Do You Zoster Vaccinate? (6.19.2026) Save

It's 06/19/2026. This is the RheumNow podcast. Hi. I'm doctor Jack Cush, executive editor of roomnow.com. This week, some big questions on the podcast.

Should you be prescribing glucosamine? Should you be talking to your interventional radiologist about treatment of NEOA? Should you be using oral or methotrexate? These are kind of important questions, right? Let's begin with a report from Scientific Advances.

This was an interesting study potentially about the pathogenesis of Sjogren's disease, where this report showed how row 60 antibodies, as you know, when you do SSA or row testing, you're really testing for row 52 and row 60. Row 52 is the big one, usually you're testing for both. But this particular report in Science was about row 60 as a driver of CD4 specific T cell responses to row 60 that led to ROS-sixty specific B cell hyperactivity and humoral activity, basically saying ROS-sixty is a driver of disease. And I thought it was interesting, which led me to look into row 52 versus row 60. And the bottom line is seventy percent of people with Sjogren's are SSA or row positive, that most of that probably is row 52.

About, I think, the number is well, first thirty percent of people are seronegative for row and law, and people who are row positive by 52 or 60 are gonna have usually more active disease. Seronegatives tend to have milder disease, just dry eyes, dry mouth, and not much more and mild at that. But it turns out that about fifty percent of people with Sjogren's disease are double positive for antibodies against row 52 and row 60, and that about ten to twenty percent are only row 60, but row 60 positivity only seems to correlate with milder disease, not major organ disease, not the really scary stuff in Sjogren's. Nonetheless, this report says there is a row, a row 60 specific T and B cell orchestrated response that could contribute to the pathogenesis of the disease. I think we'll be seeing obviously a lot more Sjogren's research and pathogenesis studies as we get into more studies for Sjogren's.

I hope that we'll see that. Another study I saw this week that kind of got my attention was GI involvement in patients with dermatomyositis. I don't usually think of dermatomyositis having much in a way GI involvement. Well, yes, you know, fifty percent of people may have dysphagia because it's the upper third of the esophagus, the skeletal muscle, skeletal muscle disease, why not dysphagia? But they can have more than that.

The prevalence of GI involvement in dermatomyositis was assessed in two different cohorts of one hundred and sixty seven patients. Overall, up to fifty percent of patients could have that, but severe GI involvement is seen mainly in NXP-two antibody positive patients, much more so than MDA-five or any of the other subgroups of dermatomyositis. So much so that NXP-two has an eight point eight fold higher risk of severe GI involvement. Those who are NXP-two positive and had severe GI disease tend to be younger, with facial edema at presentation, with, as you would expect, both active skin and muscle disease. It seems like a unique subset.

It seems to be uniquely associated with NXP two. And as you know, long, long ago, I never did a lot of myositis specific autoantibody testing. I wasn't sure about it. Now I'm doing more of it. I do think that there's something to NXP two as we know.

It's got an association with calcinosis. Right? MDA five is a bad player. So I think doing that testing is a good idea. An article from radiology hit on a subject that I think is interesting that led me to do a little more research, and that is genicular artery embolization.

We've reported on this two or three times, it looks like it's an alternative treatment for people with problematic knee OA. Basically, you use something that embolis that artery, it produces a pain benefit. So this particular study from radiology, not surprisingly, think it was two hundred patients, showed a clear cut benefit. But then I looked at this, you know, I went to open evidence, I did a PubMed search, and you know what, the bottom line is studies like this, open label, single center designs where there isn't a control group or a comparison, or meta analyses basically say that genicular artery embolization is clearly beneficial with regard to pain and should be considered. Wait a second, there's more.

There are actually three sham placebo controlled trials that show no significant benefit. So the story is out on whether you should be doing this. You know, you talk to the radiologist, let's say, Yeah, we should do that, and we should do radiation for knee OA, and that's a special kind of stupid. I would not endorse this. To back that up, far, not that the guidelines are up to date, ACR, OA treatment guidelines, I think are five years overdue, But the ACR and ULAR guidelines and OA treatment do not mention the utility of GAE, genicular artery embolization, and there are some issues about the substance you use to embolize and cut off that arterial supply.

This needs to go to the drawing board. We need more information before we start doing this. Nature published something interesting that pertains to Alzheimer's, something you don't wanna deal with, and glucosamine, something you probably don't endorse. But there's an article fairly well done showing that amongst the many mechanisms that drive Alzheimer's disease, one of it is hyperglycosylation, which, you know, if you read about it, it's kind of interesting and whatnot. But it turns out that glucosamine increases hyperglycosylation.

Glucosamine is taken by about seven percent of elderly people over age 70. Presumably, it's for arthritis prevention or arthritis management. It's, as you know from the study that I did in New England Journal, that glucosamine doesn't really work, not much better than placebo, and you can argue about whether it's got utility or not. I don't think it does. In this paper, they did mention a retrospective electronic health record study showed that in Alzheimer's patients, the use of glucosamine has been associated with progression of Alzheimer's disease or worse survival in Alzheimer's disease.

So if you're worried about Alzheimer's, make sure they're not taking glucosamine because there is no positive data, and again, it doesn't seem to produce any articular benefit that I can point to. A report a month or two before EULAR came out looked at what happens when you treat undifferentiated early arthritis. So these don't meet criteria for clinically suspect arthralgia or preclinical RA because they don't have to be, rheumatoid factor or CCP positive. So in this particular study, these were, undifferentiated arthritis, but had two or more swollen joints, but didn't meet criteria for RRA. And enrolled patients and treated them either with nonsteroidals or methotrexate starting out at 15 going up to 25, or baricitinib four milligrams a day, about twenty eight patients in each group.

These people had really mild disease at entry. Their DAS scores were 2.8. They had two or three swollen joints. Less than seventeen percent were CCP positive. At three months, baricitinib was better than nonsteroidals or methotrexate, were equivalent in their response rates, and so baricitinib lowered DAS 28 score from 2.4 down to what looks like about 1.9, a drop of minus 0.52 in DAS points, and that was significant in three months.

However, when you follow those people out to twelve months, they all did better. They all got their DAS scores down to less than 1.7, but the best at twelve months was methotrexate at 1.3, non steroidal at 1.6 DAS, and baricitinib 1.7. So baricitinib had the fastest response, but it didn't go much beyond what it achieved at three months when you looked at twelve months. This is a small study. I don't think this is an endorsement of treating undifferentiated arthritis, but the bottom line is someone who has a chronic arthropathy of more than twelve weeks of a swollen joint needs to be treated.

It needs to be treated with a DMARC. What you call them can then refer to what the success of therapy may be. If they are clinically suspect arthralgia where they shouldn't have two or three swollen joints, right? But they are seropositive, we really don't know what to do. You might do an Avatacet.

But in these undifferentiated arthritis, polyarthritis patients with two or three swollen joints, DMARDs, you know, it looks like that all these were good choices, but maybe the best choice was methotrexate, with Nosteroil and baricitinib doing about the same. Interesting. A study looked at elderly RA patients between 2,009 and twenty twenty two. So, did a percent, a twenty percent sampling of elderly Medicare patients over the age of 65 who were on TNF inhibitors and found the ones who either stopped or tapered their TNF inhibitor. So the cohort was nine forty nine patients.

And they found that only thirty eight percent of them were able to de escalate TNF inhibitor therapy, either stop it or lower the dose. But that sixty two percent had to re escalate the therapy. So, if you wanna withdraw therapy, it's only gonna be effective thirty eight percent of the time in your elderly RA patients. Re escalation was more likely in sixty percent or more patients, and it took one hundred and sixty days for them to re escalate. So it wasn't like an immediate flare of activity.

Reescalation was more likely in people who were black, Hispanic, non whites with a lower comorbidity burden. I don't know that that helps me, but maybe it helps you, and that's why I reported it. The question next in this next report is what's happening with steroid doses in newly diagnosed RA? The clinical trials say, I'm not even gonna look at this report, and say the clinical trials say that people who are bad enough to get in clinical trials, about fifty percent, sixty percent are taking corticosteroids. Usually a dose that's a little above five milligrams per day.

And that doesn't change in clinical trials, right? So this study was a Danish single center hospital, five seventy four newly diagnosed RA patients. Seventy five percent went on to receive steroids in some form in their first year. Fifty five percent received it at their first visit. The mean dose, was nine point three milligrams per day.

Half the patients who received steroids were receiving oral steroids, forty seven percent received intra articular steroids. Twenty percent had an infection in the first year with a thirteen percent increased risk, but the confidence intervals overlap one, saying that this was not a significant increase in infections when you looked at steroid exposure, but it tended that way. But the numbers here may not be large enough. Other studies have shown that at this dose, five to ten milligrams, there is an increased risk of serious infections. So anyway, I think we're still using steroids.

I think we're still using too much steroids, and we do know steroids are bad for you in RA and other inflammatory arthropathies. As you may have remembered during COVID, I was all gung ho and wild about the use of telemedicine by rheumatologists. In the first year after COVID, Rheumatologists were the second leading group using telemedicine successfully, but since COVID has died, so has your interest in telemedicine. Only a minority of you are doing this. So this report about a recent US telehealth utilization showed it increased 10% in the first quarter of twenty twenty six.

Went up from overall medical claims from five percent to five point five percent. Who's using telemedicine the most out there right now? It still is mental health, which makes up more than half of the use, which is gigantic compared to rheumatologists who are only using this for in three percent of your visits for rheumatology, three percent overall. That number is a little higher in the Western States, a little higher in the Northeast. Telehealth overall, not in rheumatology, is being used in almost sixty percent for outpatient visits, seven percent for new visits, and thirty five percent for psychotherapy services.

But again, most of this use is in psychiatry and psychotherapy. Why are you not doing telehealth? I saw a recent report from, I don't know if it was Deloitte or Becker, you know, one of these large companies that looks at healthcare in The United States, a great report about practice, and a CEO of a big group in New Jersey said that the way that they manage urgent patient appointments is they built into their system a telehealth arm, and someone assigned to telehealth every day is the one who communicates with people who need to be seen today, an hour from now, and they're always available. And when they're not doing telehealth, they're doing other productive work. But everybody has their rotation, and everybody then who calls and needs to be seen by someone right away is seen by Doctor.

Mo, Doctor. Sarah, Doctor. Ellen, whoever, and they manage the problem as opposed to trying to manage it over the phone, which is dangerous, and then make an appropriate follow-up. I still think we should be doing more telehealth because you can do it in rheumatology or other specialties can't. And if you don't think you can, look at my video on the virtual joint exam.

It's very accurate. I'm really good at telehealth. A study on polychondritis, relapsing polychondritis, proves that I'm not very good at that because I don't see very much of that. A study coming out of Kyoto University looked at fifty five patients with relapsing polychondritis followed for a total of five hundred patient years, almost ten years follow-up. And they looked at how they responded to different treatments.

So they either received a TNF inhibitor, an IL-six inhibitor, or no biologic. The relapse rates were highest with, as you might guess, no biologic, forty seven per one hundred patient years, meaning a relapsing polychondritis patient, a hundred of them, followed for one year, half of them were gonna have a flare. The relapsing rates, the relapse rates for the biologics was substantially less, twenty two per one 100 patient years with a TNF inhibitor and even lower, twelve point five per one hundred patient years with an IL-six inhibitor. Now, again, this comes from Japan where they're IL-six happy and they have the most amount of experience. Would that be something you see in your practice?

I think you would. So again, TF inhibitors lower the risk by sixty percent. The IL-six inhibitors lower the risk by eighty percent. This study was unable to comment about biologic use and risk of infections. The numbers were too imprecise to make a comment is what they said.

I don't know if you get the email that I send out every Saturday morning on the Room IQ quiz. It's been wildly successful with you and many of your colleagues. The one that went out after Euler had a lot more questions, 30 in the first week and 15 in the second week. In last week's survey, only half of you got this question right. This question being, in macrophage activation syndrome and treatment of it, which cytokine is a central target of the FDA approved drug emapalumab for MAS and MAS associated with STILs.

Emapalumab, we've covered it here before. It's an anti gamma interferon monoclonal antibody, highly successful, but only half of you got that right. Look at your inbox on Saturday morning, Room IQ coming your way. A report from the Medical College of Wisconsin and Michelle and colleagues looked at vaccination in people on JAK inhibitors. So single center study, one hundred and two patients treated with a JAK inhibitor, seventy two percent were over the age of 50, seventy seven percent were RA patients, showed that of this one hundred and two, and again, at least seventy percent are eligible by age, only 27 received at least one dose of the recombinant zoster vaccine, also known as Shingrix.

What's the deal? And only three, I'm gonna say, is that so it's three percent or three patients received the vaccine within thirty days of the JAK inhibitor. What's going on here, folks? You know the data is really clear. I'm gonna talk about vaccination recommendations at the end of this, where they say everybody on immunosuppression should get the Shingrix vaccine, but I put anybody on a JAK inhibitor, I give them the Shingrix vaccine.

I like to get it before, it doesn't have to be before. They need to get at least one dose, but two doses are better, and I'll give it at any age. It works. Again, going on a JAK inhibitor or inhibitor of an alpha interferon like anifrolimab is a gigantic increase over any of the other biologics and over just active RA or elderly RA, right? The population risk of zoster is six to ten per thousand.

On a TNF inhibitor, it's like twelve to fifteen per thousand. On a JAK inhibitor, it's like forty five per thousand. It really goes up a lot. I vaccinate everybody with the recombinant zoster vaccine that goes on a JAK inhibitor. Maybe you don't.

Tell me why. Here are the recommendations that came out of EULAR. That was a publication this week that you should look over. It's a nice, I think, quick look. The bottom line is that there were, I think, five overarching statements and 10 guideline recommendations on different vaccines.

Number one, they were very proactive about us in rheumatology using vaccines, having a plan for the vaccines as soon as you diagnose a patient, using it as soon as possible. And by the way, you should be vaccinating people independent of disease activity. As you know, it's you really do it's not independent of drugs because rituximab and methotrexate really impair vaccine responses, so you need a strategy for those. But independent of disease activity, non live vaccines can be given at any time, any situation, and don't worry about it. Live attenuated vaccines, as package insert says, should be not just avoided, but now these guidelines say they can be considered with caution because there are instances where a live attenuated vaccine could be used, like in the case of yellow fever.

Flu, they say, give the flu vaccine, hold methotrexate for one week. Any of the pneumococcal vaccines, you know, the Prevnar twenty, the Prevnar thirteen, you should based on the Vaxema study, which we covered a few weeks ago, you should hold the methotrexate for four weeks. And in both those instances, with flu and with the pneumococcal vaccines, there's not a flare of RA activity by holding the methotrexate. They say that the Shingrix vaccine is strongly recommended for patients with autoimmune and inflammatory rheumatic disease on immunosuppressive therapy. Immunogenicity is relatively well preserved, that's humoral responses, in people on JAK inhibitors.

However, cellular responses are attenuated and further reduced in people, also on methotrexate. So you need a a rule for methotrexate that applies for, when you're giving the Shingrix, maybe you should hold the methotrexate for a week like you do with the flu or the pneumococcal, but there's no study to prove that. Newborn should get a live vaccines should not get live vaccines, especially if the mother has been exposed to biologic DMARDs and hence the fetus would have been exposed. But it is safe to give the rotavirus in the first six months in mothers who had antenatal TNF exposure, they are very strong in saying everyone should be receiving, our patients should be receiving the COVID vaccine. Another recommendation guideline coming out of UR26, both of these presented on the last day of UR.

This was the recommendations for the treatment of PMR, GCA, and Takayasus. PMR and GCA go together. GCA is large vessel vasculitis. I guess they threw in the other large vessel vasculitis because there's really only one big one, that's Takayasu's. Well, it's kind of an awkward grouping if you ask me.

The bottom line here is that they say a few things you should pay attention to. One, glucocorticoid treatment in these three diseases can be delayed until diagnosis is confirmed, however, with giant cell arteritis, meaning there's urgency and you need to start steroids right away. The other thing is response to glucocorticoids is not a diagnostic test for any of these disorders, and that's something that people often talk about. With new onset PMR, the starting dose is fifteen to twenty five milligrams, that should be tapered to ten milligrams within one to two months with the aim of stopping within one year. Good luck with that.

Everyone talks a good game, but the reality is we're not so good at getting people off steroids. In relapsing or refractory PMR, cerilumab is preferred, tocilizumab is an alternative, and they say if you must, you can use methotrexate. Although, I asked the author this, the data sucks for methotrexate. They said they included it in the guidelines because these biologics are not always available in every country. And, oh, by the way, we rheumatologists are familiar with methotrexate, so why not?

Well, the data is pretty mixed on methotrexate. It's up to you whether you use it. You can say the same thing for GCA. In GCA, again, urgent referral is necessary. Urgent treatment with glucocorticoids has to be done immediately without waiting for confirmatory investigations, because it is a medical emergency.

One more thing about PMR. They say that refractory PMR should make you, and I've never thought this way, should make you think of a re evaluation about the diagnosis. Maybe it's not PMR, because PMR mimics could include myositis, inflammatory arthritis, paraneoplastic presentations, myeloma, etc. That's something that seems really smart. So again, GCA is urgent, a medical emergency, do the things you have to do, start steroids right away.

Nuance at GCA gets forty to sixty milligrams a day, tapered to fifteen or 20 within three months, with the aim to stop glucocorticoids within eighteen months. Relapses should be treated as new onset disease. Minor relapses, you can escalate to your last effective steroid dose. Steroid sparing can be accomplished with tocilizumab or padacitinib, especially in, again, those people who are refractory or relapsing, instead of using more and more steroids. They also say here methotrexate is an alternative, not in my clinic, but maybe in yours.

And they did talk in both GCA and Takayasu's about vascular complications require specialized urgent referral to vascular surgeons for management of the problem, that if there's going to be a vascular intervention for a dissection or critical ischemia, it should be done during periods of stable remission, rather than when the patient's wickedly inflammatory. But sometimes you can't do that. Again, interventions carry risks here, and you want to do the endovascular interventions to lower risks without incurring new risks. But the guidelines are really good at spelling this out. You might want to look at that report.

I would encourage you if you aren't well versed in what happened at UR twenty twenty six, many of us were there. The one way that I'm going give you three ways, and they'll be in the show notes for this that you can click and do this. First way and easy way is a fifty five minute recording called, ULA R, Room Roundup with Artie Cavanaugh and I talking about, I think, 16 or 17 of our favorite presentations. You'll get a good taste of one hour. That's, you know, one or two car rides or one sit down.

You can look at the video, you can listen to the podcast. The next best, which I think is really valuable, is listening to the topic panels. We have three topic panels. Usually, we have four or five during ACR, but for ULAAR, we only had enough staff to do three. We have a topic panel on RA, on PSA, and on CAR T cell therapies where four of us get together and talk about eight of the most important abstracts in that particular topic.

Think I you'd get a really good overview on either RAPSA or CAR T cell if you looked at one of those. And the other way, which I really like and is very, very popular, both these topic panels and daily recaps got tons of podcast listens and many hundreds of of video views. The daily recaps, we did a combined day one, day two recap, and then a day three and a day four recap. So there's three recaps, as videos or podcasts that you can listen to. Each of these topic panels and daily recaps are about thirty minutes long and have four people.

We're going over about eight abstracts, some of their favorite things, that fit for that day. So the daily recaps are different than the topic panels because it's like the best thing I saw today from the four people who were on that particular video panel that we did. They go fast. They're interesting. I hope you enjoy them.

Tune in next week for more on RheumNow.