USA: Mount Sinai PACS clinic and Dr David Putrino

"We received feedback that folks are not so eager to enter a placebo-controlled trial for fear of being in the placebo arm.

So, for our trial looking at low-dose rapamycin for Long Covid we now have an open-label extension added to the trial so everyone gets to try it! Reach out!"
 
Mij said:
"We received feedback that folks are not so eager to enter a placebo-controlled trial for fear of being in the placebo arm.

So, for our trial looking at low-dose rapamycin for Long Covid we now have an open-label extension added to the trial so everyone gets to try it! Reach out!"
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It isn't clear if there is more screening of participants, or pre-treatment stratification of people with persistent symptoms after Covd-19. I mean, is there any reason to think that both someone with e.g. breathlessness due to permanent lung damage as a result of severe Covid-19 and someone with ME/CFS following mild Covid-19 will both be improved by the treatment.

I think we need researchers in this field to start educating the public that Long COVID is an umbrella term covering a range of pathologies, and to be very clear about that fact themselves.
 
Hutan said:
It isn't clear of there is more screening of participants, or pre-treatment stratification of people with persistent symptoms after Covd-19. I mean, is there any reason to think that both someone with e.g. breathlessness due to permanent lung damage as a result of severe Covid-19 and someone with ME/CFS following mild Covid-19 will both be improved by the treatment.

I think we need researchers in this field to start educating the public that Long COVID is an umbrella term covering a range of pathologies, and to be very clear about that fact themselves.
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From https://clinicaltrials.gov/study/NCT06960928 :

Inclusion Criteria:
  • Provision of signed and dated informed consent form
  • Any sex, aged 18+
  • Must be able to attend all study visits located at 5 East 98th St, New York, NY
  • Diagnosed with:
    • Long COVID
      • Documented clinical history of confirmed or suspected acute SARS-CoV-2 infection a minimum of 6 months prior to contact with the study team
      • Formal diagnosis of Long COVID from a physician
      • At least a six-month history of one of the following symptoms following SARSCoV-2 infection:
        • headache, memory loss, insomnia, mood disturbance, chest pain, palpitations, shortness of breath, cough, muscle pains, joint pains, or GI upset
        • AND at least moderate fatigue (measured by Fatigue Severity Score)
        • AND at least moderate post-exertional malaise (PEM) (measured by DePaul PEM screener)
        • Participants who are willing and able to comply with all data collection, treatment plan, laboratory tests, lifestyle considerations, and other study procedures.
        • Baseline EQ-VAS ≤70; EQ-VAS before the index infection ≥80 (this information is collected before randomization as part of the baseline survey)

Exclusion Criteria:
  • Pre-existing conditions including, but not limited to:
    • Autoimmune conditions such as Chronic EBV, Multiple Sclerosis, Hashimoto's Disease, etc. which would impact the immunological profiling analysis.
    • A pre-2020 diagnosis of another Post-Acute Infectious Syndrome such as Chronic Lyme disease, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, etc.
    • Documented history of vaccine injury
    • History of lung or liver transplant
    • Known hepatic or renal impairment
    • Weighing less than 40 kg
    • Or any other chronic condition that has the potential to impact on immunological profiling, at the discretion of the research physician
  • Current use of sirolimus
  • Taking a medication with known interactions to sirolimus:
    • Strong CYP3A4 Inhibitors - clarithromycin, telithromycin, nefazodone, itraconazole, ketoconazole, atazanavir, darunavir, indinavir, lopinavir, nelfinavir, ritonavir, saquinavir, tipranavir, such that dose reduction may be necessary
    • Strong CYP3A4 Inducers - carbamazepine, dexamethasone, ethosuximide, glucocorticoids, griseofulvin, phenytoin, primidone, progesterone, rifabutin, rifampin, nafcillin, nelfinavir, nevirapine, oxcarbazepine, phenobarbital, phenylbutazone, rofecoxib (mild), St John's wort, sulfadimidine, sulfinpyrazone, troglitazone, and grapefruit, such that dose increase may be necessary.
    • Drugs that may increase concentration when given with sirolimus - Verapamil, such that dose reduction may be necessary
    • Other drugs that have the potential to increase sirolimus blood concentrations include (but are not limited to): fluconazole, clotrimazole, troleandomycin, nicardipine, cisapride, and metoclopramide
    • Concomitant use of angiotensin-converting enzyme (ACE) inhibitors may increase the risk of developing angioedema.
  • Febrile illness within the last 3 months of planned baseline evaluation
  • Treatment with another investigational drug or other investigational intervention within 3 months of planned baseline evaluation
  • Prophylactic use of aspirin (325 mg daily) for cardiovascular indications will be permitted in participants. All other medications for chronic medical conditions should be initiated at least two months prior to enrollment.
  • Uncontrolled diabetes, unstable ischemic heart disease, clinically significant underlying pulmonary disease, history of an immunodeficiency or receiving immunosuppressive therapy; history of coagulopathy or medication condition requiring long-term anticoagulation; history of hepatic impairment; taking angiotensin-converting enzyme (ACE) inhibitors
  • Participants who are planning to be or are pregnant
  • Participants who are nursing
Ages Eligible for Study
18 Years and older (Adult, Older Adult )
Sexes Eligible for Study
All
Accepts Healthy Volunteers
No
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So it seems like COVID-triggered ME/CFS with or without other issues caused by COVID.
 


We have known for a while that #LongCOVID pathobiology for many involves reactivation of various herpesviruses. As we continue to validate this it is great to see this work coming out in collaboration with @VirusesImmunity’s incredible team.

Paper already posted.
 
Long thread

“A thread today about Immunoglobulin G (IgG) antibodies to various pathogens and why they seem to be elevated a lot in people with #LongCOVID, #MECFS, chronic #lyme/tick- and vector-borne illnesses and other complex chronic illnesses. First, let's start basic: what is IgG?”
 
Liface said:
Do you have any actual criticism of the information proffered, or are you just here to ad hominem?
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Putrino is not an immunologist. He has been an author on several papers that make naive immunological statements and others that describe poorly designed studies. I fail to see why he should be using X to teach the world about what IgG is. It looks from the post that i can see that he overinterpreting some data.

Personally, I think it is entirely appropriate to make critical remarks about individual people claiming to be presenting cutting edge science. If nobody points out poor science we get nowhere. When I was trained someone pointing out the poor science was considered a mark of the quality of the meeting or institution. You did not get away with stuff at the Hammersmith Hospital Department of Medicine or an early Keystone Conference. Americans often complain about Europeans criticising American scientists but the Amercians are the first to criticise anyone else.
 
Liface said:
Do you have any actual criticism of the information proffered, or are you just here to ad hominem?
Click to expand...
He seems to be suggesting a subset of people with higher IgG in comparison to the “average” population. But of course these exist in healthy people as well. Either you have to demonstrate that they are more common in the total set than they are in the healthy people (and we've had countless negative study results on that front), or that you can somehow predict who they are or prove something that is specific to this set, for example via a therapeutic trial. None of this has happened, so it’s just the old folklore with circular logical, no different from arguments on recommending CBT/GET for subsets.

Other than that he seems to be talking about evidence of HLA links (HLA-DQ and HLA-DR) in Long-Covid, ME/CFS and Fibromyalgia, but as far as I’m aware previous HLA links (in the Norwegian study) for ME/CFS didn’t replicate and DecodeME found no such links (there was one remaining question surrounding HLA after the preprint, but I thought that had now been answered negatively) and for Long-Covid and Fibromyalgia there seems to be no good genetic studies to start of with that would be able to provide such evidence in the first place (and I don't recall it being discussed in studies such as https://s4me.info/threads/the-genet...lion-individuals-2025-kerrebijnet-al.46326/)?

So it just seems like babble?
 
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