Clinician-scientist, emergency physician, studies risk factors of chronic disease, advocate of health not more health care, opinions all my own.
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May 24, 2022 • 5 tweets • 2 min read
They did a study of Long COVID where they did all the standard tests that many doctors have already done and they didn't find anything either. So they concluded Long COVID should be in the same bucket as MECFS and mental health disorders. Pure gaslighting. acpjournals.org/doi/10.7326/M2…
To be precise, they did labs (BMP, CBC, CRP, Rh factor, ANA, ANCA, ACL, troponin, BNP, serum immunoglobulins, SARS-CoV-2 antibodies, and other immunologic studies), neurocognitive assessment, PFTs, 6-minute walk test, and ECHO. They call this an "extensive diagnostic evaluation."
May 8, 2022 • 6 tweets • 2 min read
Learned that there's something called type 2 asthma, which I had never heard before. It's often assigned to severe patients with poor response to standard therapy. However it's also prevalent among 50-70% of patients with asthma. Instead of "type 1" asthma, there is "non-type 2."
I see a lot of Long COVID patients get diagnosed with asthma, but then are poorly responsive to typical therapy bronchodilators. So then what is this? Type 2 asthma? I'm kind of thinking this is again our way of putting names on things that we just don't understand quite yet.
Jan 29, 2022 • 8 tweets • 3 min read
Reading this article on the disordered vascular architecture of COVID-19 lungs was fascinating, but also something that I didn't know and some long harbored feelings about how doctors approached this disease caused by SARS-CoV-2. nationalgeographic.com/science/articl…
The idea that COVID-19 was a vascular disease predated so many other theories about the damage that occurred after SARS-CoV-2 infection, and that concept was published in NEJM way back in May 2020. That's right May 2020! I wasn't aware of that. nejm.org/doi/full/10.10…
Jan 27, 2022 • 4 tweets • 1 min read
Cytotoxic T cells and activated B cells in the lungs of Long COVID patients that subsequently tested negative for SARS-CoV-2 by PCR on bronchoscopy samples. Sounds like a type of host versus host organ rejection. Note these markers were not in the blood but only in the tissues.
"Despite the presence of ongoing respiratory morbidity, the plasma proteins differentially expressed during acute disease appear to have returned to similar concentrations to those seen in healthy controls."
Dec 21, 2021 • 4 tweets • 2 min read
Though most people will develop a productive neutralizing anti-spike S1 immune response to SARS-CoV-2, here's more evidence that some will produce a non-neutralizing anti-spike S2 immune response that can result in loss of self-tolerance and autoimmunity. nature.com/articles/s4136…
In SARS-CoV-1, anti-spike S2 antibodies were found to be cross-reactive against lung epithelial cells, which suggested the possibility of SARS being an autoimmune attack of the lung. Notably, there is about 90% homology of S2 between SARS CoV-1 and CoV-2. ncbi.nlm.nih.gov/labs/pmc/artic…
Jul 10, 2021 • 9 tweets • 4 min read
Our study explaining the pathophysiology of acute COVID has been published by ERJ, the flagship scientific journal of the European Respiratory Society @ERSpublications. Here, we describe how severe COVID-19 is NOT a viral pneumonia, but a post-viral autoimmune attack of the lung.
The target of this autoimmune attack is Annexin A2, a phospholipid-binding protein, which acts as a cofactor for tPA, ensuring integrity of the pulmonary vasculature and promoting lung elasticity. Antagonism of Annexin A2 would cause lung blood clots, pulmonary edema, and ARDS.
Jun 29, 2021 • 5 tweets • 2 min read
Rheumatology consult please! When I read about Wegener’s most citations say c-ANCA antagonizes cytoplasmic proteinase 3 within neutrophils making them attack vascular walls. What about this study where proteinase 3 is expressed by the endothelium itself? sciencedirect.com/science/articl…
I guess because there were subsequent studies that showed that proteinase 3 was not expressed by endothelial cells? pubmed.ncbi.nlm.nih.gov/10792617/
Jun 26, 2021 • 7 tweets • 2 min read
Everyone hates math but I’m going to give it a shot and see if I can explain something about clinical trials and meta-analysis at least the way that I understand it. Say you have a rare event that you’re trying to prevent. It only happens maybe 1% but when it does it’s horrible.
Then you say there’s this incredible treatment that drops that bad outcome to 0.2% meaning in relative terms it’s effective 80% of the time when used. Based on power calculations you need a trial of 3000 patients to prove this point. Try it yourself here. clincalc.com/stats/samplesi…
May 16, 2021 • 8 tweets • 5 min read
@bryan_neel@farid__jalali We have to be careful not to confuse patient factors that predispose to poor outcomes with factors involved in pathogenesis. It’s an assumption that young patients are not developing this type of abnormal immune response based on statistics of mortality.
@bryan_neel@farid__jalali But I think that any patient who is more than mild or asymptomatic and enters that second stage of COVID-19 characterized by coughing and respiratory distress is experiencing this type of autoimmunity. Age and other patient factors determine who is going to survive it.
Please retweet! This new study could help us understand #LongCOVID. Consider participating if you’re in the New York City area and even if you don’t have persistent post-COVID symptoms or were never infected by SARS-CoV-2 as the study needs you too!
Post-Viral Autoantibodies in Patients with Cognitive Dysfunction and/or Postural Orthostatic Tachycardia Syndrome (POTS)
May 7, 2021 • 7 tweets • 3 min read
Does this make any sense? The endothelial damage is likely due to direct damage by the virus yet the evidence is mixed as to whether the virus actually infects endothelial cells?
Discussion about the B cell compartment states that is confusing why patients with deficiencies in antibody production don’t seem to get very sick. But then no real mention of autoimmunity?
May 1, 2021 • 4 tweets • 1 min read
There are two patterns to identify among doctors (and other health professionals) which signal evidence they might not be getting the diagnosis right. Both types are very prevalent in discussions of acute and long COVID.
Premature closure is a cognitive error where the physician fails to consider the reasonable alternatives and settles on a diagnosis that does not match the clinical characteristics of the disease. This faulty decision making process often leads to delayed diagnosis.
Apr 17, 2021 • 6 tweets • 1 min read
I’m realizing that in modern medicine there are these conditions that are viewed as unpopular siblings in certain disciplines. For instance in rheumatology it might be Sjogrens and in neurology it might be POTS.
Those who study more well defined and understood conditions scoff at the poor research in these areas, question the clinical practices, and often label patients with those conditions as difficult or likely falsely attributing symptoms that might not be real.
Apr 16, 2021 • 5 tweets • 1 min read
Aptamers. Oligonucleotide or peptide molecules that bind to a specific target molecule. I’m almost certain that this is the one big medical advances that is going to come out of this pandemic.
You already see companies including BioNTech doing something similar by deploying mRNA to treat early MS which is an autoimmune disease. These short segments of mRNA get coded into what are the equivalent of aptamers.
