currently no treatment that perfectly simulates the demand for cortisol. Hydrocortisone is given in substitute doses but it is up to you to increase the dose if you have an infection, reactivation, if you have a long period of stress, if you do sports, etc. In addition, since there are viral reservoirs that constantly maintain inflammation, it would be necessary to give doses that simulate cortisol levels during infections. In other words, it is very difficult to regulate this. Therefore, in addition to taking hydrocortisone replacement doses, you also have to control anything that increases inflammation. That is, it is no use giving you cortisol replacement doses if I don't treat the viral infection with antivirals, for example. It would only help keep you from getting worse.

Have you read Jefferies 'Safe uses of Cortisone'? I recently looked through the book as I am myself interested in low dose hydrocortisone. Nowhere in the book does he mention antivirals, yet he claims on many years of clinical practice many cases of successful treatment of chronic viral infections among others. Wondering what you think about this, and also what the basis is for your claims!!

 

[Manuel]

Have you read Jefferies 'Safe uses of Cortisone'? I recently looked through the book as I am myself interested in low dose hydrocortisone. Nowhere in the book does he mention antivirals, yet he claims on many years of clinical practice many cases of successful treatment of chronic viral infections among others. Wondering what you think about this, and also what the basis is for your claims!!

Chronic hypocortisolism leads to immunosuppression and increases the risk of both acute and chronic infections. Hence, if you replenish the levels these infections improve. But if there is a genetic predisposition to not control well a particular pathogen such as a herpesvirus or SASRS-CoV-2, this virus will continue to replicate in the viral reservoirs without your immune system being able to control it completely by having this genetic deficiency. In these cases it is necessary to treat both hypocortisolism and infections with antivirals.

 

[beingsamiracle]

Chronic hypocortisolism leads to immunosuppression and increases the risk of both acute and chronic infections. Hence, if you replenish the levels these infections improve. But if there is a genetic predisposition to not control well a particular pathogen such as a herpesvirus or SASRS-CoV-2, this virus will continue to replicate in the viral reservoirs without your immune system being able to control it completely by having this genetic deficiency. In these cases it is necessary to treat both hypocortisolism and infections with antivirals.

Yeah that definitely makes sense. Do you have any resources I could check out for supplementing with cortisone?