With respect to this thread https://www.s4me.info/threads/autoa...ic-fatigue-syndrome-2025-wohlrab-et-al.43586/ These are medications that lower IGG from 2 AI programs. I know some people don’t like it when I use these programs, but unfortunately I don’t know how to use the more sophisticated ones. Chat GPT Yes, certain medications and treatments can reduce or deplete total immunoglobulin G (IgG) levels. Here are the main categories and examples: **1. Immunosuppressive and Chemotherapy Drugs** These suppress the immune system and may reduce IgG production. - **Corticosteroids** (e.g., prednisone, dexamethasone) – reduce lymphocyte activity, including B cells that produce IgG. - **Cyclophosphamide** – cytotoxic to B cells. - **Methotrexate** – inhibits DNA synthesis, affecting B cell function. - **Azathioprine** – suppresses lymphocyte proliferation. - **Mycophenolate mofetil** – inhibits purine synthesis in B and T cells. - **Rituximab** – a monoclonal antibody that targets CD20+ B cells, directly reducing IgG production. **2. Monoclonal Antibodies Targeting B Cells** These are used in autoimmune diseases, cancers, and some transplant protocols. - **Rituximab (Rituxan)** – depletes B cells (most common cause of secondary hypogammaglobulinemia). - **Obinutuzumab**, **Ofatumumab**, and similar anti-CD20 agents – same mechanism as rituximab. - **Daratumumab** – targets CD38 on plasma cells; used in multiple myeloma, reduces IgG. - **Bortezomib** – proteasome inhibitor used in myeloma; suppresses plasma cell function. -m **3. Immunosuppressive Biologics** Used for autoimmune and inflammatory diseases. - **TNF inhibitors** (e.g., infliximab, etanercept, adalimumab) – may reduce IgG in some individuals. - **IL-6 inhibitors** (e.g., tocilizumab) – IL-6 is involved in B cell maturation. - **Belimumab** – inhibits B cell activating factor (BAFF); reduces B cell survival. **4. Plasma Exchange (Plasmapheresis)** Physically removes IgG from the blood. - Often used in conditions like myasthenia gravis or Guillain-Barré syndrome. - Rapid, temporary depletion of circulating IgG. **5. Other Treatments** - **Radiation therapy** (especially total body irradiation) – can deplete B cells and reduce IgG over time. - **Stem cell or bone marrow transplantation** – immune system "reset" can reduce or delay IgG recovery. - **Long-term use of antiepileptics** (e.g., phenytoin, carbamazepine) – rarely, may reduce immunoglobulin levels. --- Deep seek Certainly! Several medications can reduce or deplete **total immunoglobulins (IgG)** by affecting B-cell function, suppressing the immune system, or increasing IgG catabolism. Here are some key drug classes and examples: **1. Immunosuppressants & B-cell Depleting Agents** - **Rituximab (anti-CD20 monoclonal antibody)** – Depletes B cells, leading to reduced IgG production. - **Ocrelizumab, Ofatumumab (anti-CD20 therapies)** – Similar mechanism to rituximab. - **Belimumab (anti-BAFF monoclonal antibody)** – Inhibits B-cell survival, lowering IgG over time. **2. Corticosteroids (Prolonged High-Dose Use)** - **Prednisone, Dexamethasone** – Can suppress B-cell function and IgG synthesis with long-term use. **3. Alkylating Agents (Chemotherapy Drugs)** - **Cyclophosphamide** – Suppresses B-cell proliferation, reducing IgG levels. **4. Proteasome Inhibitors (Plasma Cell-Targeting Drugs)** - **Bortezomib, Carfilzomib** – Used in multiple myeloma; can decrease IgG by killing plasma cells. **5. mTOR Inhibitors** - **Sirolimus (Rapamycin), Everolimus** – May reduce IgG by modulating B-cell activity. **6. Other Immunomodulators** - **Mycophenolate Mofetil (MMF)** – Inhibits B-cell proliferation, leading to lower IgG over time. - **Azathioprine** – Suppresses B-cell function, potentially decreasing IgG. **7. IVIG-Competing Therapies** - **Imiglucerase (Enzyme Replacement Therapy in Gaucher’s Disease)** – Some reports suggest IgG reduction due to unknown mechanisms. **Important Considerations:** - IgG depletion is more common with **long-term use** of B-cell-depleting therapies (e.g., rituximab). - Monitoring IgG levels is crucial in patients on these drugs, as **hypogammaglobulinemia** increases infection risk. **IVIG (intravenous immunoglobulin) replacement** may be needed if IgG falls too low. —————- END AI Interesting that phenytoin came up as there are some patients who reported significant improvements on this.
All of the ### and *** makes this very hard to read. Do you have a version without it? I assume it’s from the formatting by the LLMs.
I'm not sure what the point of this is supposed to be, but it seems like it misses some drugs like Efgartigimod (which has been studied in LC), a whole range of other biologics, newer B-cell targeting mAbs, CAR-T cells and other drugs. I would reiterate what @Utsikt has said, writing a list of different drugs using different categories and manually adding drugs rather than using the AI generated lists seems more useful even when I'm not sure if there is any use. If I'd had to guess a simple google search will outperform an AI search here.
Correct about Efgartigimod https://pmc.ncbi.nlm.nih.gov/articles/PMC6159959/ Neonatal Fc receptor antagonist efgartigimod safely and sustainably reduces IgGs in humans BACKGROUND. Intravenous Ig (IVIg), plasma exchange, and immunoadsorption are frequently used in the management of severe autoimmune diseases mediated by pathogenic IgG autoantibodies. These approaches modulating IgG levels can, however, be associated with some severe adverse reactions and a substantial burden to patients. Targeting the neonatal Fc receptor (FcRn) presents an innovative and potentially more effective, safer, and more convenient alternative for clearing pathogenic IgGs. METHODS. A randomized, double-blind, placebo-controlled first-in-human study was conducted in 62 healthy volunteers to explore single and multiple ascending intravenous doses of the FcRn antagonist efgartigimod. The study objectives were to assess safety, tolerability, pharmacokinetics, pharmacodynamics, and immunogenicity. The findings of this study were compared with the pharmacodynamics profile elicited by efgartigimod in cynomolgus monkeys. RESULTS. Efgartigimod treatment resulted in a rapid and specific clearance of serum IgG levels in both cynomolgus monkeys and healthy volunteers. In humans, single administration of efgartigimod reduced IgG levels up to 50%, while multiple dosing further lowered IgGs on average by 75% of baseline levels. Approximately 8 weeks following the last administration, IgG levels returned to baseline. Efgartigimod did not alter the homeostasis of albumin or Igs other than IgG, and no serious adverse events related to efgartigimod infusion were observed. CONCLUSION. Antagonizing FcRn using efgartigimod is safe and results in a specific, profound, and sustained reduction of serum IgG levels. These results warrant further evaluation of this therapeutic approach in IgG-driven autoimmune diseases.
Efgart failed for POTS. https://www.s4me.info/threads/efgartigimod-vyvgart-what-could-the-trial-data-possibly-tell-us.37316/ Did they look at fatigue/brain fog/sleep?
FYI, you can include "Please use XenForo syntax" in your prompt to the AI and it'll give you text that looks good here. When pasting it into the message box, first click the button at the top right of the message box to use the BB Code Editor:
And pretty much an abundance of other biologics or drugs acting on FcRn (Nipocalimab, Batoclimab, Rozanolixizumab...) as well as newer mAbs to pretty much all targets mentioned above! If you want the list to be complete (I'm not sure why you want this list in the first place) you'll find tons of others drugs by googling something along the lines of "drugs that work similar to..." and then have a look at whether they lower IgG.
I'm not sure what the reference to IgG reduction and the other post is supposed to be. As far as I understand Jonathan has said that total IgG levels probably mean very little and understanding specific pathways and targeting those is all that matters. What is the point of the list supposed to be? A complete list of drugs that lower IgG (then there are many more to the ones above)? Drugs that cause a higher reduction of IgG? Drugs that are more commonly prescribed and reduce IgG to understand if ME/CFS recovery reports should have existed if IgG reduction was important?
Hearing from people who knew of people in the Efgart trial that trial was poorly done and that many patients reported getting a lot better, including severe bed bound patients.
Without any evidence of the opposite, all that tells us currently is that presumably as many people in the placebo group also got better!
Removed some of the visual clutter: 1. Immunosuppressive and Chemotherapy Drugs These suppress the immune system and may reduce IgG production. Corticosteroids (e.g., prednisone, dexamethasone) – reduce lymphocyte activity, including B cells that produce IgG. Cyclophosphamide – cytotoxic to B cells. Methotrexate – inhibits DNA synthesis, affecting B cell function. Azathioprine – suppresses lymphocyte proliferation. Mycophenolate mofetil – inhibits purine synthesis in B and T cells. Rituximab – a monoclonal antibody that targets CD20+ B cells, directly reducing IgG production. 2. Monoclonal Antibodies Targeting B Cells These are used in autoimmune diseases, cancers, and some transplant protocols. Rituximab (Rituxan) – depletes B cells (most common cause of secondary hypogammaglobulinemia). Obinutuzumab, Ofatumumab, and similar anti-CD20 agents – same mechanism as rituximab. Daratumumab – targets CD38 on plasma cells; used in multiple myeloma, reduces IgG. Bortezomib – proteasome inhibitor used in myeloma; suppresses plasma cell function. 3. Immunosuppressive Biologics Used for autoimmune and inflammatory diseases. TNF inhibitors (e.g., infliximab, etanercept, adalimumab) – may reduce IgG in some individuals. IL-6 inhibitors (e.g., tocilizumab) – IL-6 is involved in B cell maturation. Belimumab – inhibits B cell activating factor (BAFF); reduces B cell survival. 4. Plasma Exchange (Plasmapheresis) Physically removes IgG from the blood. - Often used in conditions like myasthenia gravis or Guillain-Barré syndrome. - Rapid, temporary depletion of circulating IgG. 5. Other Treatments Radiation therapy (especially total body irradiation) – can deplete B cells and reduce IgG over time. Stem cell or bone marrow transplantation – immune system "reset" can reduce or delay IgG recovery. Long-term use of antiepileptics (e.g., phenytoin, carbamazepine) – rarely, may reduce immunoglobulin levels. --- Deep Seek Certainly! Several medications can reduce or deplete total immunoglobulins (IgG) by affecting B-cell function, suppressing the immune system, or increasing IgG catabolism. Here are some key drug classes and examples: 1. Immunosuppressants & B-cell Depleting Agents Rituximab (anti-CD20 monoclonal antibody) – Depletes B cells, leading to reduced IgG production. Ocrelizumab, Ofatumumab (anti-CD20 therapies) – Similar mechanism to rituximab. Belimumab (anti-BAFF monoclonal antibody) – Inhibits B-cell survival, lowering IgG over time. 2. Corticosteroids (Prolonged High-Dose Use) Prednisone, Dexamethasone – Can suppress B-cell function and IgG synthesis with long-term use. 3. Alkylating Agents (Chemotherapy Drugs) Cyclophosphamide – Suppresses B-cell proliferation, reducing IgG levels. 4. Proteasome Inhibitors (Plasma Cell-Targeting Drugs) Bortezomib, Carfilzomib – Used in multiple myeloma; can decrease IgG by killing plasma cells. 5. mTOR Inhibitors Sirolimus (Rapamycin), Everolimus – May reduce IgG by modulating B-cell activity. 6. Other Immunomodulators Mycophenolate Mofetil (MMF) – Inhibits B-cell proliferation, leading to lower IgG over time. Azathioprine – Suppresses B-cell function, potentially decreasing IgG. 7. IVIG-Competing Therapies Imiglucerase (Enzyme Replacement Therapy in Gaucher’s Disease) – Some reports suggest IgG reduction due to unknown mechanisms. Important Considerations: - IgG depletion is more common with long-term use of B-cell-depleting therapies (e.g., rituximab). - Monitoring IgG levels is crucial in patients on these drugs, as hypogammaglobulinemia increases infection risk. IVIG (intravenous immunoglobulin) replacement may be needed if IgG falls too low.
Here is what JE said Until JE drops the next chapter of the ME/CFS chronicles, that’s about as much as we know.
Doesn't sound like anything much to do with IgG reduction to my ears (more like something along the lines of very specific interactions of immune complexes, T-cells and IFN-gamma production and various feedbakc loops or something else I know equally nothing of).
The efgartigimod trial had a symptom questionnaire as an outcome (compass?) that many POTS patients say is not a good measurement for the condition. People reportedly had huge reductions in HR and symptoms during tilts, massively reduced PEM and increased step count. None of this was taken into account and the drug company has refused to release the raw data. It could well be placebo but it could well be a real effect. I wish a better designed trial could be conducted but I'm not holding my breath...
Yes, there was even a discord channel where a substantial part of the total trial participants were sharing their experiences (I think that is probably a bad idea, I think many trials aren't set up in a way that particpants should be talking about their experiences publicly to each other). Presumably there might have been some problems in the trial making it hard to even track differences in POTS (it was not an ME/CFS study after all), as one should expect in a trial of Long-Covid! They also used Malmö (Federowski was part of the trial) but of course PEM was not part of the trial (presumably some of the Malmö measurements could pick up some changes if there are indeed significant differences in PEM, but needn't be the case if participants simply increase their activity) and as such was not studied in any way. I have heard that a lot of patients that thought they got the drug said that their TTTs looked normal after 24 weeks and I've also heard of many saying that there were a lot infections. But none of that tells us anything about the study, just like how a reduced HR probably tells us nothing because it's equally possibly that participants in the placebo group had similar improvements, which might not be unexpected in a Long-Covid trial.
