Infectious Rheumatology (5.15.2026) Save

Hi, everyone. This is the Room Now podcast for 05/15/2026. I'm Jack Cush with RheumNow. Before we get into the podcast, I want to remind you about a series of videos that are on the website. They're called advanced practice room.

These are designed to be short, mini lectures, ten to fifteen minutes on topics, and I did these really for people who are just starting out in rheumatology. And I think you should refer your residents, your students, your fellows, new hires, physician assistants, and nurse practitioners who are starting out with you to check these out. Again, there'll be about 13 or 14 of them. The ones that are up there right now include these mini lectures, again up to about fifteen minutes, on evaluation of musculoskeletal complaints, evaluation by laboratory tests including rheumatoid factor, CCP, and another one on acute phase reactants, sed rate, CRP. I have lectures on lupus, fibromyalgia, difficult to treat RA, Still's disease, and glucocorticoids.

And soon to follow is going to be spondyloarthropathies and psoriatic arthritis. So they're there, they're for the people that you want to get up to speed on, topics in rheumatology and the evaluation and care of the patients that we take care of. This week on the podcast, a lot of, interesting reports. There was a letter to the New England Journal about a week or two weeks ago, wherein someone reported on their ten year study of one hundred and forty seven patients undergoing, partial meniscectomies by arthroscopy. And, you know, this is a sort of standard of care where they do, you know, they fashion the damaged meniscus, by arthroscopic repair of it and, leaving some in place.

And they do these for degenerative tears. In this specific study, one hundred and forty seven patients who did not have a coexistent knee OA were either treated with partial meniscectomies or with sham surgery. And they looked at ten year outcomes and showed no benefit to the meniscus surgery over sham surgery. In fact, they may have in fact done worse. And there is some literature out there about, and especially in people who have OA, that if you do, meniscal surgery that or you try to clean things up in the knee with the meniscus and such structures, you may worsen the OA and whatever.

So that's why there has been this move, over the last ten years to manage those conservatively, and not take them to surgery. A number of good reports this week relating to rheumatology but being infectious in nature. JAMA Insights presented a case of chikungunya, I'm sorry. It was a review of Chikungunya, basically saying that it's a worldwide disorder affecting thirty five million people, and it's mainly in the tropics and subtropics. It can be in The Caribbean.

The people who are affected here are those who live there or people who travel there. As you know, this is a mosquito borne alpha virus, and, I've seen a number of cases in the last several years since we started reporting this. They do have fever, they do get arthritis and polyarthritis. Less so do they have rashes, myalgias, nausea, vomiting, constitutional things, conjunctivitis, rarely myocarditis. But I like these reports because I think I like saying the word chicken ganya.

It sounds to me like an entree item on a fusion restaurant that I might have visited in Jamaica, but actually the word chicken ganya comes from, the local language in Tanzania and Mozambique where the word means to bend up or to become contorted. Yes. I did look this up. And what they're describing really is the bent over posture of those who are suffering with severe joint pain and arthralgia. So the word chikungunya comes from the musculoskeletal manifestations of chikungunya.

That's rheumatology trivia, advanced trivia that you now know. JAMA Dermatology did a case of parvovirus b19 affecting an adult. That was kind of cool. 40 year old, two days of asymptomatic red rash on the cheeks, but also in the inguinal region, flanks, axilla, fever 39, arthralgias, the rash, the white count was 2,000, the rest of the CBC was normal, the sed rate was normal, the CRP was really elevated 1.24 milligrams per deciliter, that's 12 milligrams per liter, and it was diagnosed by PCR to identify the parvovirus. Again, as we get older, we are all going to be exposed to parvovirus and we may not get the infection, the vast majority of us won't.

And by the time you get above 60, the majority of the population has, you know, IgG antibodies to parvovirus and should be protected. The group that's probably least protected serologically, meaning they've not had exposure, are in fact, women in their childbearing years, which is why this is an issue when women get infected that they could pass this on, to the child. So the point here is this does happen, this does happen in adults, and, serologies are not useful. You need to do PCR to make the diagnosis. When it happens, symptomatic management, although I've had, I think I've had like two or three patients that started out with proven parvovirus B19 that ended up with a chronic arthropathy that I then had to at some point, you know flip the switch and stop calling it parovirus B19 polyarthritis and start calling it seronegative RA.

That happens too. One of the most common complications in clinical trials, in RA trials that I've done and other the most common adverse event that gets reported is non serious infectious events, NSIEs. I've written about that in the past with Katherine Dow, Will Dixon, and the BSR has written about that. This is the most common thing. It may occur in thirty to sixty percent of patients.

But the question always is, do our drugs, advanced drugs especially, target synthetics, do they cause more NSIEs? And the answer has always been no. But and this is far far far more common than the serious infectious events, which are hospitalizable, needing IV antibiotics, etc. A patient survey study coming from the arthritis power registry, it's now also called the patient spot registry, looked at three fifty one patients who were doing periodic surveys. And against these three fifty patients they had four thirty nine non seriously infectious events.

So the important thing here is that the thing that was associated with these events was steroids at ten milligrams per day or greater. But biologics and JAKs had no greater risk compared to patients who were just taking conventional DMARTs. So, again, that may have some teaching value for you or not, but the real thing is what you're probably not doing. Still, way too many of you are stopping biologics or halting and delaying infusions in people who have the sniffles. You know, it's a non serious infectious event.

They're not going to get hospitalized. They usually don't have any fever. You know, I've always treated them on and told them don't stop. Don't stop until I tell you to stop. Because once they stop, they don't know when to go back on and then they flare and they get worse and the main driver of infection non serious and serious is going to be disease not under control.

So I say don't halt the infusion, hold the infusion unless the patient's got a serious high fever or gets hospitalized. Otherwise power through, it is the right thing to do, and there are many sources that say that not just me. We've talked a lot in the past about the risk of TB and mycobacterial infections, and many of you worry about what can I do, you know, when the patient's got a history of TB or positive QuantiFERON IGRA test, and what can I do? Again, the linkage between, biologics and mycobacterial and TB is with TNF TNF TNF TNF, and maybe a little bit of gamma interferon. So, if you inhibit TNF or maybe gamma interferon, that puts the patient at risk, or for getting a mycobacterial infection and or for spread of mycobacterial.

So, again, if TB is in the story and mycobacteria is in the story, give them a non TNF drug: IL-six, abatacept, B cell inhibitors, even JAKs although you could say JAKs may have some effect on gamma interferon, their rates are not any higher than that was seen with IL-six or abatapsid. Again, so again, the risk of reactivation with those non TNF biologics targeted drugs is at least a log 10 or a 100 fold less than with TNF inhibitors. Don't use a TNF inhibitor if that's what you're worried about. Anyway, I bring all this up because a retrospective report of almost fifteen hundred patients with non tuberculous mycobacterial infections, NTMs, used to call this atypical mycobacterium, MAIs, MAC, M. Cancassi, M.

Fortuitum, all those bugs First off, those bugs are far more common than TB, MTB. And they're usually not as morbid or mortal as far as risk, but in this study of fourteen twenty NTM patients, sixty six had RA four point six percent. The combination of RA and NTM was a predictor for respiratory related deaths, meaning RA patients NTM patients who had RA have almost a four over a fourfold higher risk of dying. So it's not a good combo, but it was a good opportunity to talk about mycobacterial infections in RA and inflammatory arthritis. Another RA, abstract comes from Core Evitas, and which used to be called Corona.

CorEvitas has a registry of, you know, tons of patients. They did an analysis of RA patients starting either on a biologic or targeted synthetic, but also had a renal insufficiency. They were a CKD what's that? Stage four with an eGFR of less than 60 ccmin. Okay?

So they found amongst nine thousand six hundred patients, fifty two thousand years of follow-up, that ten percent had this degree of renal insufficiency. The point of this was those RA patients don't do well. RA patients, comorbidity, we know they don't do well. But here specifically, RA patients with renal insufficiency were less likely to achieve C. Diff remission and low disease activity state.

So if they didn't have, renal insufficiency, twenty eight percent were in remission. But if they did, it was only nineteen percent, that's a twenty four percent reduction that was significant. So the effectiveness of biologics and targeted synthetics can be curtailed, hampered, by the presence of chronic kidney disease. Alright. The Society of Interventional Radiology, who's a card carrying member of that, issued a position statement this past week about the appropriateness of genicular artery embolization, GAE, in symptomatic OA patients.

We've written about that before. There have been a number of reports in JAMA about that. We I'd have never used it, but it works. It works really well. And their position statement says it should be considered in people who have failed conservative therapy, and especially if they're not candidates for knee replacement.

I think we should be doing more of that. And by the way, I don't know if you've seen what I've seen, but there's a lot of reports out there about the use of, or people touting the value of radiation therapy for knee o a, that's a special kind of stupid. That's people just trying to get some business. The evidence for that is weak, weak, weak. I would not do that to any of my patients, and shame on those people who think it's an appropriate, intervention.

This on the other hand, done by interventional radiology, has in every study I've reported and found, has been a positive result should be considered. PNAS, Proceedings of the National Academy of Sciences, you know, a very prestigious journal, published a report this week about PTPN22. PTPN22 I know that that gene is associated with RA risk it doubles the RA risk. It's one of the few genetic associations that strongly is linked to RA, that's not an HLA gene, right? And we know that this gene is also associated with risk of other autoimmune disease.

This gene, PTPN22, is found in up to five to fifteen percent of people in The United States. But in autoimmune disease, it's found at more than double the rate. In RA, I think the number is, you know, above thirty percent, for instance. And it is involved in RA in many of the immunologic abnormalities. For instance, the gene is important in augmenting citrullinization that then leads to risk and or to worse disease in the form of CCP antibodies.

Anyway, this gene not only augments, you know, centralization, it augments innate immunity, enhances NK cell activity, but while these are bad things, the PNAS article said it protected people against coronavirus infection. What? Sort of like, you know, these gain of function mutations that sometimes have really bad things happen to them, but conversely might have some good things happen. This is one such example. There is a positive side to one particular allele of the PTPN22, that's the eighteen fifty eight C, allele.

But anyway, I thought that was interesting enough to bring to your attention. A registry study coming out of the NIH, was it the NIH? I think it was. Looked at, let me think about this a second no, that's another study on mortality from the NIH. This was a registry study that looked at five eighty seven patients with lupus, and examined the importance of RNP antibodies.

Now I would thought, you know, RNP antibodies, who cares? It's sort of like one of the antibodies that is almost always found in people who have a speckled pattern ANA, which is almost always found in anyone with a positive ANA. So, when you order RNP you get RNP and SM together, do you not? Well, they found that thirty percent of their five eighty seven patients were RNP positive, and they showed, compared to RNP negative people, that RNP positives had more disease activity, had higher SLEDAI scores, eight versus four, and more use of drugs, including glucocorticoids, seven milligrams a day versus three milligrams a day. RNP positive patients had more renal disease, skin disease, serologic activity, and were less likely to achieve LL DOS (twenty percent versus thirty two percent or remission (twelve percent versus twenty three percent More importantly, or less I don't know, co associated here, is that if they were RNP positive they had an eighteen fold higher likelihood of being SM positive.

SM, we know, is more specific for lupus and also more prognostic for more severe disease. So the benign nature of RNP was sort of busted in my brain by this report, and, and this is why, I do note it I do test for it, and do note it in the chart of peep people who I do subserologies in. I'm gonna get to another lupus report later, but there was a report about, renal crisis in scleroderma and pulmonary artery hypertension basically showing amongst two thirty four patients with scleroderma seven percent had both, pulmonary hypertension and renal crisis and that surprisingly to me, that the pulmonary hypertension can precede the renal crisis, but it can also come on at the same time. So there is no clear sequence of development here, and, you know, I don't usually be I'm not usually looking that hard for pulmonary artery hypertension, usually in people with limited disease, crest disease, and usually over a long period of time. But, you know, it does happen in diffuse disease as well, which is where you see more, renal crisis cases, do you not?

Nonetheless, people with systemic sclerosis who have, both pulmonary hypertension and scleroderma renal crisis, as if that isn't enough, have almost a tenfold risk of GI bleeds. Oh my goodness, really? So, again, never good news with scleroderma, but these are the you can identify these people by these occurrences, by these features. Again, those two occurrences are also more likely with age, and people who are more likely to have elevated NT proBNP, you know, often associated with heart and or lung disease, I guess. Found a report this week about an inverse relationship between femoral bone mineral density and osteoporosis, levels of depressed BMDs, and all cause mortality.

This has been reported before, that osteoporosis is a risk factor for all cause mortality. In this report of almost three thousand postmenopausal women, this is from NHANES, done over a thirteen year period, that there was a forty seven percent increase in mortality hazard ratio of one point four seven. Why do they die? Why does osteoporosis lead to increased mortality? Two reasons: fracture related mortalities, which are real, especially in the elderly, and are more of a problem with hip fractures than other fractures related to osteoporosis.

And then osteoporosis itself is a sign of frailty, and frailty being a risk factor for, mortal, if not morbid, outcomes. Kind of interesting. I'm not familiar, maybe you are, with ANCA associated pachymeningitis. The report that I put up says it's rare. The report was about two thirty patients with systemic vasculitis from one hundred and seventy reports.

One hundred and eight of those were NPO positive, seventy one were PR3 positive. ANCA associated pachymeningitis has been more, in the literature, reported with GPA than other forms like MPA and other forms of ANCA associated vasculitis. They usually present with headaches, cranial neuropathy and acute phase reactants. The cranial neuropathies can present with visual issues, diplopia, vision loss, hearing problems, ocular palsies, etc. These people all had other systemic features, usually ENT lungs, kidney orbits.

The acute phase reactants are abnormal and high, the CSF is abnormal, again it is a rare manifestation of ANCA associated vasculitis, probably less than five percent of cases. And when and the diagnosis is made by thickening of the meninges, okay, and these abnormal tests, but this pachymeningitis picture you shouldn't automatically assume is due to the ANCA associated vasculitis because the differential diagnosis includes other infections and cancers and RA and other rheumatic diseases, sarcoidosis, and IgG4 related disease. ANCA associated pancie meningitis kind of gives you a clue that they may have the vasculitis. Osteoporosis International had an interesting paper from Buenos Aires, Doctor. Osvaldo Messina, a good friend, brought this to my attention.

It was a sort of a systematic review of vitamin D deficiency, looking at many sources to find out what's the deal, you know, with vitamin D deficiencies and rheumatic diseases. And we certainly know that vitamin D deficiency is very high in patients with autoimmune and rheumatic disease. The paper that looked at association says it was associated with higher disease activity, with fatigue, and poor, musculoskeletal outcomes. They did say that there's ample evidence that supplementation works. They also did not show that supplementation, while it may work in increasing vitamin D levels, doesn't fix anything that you can measure.

That when it comes to large trials and Mendelian randomization studies that vitamin d doesn't cause disease and isn't associated with sustained remission, meaning that when you treat it, doesn't make people better. Do I recommend it? Yes. Do I take it myself? Yes.

It's good for bone health. It's good for B cells and immune function. It's very important patients. But the problem is the research is crappy. A lot of heterogeneity, a lot of non standard study designs.

But rheumatologists just love vitamin D, and I just love to make fun of it. Fault me, if you will. But, just test it, treat it, and don't think you're treating their fatigue. I don't believe that fatigue gets better or disease activity gets better. Although Michel Petrie's got some data about lupus patients doing better on supplementation.

So, you know, maybe I'll back off on that a little bit. This NIH study was published in ACR Open Rheumatology that, was a, an analysis of, I think, many well, I don't know if this was the NIH. I think the other one was the NIH study. Anyway, this particular study that appeared in MedPage Today, which is coming from the original journal article, found that lupus, in young women, leads to death. So lupus patients die, yes, we know that, and it's less and less, as time has gone on.

But, to my surprise, and it really shouldn't be, that a lot of it happens during the age bearing years, in lupus patients. So when they looked at years of life lost, lupus was the cause, and it was fourteenth as a cause in women between the ages of 15 and 44. It was ninth between the ages of 15 and 25. Amongst the autoimmune diseases, it was either the first or second greatest cause for years of life lost. It was behind other causes of death in these women, and that would include diabetes, HIV, lung disease, anemia, cardiovascular and cerebrovascular disease, and nephritis.

But it still is, you know, lupus can be deadly, and we know that. And but luckily, we're getting more therapies, we're being more aggressive, we're eliminating our use of steroids. I like the way lupus is gone. Another report, the final report for this podcast, was about drugs that target toll like receptors. You know, usually there are drugs out there targeting TLR7, this one, and padaran.

And padaran is a small molecule inhibitor of TLR7 and TLR8, and was reported in the WILLOW study, a phase two trial of four sixty three patients with cutaneous lupus erythematosus, CLE, or systemic patients who did not have extramucaneous extramucaneous disease, and they looked at whether this drug would affect the skin outcomes and measured that by a Classy A outcome score at week sixteen. So they either got placebo or the TLR seveneight inhibitor, and they showed that it was highly effective with fifty to 70% better responses compared to the placebo. So, again, this is important because the TLL, the toll like receptor activation very much involved in the innate immune response, which is important in handling of viruses, but also in the genesis of then adaptive immune responses in autoimmune disease. There are mutations of TLR7, that have been linked to, excessive activity that then leads to childhood lupus. Right?

So these therapies, are have been reported the last few ACR ULAR meetings, are getting closer to the market, and I think that they'll be an add on. And of course, some people believe that hydroxychloroquine, one of its many effects, most of which are unknown and truly unclear, but we know it's good enough that we give everyone with lupus hydroxychloroquine because it's so safe, that maybe its mechanism of action is through inhibition of TLR seven or I think not nine. So, what about the safety of the TLR inhibitors? Looks really good. There's nothing there that looks scary at all, and nothing learned from knockout models or mutation models for, the toll like receptors.

So, maybe it will compete with hydroxychloroquine for safety as well as efficacy. Anyway, that's it for a long edition of this podcast. We're going to do it again next week. I want you to know we're getting ready to cover EULAR, which is, about two weeks or two and a half weeks away. We'll be there.

Hope you'll be following us. Hope you are going to enjoy that as you have in the past. Take care of yourselves. We'll talk next week.