Chapters Transcript Long Covid for the Rheumatologist Course: NYU Langone Seminar in Advanced Rheumatology So today we're gonna talk about uh long COVID or post-COVID. It goes under a number of different names and I've had the pleasure of treating patients now as part of our program over the past 3 years, and there are lots of challenges, uh, for rheumatologists and as well as for other specialists so I the, the talk here is to try to understand a little bit about what post COVID is and uh um talk a little bit about how we might think about approaching it and treating it. So, um, the definition of, uh, post of long COVID or what they call post acute sequelae of COVID-19 is broadly defined as the sign symptoms and conditions that continue to develop after COVID-19 infection. Common symptoms includes fatigue, post-exertion, malaise, shortness of breath, uh, muscle pain, joint pain, paraesthesias, weakness, uh, neurocognitive and neuropsychiatric symptoms. Uh, the CDC actually has tried to separate the different entities and long COVID is really a definition that's more of a definition that has been patient created as opposed to doctor created, and it talks about signs and symptom of disease that last for more than 4 weeks after the initial phase of infection. Uh, may be multi-systemic, may be, uh, relapsing and remitting, uh, may worsen over time, and it may be an overlapping entity. Uh, post-COVID-19 is also similar to long COVID, and it's used to describe any new returning or ongoing health problems after COVID-19. Uh, the medical definition of the medical term is really post acute sequela of SARS-COV-2 infection, and that's used by the medical community and refers to ongoing relapsing or new symptoms or health effects. Uh, occurring after the acute phase of SARS-COV-2 infection. So when we talk about post-COVID syndrome, people talk about it in different ways. So one type of post COVID syndrome people talk about is persistent disease patients who become sick and remain sick. This isn't a different disease, it's really a continuation of their acute, uh, COVID illness. Um, some people talk about diseases that are triggered by COVID, so things like, uh, maybe rheumatoid arthritis, lupus, vasculitis that may be, uh, triggered or caused by, um, COVID, and then the more typical disease, the one we're really here to talk about today is the, uh, PSC, you know, it's a novel disease which has some features of myalgic encephalomyelitis, chronic fatigue syndrome. Persistent disease I'll just touch on, but certainly there are patients who had COVID who then uh go on to have chronic lung disease, they have myocardial damage, kidney failure. Uh, patients who've had stroke or viral encephalitis, hypoxemic brain damage, sequela of vascular events like DVTs or, um, peripheral vascular disease, or acute illness neuropathy, and those we all sort of understand they're not really diseases that are new or novel, they're seen in uh as a sequela of many other, uh, infectious diseases. Um, and persistent disease, um, you know, can occur because there are patients who don't clear their virus. Um, this, um, report by Stein and Nature in 2022 showed that, um, patients even out to, um, 230 days, a virus can still be identified in patients, uh, mostly in the brain, uh, heart and lungs, so patients can have persistent disease, particularly those who are elderly or patients who are immunosuppressed. Now we'll talk a little bit about um what I think we as rheumatologists have been sort of thinking about wondering about can you get rheumatic disease after COVID-19? Will it trigger diseases? So this was the report that was published in the Egyptian uh rheumatologists looking at eight patients who developed rheumatoid arthritis after COVID-19. 4 of them at least do seem to meet what uh what we would consider criteria for rheumatoid arthritis. They had rheumatoid factor, CCP, and at least one of them shown here on the, uh, ultrasound, um, you can see has um evidence of synovitis with blood flow into the synovial tissue, um, and erosive disease. There have been at least 2 case reports of uh systemic lupus erythematosis following COVID-19 new onset. Um, these patients seem like, you know, what we would call lupus. They have ANA DNA antibodies, uh, abnormal kidney biopsy. This patient was treated with cyclophosphamide. Um, the second case is again a patient who presented with nausea and vomiting, found a creatinine of 7.1, high tide or ANA DNA antibodies, low compliments. Had a biopsy that showed stage 4 lupus nephritis and was treated uh appropriately so we know that these cases can occur after COVID-19. Um, there have been reports of newly diagnosed anchor associated vasculitis after COVID-19. There are a number of case reports and then that led to a series here, um, detailing 48 patients who um are reported to have had vasculitis following, um, COVID. This is also a report on um the uh in uh family practice from 2022, uh, looking at um a review of literature of cases of arthritis that have been reported following the um uh COVID-19 infection, and what you can see here is there are cases that reported of reactive arthritis, viral arthritis, new onset rheumatoid arthritis. There are actually reports of gout of an increased incidence of gout following um COVID. Um, so we, we do see reports, we do have at least some people who believe that you can develop, uh, inflammatory conditions after COVID-19. However, the one, group that looked at this, it just was published in, um, in January in, um, arthritis and Care Research, um, and what this group did is they looked at, um, all of the different studies, um, reporting, uh, rheumatic disease following um. Following COVID-19 infections and their conclusion really is that the level of evidence included is very low and it's generally poor and without prospective studies we really don't know if there is an increased incidence of rheumatic disease following COVID-19 infection and this was just a um what they did in the study, how they um. They went through data, identified all the different, uh, cases, they excluded studies, and they found 8080 case reports or small series that seemed to be reasonable and then concluded there wasn't really enough, uh, enough data. All right, so I'm gonna talk a little bit about some of the epidemiology of long COVID. This was from, um, a report by, uh, the CDC, uh, in September. And what we can see and, uh, I think this was uh probably touched on earlier, but we do see that most of the cases of, um, Of long COVID occur uh not in children and not so much in the elderly but really between 18 and 64 years of age, uh, is where most of the um cases are, um, and it's more common in, in, um, women than men which I'll show you in a second, um, but the prevalence is is fairly significant. Uh, this is from, uh, morbidity Mortality Weekly report in August of 2023, and it does show that the incidence of, uh, long COVID is going down, uh, between, uh, 2022 and 2023. The prevalence decreased from around 20% of. Uh, of patients who had COVID down more to about 10%. So it does appear to drop, um, probably because we're not seeing as many severe new cases and patients do sometimes get better, which we'll talk about later also. Uh, this is the crude, uh, incidence ratio about, um, the prevalence of long COVID, uh, in patients who've had COVID 7.3% total, more common in female, more common in people who have had comorbidities, and it also appears to be less common in patients who have had not just one vaccine, not just two vaccines, but two vaccines and a booster seems to offer some, uh, protection against developing long COVID. What are the symptom complexes that we see? This is a study from Bommers, um, which were published in 2022, and the most common symptoms really are neurologic, um, neurologic ailments, uh, mostly what we would call brain fog or trouble focusing, trouble concentrating memory, uh, fatigue is just as common, seen in, um, about 60% sleeping disturbances. Uh, exercise, uh, intolerance, what we call post-exertional malaise, um, joint and muscle symptoms are less common, probably less than 20%, somewhere between 10 and 20%. So it's not something a lot of these patients are not going to necessarily present to a rheumatologist who doesn't particularly specialize in in long COVID, so you may not be seeing these. These were from the Covidome group, which is a German group that basically similar to what NIH is doing. They are uh capturing all their cases and um uh following them longitudinally. So what causes um the um post acute sequela of COVID-19 disease the long COVID. It's still elusive and there have been many postulated ideologies, viral infections, autoimmunity, activation of glial cells, mast cell activation, micro clots, muscle dysfunction, adrenal dysfunction. Uh, and decrease serotonin, and I'm sure all of you, not necessarily even in the medical literature, but just on your, uh, your Facebook or your computer feeds on the news, uh, every couple of weeks you'll hear a new cause of we've understand why people have long COVID, um, and everybody gets excited that we have a new etiology and the patients come in and they say I want to take this supplement or this medication. So I just think we'll look at some of these things and we'll see what the data really shows. So what are the hypo hypothesized mechanism of long COVID, um, immune dysregulation, uh, gut, uh, dysbiosis, uh, vascular clotting, uh, activation of the central nervous system. We'll look at a little more detail. This is just a cartoon from a, um, also was in the um Rheumatology International, and this was at um. Uh, an article on, um, pathogenic method of long COVID in, in rheumato in rheumatologic diseases and obviously in rheumatology we look at antibodies and their, you know, antibody levels being elevated, um, cytokines and, um, such. I'm not gonna go into this in detail, but this is a just a slide, and you could probably look at this if you look at the slides later of the pathophysiologic mechanism may be involved in longOI it's a combination of direct tissue damage, activation of the immunologic systems, um, and activation of the central nervous system, as well as uh psychiatric and uh functional things that may play a role. This is a study from uh Opstein was published in 2023 looking at immune system activation and uh what they showed in the study that there were activation, the expression of activation markers on CD4 and CDH cells in long COVID is increased in patients who continue to have long COVID symptoms versus those who have recovered and what they actually did in. They looked at early long COVID, intermediate long COVID, and then long long COVID and in all cases, they showed that there seemed to be increased activation markers, uh, in patients who had long COVID versus those who had recovered at all three, time frames. Uh, this is another similar study was done by CA, was published in Nature Immunology, uh, just this February, uh, February 2024, and they looked at, um. Uh, that the T cells from individual of long COVID express homing receptor associated with migration to inflamed tissue. So if you look, there, there, there are increased expression of these um receptors on the surface, uh, and the red is the long COVID and in the uh uh blue are the patients who had recovered and you can see that there are increased, um, uh, surface molecules in patients who had, um, who had long COVID. This is from um 2022 Christoph Schulte, um, and his group they published on that IL1 IL6 and TNF cytokine are associated with, uh, post COVID and if you look, I know it kind of comes a little bit small. Let me see if I can go up here, but if you look. Yeah Let me see here. So this is the um the TNF, the IL 1 IL 6, and in all of them, you can see that in the patients in the um the first lines are patients who had um. Who were um healthy controls, patients who had COVID, um, who recovered, patients who had long COVID and then recovered from long COVID and the last group is the one with persistent disease and you could see that in the persistent disease, the cytokine levels remain higher. This is, this, um, is another study looking this time at uh interferon release uh um spontaneous interferon relates from T cells in patients with long COVID and what you can see if you looked at the. That the this is unexposed. These are patients with long COVID or at higher levels of interferon in the next one you have the unexposed patients or the patients who had COVID and recovered versus the long COVID and we can see that they have higher levels of interferon. This is um from a mouse model of um COVID where a mouse were um exposed to COVID had lung infections, and later on showed that um uh post um exposure they had increased um activation of their microglial cells, uh, which affected brain function, hippocampal function, so. Um, certainly we think that COVID may, uh, activation of the central nervous system may play a role in the development of some of the symptoms we talked about, uh, the fatigue and the, uh, cognitive dysfunction as well as the post-exertional fatigue. Gut dysbiosis is another area that has um developed a significant amount of interest, and this was a study that was published in the Journal of the Korean Medical Science in 2023 and showing that there are differences in the, uh, gut, um, microbiome and the different bacteria that are present. Uh, in patients who had, um, um, uh, healthy controls, patients who had COVID and recovered, and, uh, long COVID patients, suggesting that, uh, the gut, uh, flora may play a role in, um. In who has uh will develop long COVID. Um, other people have postulated that the problem is not just that, um, the, uh, COVID-19 virus is a, um, causes the long COVID, but it's reactivation of other viruses and things like HIV-6, CMV, and EBV have been postulated to possibly play a role in the patients developing, um, post-COVID syndrome, and this was a, um, a study done in virus research in 2023 showed that by PCR that patients who had, um. Long COVID compared to those who recovered they had higher levels of uh EBV. This is not a post COVID study. This just showed that patients who had COVID-19 um had higher levels of EBV, so suggesting that um that EBV may be activated by COVID-19 infection. Um, this is something that you may have seen a lot of it's, it's been, um, brought up a lot in the late press and probably brought up by patients. The issue of that micro clots or small clots in the circulation are the cause of, um, long COVID, and most of the data on this came from one group, uh, Pretorius in South Africa, and they published a number of, um, mechanistic studies basically taking um. Uh, uh, blood centrifuging out the serum, um, uh, using, um, Taking the healthy plasma, um, degrading it, and then having it looked at, um, using fluoresce, um, microscopy and what they show is that I'm sure you may have seen some of these pictures, um, but the patients with, um, persistent, um. You know, with COVID-19 active have been shown to have these micro clots they're not seen in controls, they're not seen in diabetics and then here are the long COVID patients with these little squiggly lines, these green squiggles that are supposed to represent micro clots. um, it's really all of the data is from the one group and um it's a proprietary system that they um that they will sell to doctors, um, and they are advocating in some cases, uh, anticoagulation. Uh, as treatment in patients who have these so-called micro clots, um, we can talk, we'll talk about that a little bit more later. Uh, this was recently published in Cell in, um, October of this year and has again gotten a lot of, uh, play. I mean, a lot of my patients are calling up and saying they want to be tested for their serotonin levels. They want to be treated, and this was published in Cell, um, showing, uh, that there are reduced serotonin in patients who have, um, post-COVID syndrome. Um, and if you look here on the slide, I think some of this, this study was basically they, they did some data with humans and some mouse models, but if you look here at J in the corner, um, you can look at patients who are healthy controls, patients who had. Healthy controls patients who um had COVID patients who recovered, and then patients with long COVID and the level of serotonin is much lower in patients with um post COVID than patients who've recovered um it's actually at the same level. I so I go back to the first two. Um, are patients who had who have active COVID-19, so the level of serotonin decrease with active COVID-19 increases in patients who recover and then decreases in patients who who have persistent, uh, long COVID symptoms and then through their mouse model they looked and they found that um this is probably caused by decreased intensive absorption of serotonin, increased conversion of serotonin to its metabolites. Um, and what they were able to show in their animal models is that you can inhibit, uh, hippocampal function, uh, mediated by the vagus nerve by having the low, uh, serotonin and that by giving, uh, fluoxetine, uh, it can, um, reduce the effect of the diminished serotonin. And again, these are in mouse models. Recently there was this article published which was published just in this February showing that there are muscle abnormalities in patients with uh COVID, and it may correlate with the post-exertion and malaise. They showed that there's decreased oxygen and utilization, decreased strength and decreased exercise ability, and then if they did um muscle biopsies on these patients, they would find that there were abnormalities in the muscles, um, decreased, um. Decreased mitochondria, abnormal, uh, uh, red fibers, uh, replacement of the type 2 fibers so it really suggests that there is a muscle issue. Now one thing that this doesn't really address is, is this a problem just that patients are deconditioned, um, this may not necessarily be a cause, but it may more be the effect of the uh long COVID rather than the cause of it. Some people have suggested that the reason for long COVID is just a persistent disease and there's still low grade disease. Uh, this was a report from 2022 report on two patients who had persistent virus, uh, in long COVID, even, uh, two years after their initial diagnosis, and they found one was in the skin and one was in the, uh, appendix. People have talked about mast cell activation being uh present in COVID. There's really no, uh, scientific studies looking at mass cells, looking at histamine and such. This is really just a Uh, study where, um, basically taking, um, calling patients and asking them about their symptoms and this reports that there are symptoms of mass cell activation but if you look at the symptoms they're really the same symptoms that we see with long COVID, so patients will have fatigue, achiness, tiredness, brain fog, and then a few other things like uh. Rashes, um, you know, finding that they, um, feel worse if they have a, if they eat a high histamine diet. So I don't think this really tells us very much, but it just brings up the idea that mast cells potentially could be important. Uh, this was recently published, um, and in, um. Um, in nature, uh, came out, uh, just this, um, December, uh, from Sinai and Yale, uh, David Petrino's group, and they were looking at different biomarkers, uh, that might help us, and what this study showed is that there appears to be decreased cortisol in patients with long COVID. So if you look at healthy controls. Um, this is healthy controls. This is patients who had COVID and recovered. These are the patients with long COVID and they had much lower, and this was an external group, another group of patients, not from their group who had long COVID, and they also had low levels of cortisol, and you can just see it also here, the big purple one here are the long COVID patients and they had low cortisol. So adrenal dysfunction may play a role and certainly a potential target would be to um. To repeat the uh cortisol deficiency. So as of now there is still no FDA approved treatments for um for long COVID. Everything that I'll talk about here are based on um you know, speculation and um uh small small um studies but right now I can't say to you that anything has been proven uh to work. Um, so people have different approaches. So this is an article by, um, Don Goldenberg, which is published in Arthritis Care Research in 2023 where his suggestion is that if you, when you have a patient that has symptoms after COVID, if they have evidence of inflammation, ongoing infection, they should be treated but if you cannot identify. Organ damage either from from clinical exam blood testing that you should use um our models like fibromyalgia and chronic fatigue and try to treat the patient symptomatically so multidisciplinary clinics um trying to treat sleep pacing, take patients appropriate rest and then medication maybe when needed, but he is um. Um, cashing against aggressive, unproven treatments until we have a better understanding of the, uh, illness. Um, so this is interesting. So we, um, we're talking about like what is out there and, um, what is being, uh, studied for, um, long COVID, and this was a sympto uh systematic review of all the trials that were ongoing based on the WHO registry and basically they were able to look at all studies for COVID and we're able to identify that there are 388. Uh, registered trials to treat long COVID and here's a list of all the things that are being studied. There are a number of different medications. There are 5 trials with colchicine. Um, there are trials with a number of antivirals. There are trials of hyperbaric oxygen, electrical stimulation, trials of rest, trials of, uh, education, so many different things out there and unfortunately most of the drug trials here, uh, don't seem to be published, uh. We all think about steroids. I certainly as a uh clinician and a rheumatologist, and I have patients who have long COVID and they're having lots of symptoms, joint pain, uh, fatigue and stuff, you think about giving steroids, well, this is the only study that I could find a study a report of um. Of looking at uh prednisone for um long COVID and they were able to show that you're able to decrease immuno you know immunologic, decrease sed rates, CRP, uh, cytokines, but basically if you look clinically it wasn't that impressive. These patients received 30 mg of prednisone. Uh, for 4 days, so it was not necessarily a long course and some of the patients that they had in the study had some mild improvement in their or partial improvement in their pain, their fatigue, but there was no dramatic improvement in most of the patients. Colchicine, um, we have no published data. There are again 5 clinical trials ongoing. I have personal communication from Doctor Michael Pilinger that it helps. Um, I've used it a few times, um, you know, I'm not sure that I would recommend it as a first line, um, but it's something that we'll, um, continue to think about. Uh, low dose naltrexone, which I think a lot of us, uh, who are treating, um, long COVID think, uh, has potential benefit, um, and there were, there were two clinical studies that were done, um, this, uh, first one definitely showed, uh, and it's a, it was a observational study, so there was no no control group, but the patient did respond in terms of fatigue, sleep, uh, and overall function. Um, and again it was a positive study. This is the 2nd 1 looking at the safety of, um, naltrexone, um, 36 patients, and there was a significant improvement in overall feeling better, um, energy, um, ability to, uh, concentrate again positive studies, but these were, um, had no control groups. These were just, um, you know, just, um, uh, patients treated and then monitored, uh, two months later. Um, all of you probably know about this. Um, there was a report that came out in this neuroimmunology reports of the combination of, uh, Guanfasine with NAC for, um, for post COVID syndrome, and it got a lot of press and patients were coming in asking for this, um, basically with a report of. 12 patients, 4 of whom dropped out, uh, and 8 patients reported improvement and again there are theoretical reasons why these things would work, would work, um, in helping, you know, deactivate the glial cells, helping with neurotransmission, but certainly you know the you know 8 patients, uh, um, um, reported it's certainly not a study. This is, um, especially on, uh, with knowing that, uh, serotonin levels appear to be low. Here's a study of 95 post-COVID patients treated with SSRIs, um, significant positive study, um, but no control group, uh, patients got better in terms. In terms of uh depression, not not unexpected fatigue, um, cognitive function, it was actually quite a positive study but again no control group and we don't know if it's really affecting the mechanism or it's just helping patients function better. This is an open label trial of Amantadine on uh post-COVID fatigue, uh, again, no, no control group, but a very positive study in patients fatigue, uh, did, did get better. It is something I think to consider now in your post COVID patients who have a lot of fatigue. Um, this, um, this, um, report is from, uh, Germany. In Germany, um, there has been a push to treat patients with long COVID with therapeutic apheresis, and again, most of here is this study reported that, um. They, they were able to show that they were able to remove autoantibodies, cytokines, uh, toxins, which is not unexpected since we know the technique works, but they didn't really report on how the patients did. They, they referenced their prior study where they talked about a 100. Um, 1,111 patients with either MECSF, uh, 13% they classified as long COVID, and they said that all the patients reported to get better. So that's all, all we know, but I'm certainly, um, you know, we don't have any real data on apheresis. Hydroxychloroquine is something that obviously as rheumatologists we're all, um, you know, we think maybe this will work. We've we've all used it in our patients with autoimmune disease who have fatigue, but again, no, no published data. There was one letter by um Wand and zoo and clinical rheumatology suggesting that it may work based on the mechanisms and it's probably a low risk drug. I would love to get some data on um hydroxychloroquine. Uh, statins have been shown to reduce mortality and hospitalized patients with COVID-19. It has immunomodulatory and anti-inflammatory effects, but there's really no data as monotherapy. Uh, Patterson reported in a group of patients with, again, no control group using Pravastatin with uh meraviro, which is an antiviral, it's a, um. Uh, uh, CCR5 receptor antagonist to try to disrupt monocyte endothelial platelet access and they reported that, um, that there was improvement in biomarkers and then a statement that the patients also felt better. Hyperbaric oxygen might make sense, um, and this is the follow up um this group did a controlled study and seemed to show a benefit uh they then they followed their patient out for um one year and showed that compared to baseline patients did have improvement and improvement in a general global assessment score on the left, uh, in the middle, this is a sleep study, a sleep score which improved. And the third one is just uh uh a group of symptoms, fatigue, pain, cognitive function and again that out going out long term, the patients continued to have some benefit with the hyperbaric oxygen. Vaccines. So you would think, do we talked a little bit, um, when I showed you the CDC data that vaccines may help prevent long COVID. Um, so the question is, can it be used as a treatment? And while it isn't that impressive in all of the studies on post-COVID, getting vaccine either before or after, the trend seems to indicate that patients who are vaccinated have fewer long COVID symptoms, so it would be a very reasonable thing to offer your patients who haven't been vaccinated the vaccine if they have long COVID. Um, we talked a little bit earlier on about the micro clots. This is the same group that, um, had published the data that showed you the green squiggly lines, um, and this, this would they published their, um, efficacy on treatment with triple anticoagulation, which is, uh, aspirin, um, abixaban, and clopidogrel. Um, and this was their pre-publication report which showed, you know, dramatic improvements in joint pain, palpitation, shortness of breath, cognation, and fatigue, and it looks very impressive except this has not been published anywhere, so it was listed as a pre-publication report, uh, not peer reviewed, uh, and it's never actually been published, so we don't know if this data really is, um. Is reliable so I certainly have not treated patients with um anticoagulation in this way it's a pretty aggressive therapy. Um, hi, um. I, um, using, um, IVIG, um, there was this one this is one report from Frontiers in Immunology in 2022, uh, looking at, um, the, uh, the potential benefits on pulmonary neurologic and cardiac symptoms, uh, in this group, they had, they had 9 patients, they treated 6 with no control group. They gave 0.5 g per kilogram of IVIG every two weeks and their report was that all their patients felt better, um, and the NH is actually now in the process of funding an IVIG study so we should get some data at some point soon. Other treatments we do know that Paxlovid does not prevent post-COVID syndrome. We don't know yet whether Paxlovid can improve established post-COVID syndrome. There are a number of studies that uh were ongoing on this. There were case reports suggesting the benefits of uh antihistamines. One of the things that I've been interested in are any of our biologics going to be helpful? So should we be using um. IL-6 inhibition should be using um anti TNFs or anti-interferons um and the answer is we we don't know yet. There was one case of a patient who had RA who had was off their biologics when they had COVID, developed long COVID, went back on the biologic uh the tosillizumab and seemed to be better after restarting it. Obviously one patient does not make a, uh, a recommendation. So conclusions we really have no FDA approved therapy we have no real convincing data um we're starting to understand the pathophysiology hopefully that will help lead somewhere. Remember, just because we can show that there is a high cytokine or an abnormality doesn't mean that's the cause of the disease or that giving that medication is going to help. So just because we can inhibit things we we don't know. Um, I think right now the appropriate approach is to try to treat your patients symptomatically if they need sleep medication, anxiety, or antidepressants. I think if they have neuropathic or inflammatory pain, that should be treated. Uh, consider low dose naltrexone. Uh, patients with post-exertional malaise should be encouraged to rest. That was one of the things that was. You know, a big discussion early on in our post-COVID group and really across the country, patients should not be pushed to exercise and get up and do things. They really do need to rest. Many patients do get better over time. Uh, the COVIDone group in Germany just reported it just came out a couple of weeks ago, and I didn't have a chance to make a slide, but about 50% of their patients over two years got better. Uh, the patients who are the least likely to get better were patients who were male. Uh, older age, uh, and, um, less than 12 years of education. So we do know that patients get better and so that is something that you can tell your patients and um. And hopefully that will give some hope. So I think we're gonna see patients get better. I think it's important to be supportive and respectful. These patients are very, it's a very difficult thing with the post-exertion malaise. uh, the patients are very disturbed. They're often young healthy people who are now, you know, can't work and can't function. So hopefully we're gonna get more data and uh we're gonna learn more about the uh illness. Thank you very much. Yeah, then got time. OK, so I, I guess it's maybe more of a long winded comment, but maybe there's a question. So, and I'm gonna blame my comment on Jerry Weissman because if Jerry Weissman were here, he would stand up and he would say, we all, a lot of us in this room trained under him and you know what I'm gonna say he would say that you know that this area of study now and not to disparage anybody uh including yourself but that this is just another iteration of. Of, uh, uh, silicone breast implant patients who develop pain syndromes and post-ly fibromyalgia and then it's all just a tautology and it's kind of a, it is what it is because it's true because it's true and these patients must have a disease and again I'm not commenting whether I believe all of that, but Jerry would say something like that so in in keeping with. You know, kind of primum no no sere and you know how do you, Bruce, I mean, I know you see a lot of these patients, um, how do you reconcile kind of doing something productive for your for your patients but not giving them plasma foresis, you know, I, I think that is, that is a problem because there are, you know, a huge number. There are Facebook groups and. All kinds of patient advocacy groups who are proposing the very aggressive treatments and there are doctors there are concierge post COVID clinics and experimental post COVID clinics who are doing rituximab and. Um, in those treatments, um, I will tell you, and again, you're talking to somebody who has treated people with fibromyalgia for many, many years, and I've been post-yme disease. The demographic of this is different. Um, you know, it really cuts across all groups. I mean, I don't say, but, you know, we see, I've seen, you know, men, women, people who were, you know, varsity athletes, people who were, you know, people who were not people who had. Medical illnesses previously. I, I, I don't think this is what you're getting at that this is a large group of hysterics or any anything like that. I think that if you look at the demographics, it really cuts across in a way that I feel very comfortable, you know, accepting that this is, is a, is a, is a true illness and, and the patients are very unhappy with their, their symptoms, but. I don't know that the answer is gonna be what we want, which is, you know, take this pill, take this shot and you're gonna get better. I try to, when you look at it, there are patients who have post COVID who have very high cytokines who have high sed rates who are ill, and then others who aren't and maybe they're different groups. And you know, certainly I have given people, you know, short courses of steroid and seen some improvement. Now again, you could say that anything will, you know, can have a placebo effect, but I, but I think that there is more to this, and I think the patients are clearly different if you look at all the things that I've, I've talked about, um, but it may just be one of these things that you know we're not gonna see as much COVID people aren't gonna be as sick it may go away without us ever getting an answer so. Just hi so I just um going along with trying to be supportive of these patients and you've mentioned that many of them can't work and I think as part of physician do no harm is trying to balance understanding the patient and trying to be supportive but I hate seeing young people ruin their career and going. And supporting disability because often the insurance companies, the disability insurance companies end up not supporting it and then they have. You know, a gap in their career and that sort of long term effects of that so I'm just wondering what your experience has been and how you handle this being off work. Well, I think that, you know, again I, you know, I see obviously a lot of patients and, and I think these are patients who are sick and I think a lot of these patients legitimately can work. Um, insurance companies have been, I think, more receptive to post-COVID than they had been to fibromyalgia, MECSF historically, and I've certainly not had a lot of difficulty with patients who need short-term disability, and a lot of my patients over the course of a year or two have gotten better, gone back to work, um, some patients, so, so I've seen this. As a, you know, when patients are, have, you know, have their acute process and, you know, take a 234 months disability, a lot of them, it has been very therapeutic, um, so unlike other illnesses, you know, fibromyalgia, there, there's a lot of data suggesting that exercise can be helpful in these patients that's not been what most of the experts have. Suggested so I think there is a legitimate need in some of these patients for disability and I think you have to be a little bit supportive of that until at least we get more data on it. A quick question, um, since most of the symptoms have to do with neuropsychiatric manifestations, are there any, uh, uh, imaging studies, any control studies about imaging MRI, PET scans, uh, with the head I mean there are, there are, there are some, uh, something that I've seen. I mean, fairly conventional imaging has not shown anything very interesting, but there are some suggestions that on that you can see differences on advanced imaging, um. You know things like quantitative uh MRI's and, um, you know, advanced imaging that there may be some differences in some of these patients but not on most conventional uh imaging that we do and you know LPs most of the time have been normal as well so it's really looking at cytokines and probably advanced imaging that we get a sense that there are differences here. OK Published March 14, 2024 Created by Related Presenters Bruce Solitar, MD View full profile
CME Knowledge Hub
