Hmmm Really_?(7.11.2025) Save

Hello everyone. It's 07/11/2025. This is the Room Now podcast. Hi. I'm doctor Jack Cush, executive editor with roomnow.com.

This week on the podcast, a few new thoughts, some things that are painfully obvious, but. And let's begin with some things that fall into the category of really? Really? I'm gonna start with DISH, diffuse idiopathic skeletal hyperostosis, also known as Farestier's disease, you know, for contiguous segments with those bulky osteophytes. I like this article that I found because it reviewed the issue of dysphasia with DSH.

It's a known cause. I wouldn't have been able to guess how known or how common that is. I can't say it's ever come up. I've seen a few DSH cases, usually not in cervical spine, but in this study. Two zero eight patients with dysphagia, so they're looking at it from that angle, who underwent CT of the head and neck.

They found that dish was the cause of dysphagia in thirty nine percent. Really? Thirty nine percent. And if that's not surprising, and it was usually they had anterior dysphagia, again it's usually from the anterior osteophytes that are occurring as opposed to the lateral. But the real surprising thing is, what were the predictors of patients with dysphagia who will have DISH?

The predictors were: one, a low serum albumin two, COPD three, chronic pain, I assume chronic neck pain three, I get. The other two is like, what? And I must say the article did not really get into it other than to say serum albumin may reflect malnutrition. Malnutrition related to dysphagia, you say? Well, they didn't say.

I guess that's the implication. And or they said that the lower albumin was due to inflammation. Well, you wouldn't think DISH has got a whole lot of inflammation going on, and nothing else in the paper suggested that other than this finding of COPD. COPD, inflammatory disease, maybe that's driving a little albumin, but what's that got to do with bulky osteophytes of the cervical spine? I find this interesting.

I think that the point is that DISCH belongs in your differential diagnosis of dysphagia. And don't get me started on dysphagia. It's too late, it's already happened. There's two kinds of dysphagia, there's the dysphagia up here in the throat, and then there's the dysphagia down below the sternum. Substernal dysphagia is smooth muscle, is achalasia, is esophageal dysmotility is masses, right?

Up here in the throat, up high, it's usually from a lack of saliva associated with xerostomia, Sjogren's syndrome, and whatnot, or it's psychiatric, bulbar hysteria kind of things, you see a lot of upper pharyngeal dysphagia with fibromyalgia. I don't know if it's psychologic or if it's the dry mouth that they may have, but this kind of dysphagia with here, we're talking about substernal dysphagia, I guess it could be cervical, if that's being found on cervical CT. See, told you, don't get me started on dysphagia. Another interesting report was a full read review, nice review, pretty expansive, kind of a little maybe too expansive, from Joint, Bone, and Spine, the journal Joint, Bone, and Spine. It is a full read review on idiopathic inflammatory myositis and new treatments, and it go into IVIG and FcRn receptor blockade and rituximab and all kinds of things.

But it begins with sort of an overview of myositis, and I like the way it began because it asked the question, is the term polymyositis obsolete? Dramatomyositis, we use all the time. How often are using the term polymyositis? Their contention was that it's been replaced by better understanding of idiopathic inflammatory myositis in all its labels, including necrotizing myopathy, inclusion body myositis, antisynthetase syndrome, overlap myositis, and now we have NXP two, a TIF one gamma myositis that we're just not using the term polymyositis much anymore. Really?

Or if you're interested in the therapies, you can look at that free, full read reference. Some new thoughts from some new papers. A one year study looked at the risk of falls in inflammatory arthritis patients. It happens. It should happen.

They're weak, they have pain. In this study, from one hundred RA patients, thirty three percent reported a fall in a twelve month period. From eighty patients that they followed, forty six percent had a fall in, the prior twelve months, making it much more common in PSA, and they noted in their discussion that this has been reported before when compared to RA. PSA patients have more falls. Falls were associated with disease duration and HACS score.

HACS score, underline that, bookmark that. That's your invitation. You see patients who are checking all those boxes to the right on the HAC score, or on the MD HAC, that's your invitation to ask about, have you had any falls? Falls, because they are associated with morbidity and mortality, is something we should be asking about. And as I mentioned, because you bookmarked it, when the HAC score is high, maybe that's when the risk is also high.

I found this interesting report, about what's the predictive utility of finding MRIs in patients with very, very early arthritis. Patients who are clinically suspect arthralgia, they don't have synovitis, so I'm thinking, why are they having MRIs if they don't have synovitis but they have maybe chronic hand pain or whatever? And yes, some of those people do in fact have erosions when it's found. This particular study of four zero five, this is from the Leeds Early Arthritis Clinic, I believe, CSA patients, forty seven percent had MRI erosions. Forty seven percent, what?

But again, this is sort of a select group doing advanced research. And they did say that if you had an MRI erosion, you had a five times greater risk of having a later subsequent radiographic erosion, odds ratio of five. But in the overall scheme of things, ninety six percent of MRI detected erosions had no associated x-ray abnormality. Meaning that finding an MRI early on, if someone doesn't yet have synovitis, may not yet have RA, and MRI erosions, not meeting criteria RA, not yet having synovitis, does not signify proof that they have erosive arthritis. Ultimately that has to be diagnosed by X-ray.

This is like all those studies of hockey players and manual workers who have abnormal MRIs of the SI joint. The greater the sensitivity of the imaging test, the more you'll be finding things that don't mean anything. So don't get carried away just because you find MRI erosions. Maybe the thing is not to do your MRIs on people with CSA, pre clinical RA, but I don't. Maybe you do.

They certainly do in leads. RA patients have a forty percent higher risk of serious dental infections. A study of the national inpatient sample over a six year period looks at all US hospitalizations, a retrospective study of fifteen million hospitalizations and records, ten ks or zero point seven percent were hospitalized for serious oral infections. What were the risk factors? RA, two percent.

Being male and being black, and having smoking as part of your history. But RA is a risk factor for serious dental infections, serious enough to get you hospitalized. And you've heard many times before about the parallels between gingivitis and R. Acynovitis, both at the histologic and cytokine level, and as far as the damage they can do to local tissues, and about the cross associations between the two. So this finding is really not that surprising.

We've talked before about nerve blocks, specifically genicular nerve blocks, as an effective therapy for knee OA. I've seen these studies, I've never done it. Now, I'm looking at a meta analysis of six randomized control trials that involve four twenty patients with knee osteoarthritis, and they showed significantly, you know, like for pain it was P less than point zero zero zero one, and for function, significantly better with p less than point zero zero three, with relief as early as two weeks, as far as pain, and functional improvement by as early as twelve weeks. We're not doing this in rheumatology. Maybe we should.

Would you do this instead of a steroid injection? Well, got steroid in the closet and in a tray. Can just do that in twelve seconds. But actually, you don't want to keep doing steroid injections into osteoarthritic knees. I think we should be doing more of these.

I will. I'll be asking about them at least. And they're supposedly done by your interventional radiologist. I found an interesting study about autoinflammatory disease from a UK National Referral Center. They reported their 2022 experience with three zero four referrals for suspected systemic auto inflammatory disease, the abbreviation is SAID, S A I D.

Thirty nine percent were diagnosed with a SAID, meaning the majority of patients referred did not have an auto inflammatory disease, and half of those that were diagnosed had monogenic disease. And most of these referrals, by the way, were in an adult population. They found there was a significant delay in, from symptoms to, diagnosis, two to six years, especially in those who are adults, especially in those who are having a late onset of their auto inflammatory disease. What were the diagnoses that you saw? You know, would have guessed a predominantly adult population had been Still's disease.

No, Still's was number five. Number one was FMF. Number two was recurrent idiopathic pericarditis. Number three was undifferentiated auto inflammatory disease. Number four was CAPS, the Cryopyrin Associated Periodic Syndromes.

And five, my disease, Still's disease, coming in at a modest position. A lot of things after that. FAPA, TRAPS, Schnitzler's, Vexus, ROSA, MKD, Mevalonic Kinase Deficiency, PFID, PFIT, DADA2, and Blau syndrome. That's the experience of others. What's your experience?

So now I got a bunch of reports that I think are kind of duh, painfully obvious, but they do have a caveat and worth discussing. I began this tweet with, don't stop the DMARs. You've heard me before saying, please don't encourage people to stop their DMAR therapies working. This is a retrospective study of ninety one JIA patients. A third of them had oligoarticular disease, twenty five for twenty seven percent had polyarticular disease, but they had all types being represented in there, including era and systemics and whatnot.

And they talked about, because of the sometimes the self limiting nature of JIA and its many forms, that patients get cycles of therapy, and then when they go into remission, they stop the cycle. So in this study, they included patients who got up to four different cycles of therapy, and they showed that consistently, whether it was the first time, the second time, the third time, that when you stop therapy because they're in persistent remission, let's say six months, two thirds of them are going to flare, and relapse and require therapy again. And only one third are able to remain off the DMARD. Bad news here is you don't know who they are. So those are the realistic odds and maybe why you shouldn't stop the DMARD or the biologic.

Again, about a third of these patients initially were taking methotrexate and a biologic, two thirds were on methotrexate. And then with subsequent courses, they went on different therapies. In Erlangen, the home of a lot of novel studies led by Doctor. Shet and colleagues, 1,500 patients that were entered into clinical trials, I guess. They looked at how you could predict remission at six months, irrespective, I guess, of the therapies.

They did show that they could do this with great accuracy using the ADA Boost modeling, had the strongest predictive accuracy at eighty six percent. And what did they base the prediction on? Alright. This is machine learning, AI predicting who has a greater risk of going into remission. It was based on duh, dash 28, activity, age, VAS scores for pain, and the number of swollen joints.

But while this is a duh moment, these are things that you use in your decision making. But wouldn't it be great if you actually had an AI program that told you what the likelihood of remission at six months was going to be, and maybe that would further inform your therapy? I think that's where we're going in the near future. The near future is often guided by our recent past. Some of our biggest questions are in scleroderma, and one of the better or often referred to studies is the U Star study.

It's a multinational prospective study of patients with scleroderma. In this sub study, eight ninety three patients with ILD related to scleroderma, they found that ten percent of them died. So getting ILD with scleroderma, any of our diseases, RA, maybe not myositis, but most of our diseases has a significant morbidity and if not mortality risk. These patients were followed up to thirty nine months, ten percent died, predictors of mortality was sort of rapid deterioration of greater than ten percent within the first twelve months. That's kind of a dumb moment, And a significant decline as measured by their modified Rodnan Skin scores, so rapidly changing skin, rapidly changing lung.

Again, these people have a three to fourfold higher risk of death. Things that were not predictive were DLCO, you like to look at DLCO. I have always liked to look at DLCO, usually not that predictive. An absolute score on the modified Rodnan score, it was a change that made the difference, or the number of digital ulcers were not predictive. I thought this was interesting.

Another study of systemic sclerosis, seventy four patients, were examined by a number of different parameters, and this study showed that nail fold video capillaroscopy had a significant correlation with future ILD progression, as measured by worsening of PFTs. And also, nail fold capillaroscopy also predicted worsening of the modified Rodnan Skin score over a two year period. The interesting thing, and they did many, many measures on here, including biologic and clinical and lab, they found that KL6, something that you don't measure, that the lung guys measure a lot, correlated with the nail fold video capillaroscopy scores, and also the decline in PFTs. In this period that they watched patients, the ILD rate at baseline was thirty eight percent, but went up to fifty one percent. So if some patients do progress, and maybe you can get insight into those who are at greater risk by looking at their nail folds.

The predictive features were capillary disorganization and late pattern changes. That would mean big dropout, asymmetric morphology, large dilated vessels. That's late pattern changes. You know that cannabis is sort of like all over the place these days. It's legal in 24 states.

It's decriminalized in seven states. It's in the District of Columbia in three territories it's legal, and there are more coming on board. Unfortunately, HHS, as of this year, still has cannabis scheduled as a schedule one drug, meaning it has no medical use and high abuse potential. Then 2024, there were laws being introduced to decriminalize it on a federal level, bumping it down to a schedule three drug, but that didn't happen. So we still have a lot of conflict here, do we not?

It is a schedule one drug according to the FDA and the federal government, but everyone's using it, and oh, there's no guidelines? Oh, and all the benefits and merits of cannabis use are coming from who? The authority behind the counter named Paco. This is a little problematic. I believe in the use of cannabis.

I just wish there was some real research and evidence in this area. BMJ had a nice report on a UK population study of 15,000,000 adults showing that if you have autoimmune disease, that you have twice the risk of having an effective disorder. That includes depression, bipolar disease, and anxiety. Significantly higher in autoimmune patients, like twenty nine percent, compared to general population, eighteen percent, and this was regardless of age, sex, ethnicity, income, family history, etc. Study, two studies on cancer that were interesting this week, a case control study from, let's see, twenty fourteen, twenty nineteen, an RA patients over the age of 65 compared cancer risk in RA patients to US population risk using the SEER database.

The overall cancer risk was not increased with JAK inhibitors, was not increased with TNF inhibitors, was not increased with other non TNF biologics. However, JAK inhibitor use was associated with increased risk of lung cancer odds. The ones that weren't increased, the odds ratio was one. The ones that are increased, JAK inhibitors increased with lung cancer, odds ratio one point four zero, especially in males two point one two, and if you were on a JAK for greater than two years. Lower rates of breast cancer with JAK inhibitors in women on JAK inhibitors.

Wait a second, what did they just say? They just said what you've always heard, the risk of cancer in RA is one, it's not increased. But actually that's wrong because certain cancers are increased and others are decreased. The decreased ones are breast, the increased ones are lung and skin and leukemia, right? These are the things, lymphoma.

That's the risk they found associated with JAKs. So is this a JAK issue, or is it an RA issue? I believe that's an RA issue. But wait, my next report from the German biologics registry, the rabbit registry, does great research, really fabulous research. Shows an overall very small increased risk of malignancy with JAK inhibitors versus other biologics.

The risk they found was greatest in, and listen to this and tell me what it sounds like, those 60, those with high disease activity, those who were on three or more prior DMARDs, wait, that sounds like the entry criteria for oral surveillance. A JAK inhibitor study that showed an increased risk of C, I think this data kind of confirms the results of oral surveillance. So this is like two thousand two hundred on JAK inhibitors, four thousand two hundred on biologic DMARDs, the rates, again, one point four higher for JAKs, the incidence rates was eleven point six versus eight point nine, but the JAK risk only appeared after sixteen months of therapy. It was not there in the first year or year and a half. Again, this is kind of confirming data from the oral surveillance study.

We're gonna end with two reports on psoriasis. We've talked about it here, I've had lectures at RheumNow live on this. Does having severe psoriasis increase the risk of psoriatic arthritis? The answer is yes. Does aggressive treatment of severe psoriasis with biologics reduce the risk of psoriatic arthritis?

A lot of reports say yes, some reports say no. People that argue about this talk about all kinds of methodologic issues in the analyses. This is another analysis coming from Dennis McGonigal, another cohort that he was working with, retrospective analysis of severe psoriasis patients who were either treated with TNF inhibitors or with phototherapy. They were followed on average of nine years, there was almost a thousand patients, almost five hundred on a TNF, almost four fifty on UVB therapy, and compared to phototherapy, the anti TNF inhibitor treated patients had half the risk of incident or future PSA. The rate in PSA was one point one eight per 100 patient years, the rate in, with UVB therapy was two point four eight.

So the predictors of developing PSA, if you've got just psoriasis, is having a higher Posse score, greater severity of skin, the presence of arthralgia, nail involvement, and a family history. I think that's a nice report. I like this next report from Philip Meese and colleagues. It was published in Arthritis and Rheumatology. This looks at what happens when you, the benefits of early intervention of DMARR therapy in patients with psoriatic arthritis.

So in this study, two ninety one patients entering into the core Evitas, core Evitas, used to be the Corona database, two ninety one patients. You're said to get early DMARR therapy if you were initiated on DMARDs within the first year, late if it was after the first year, seventy nine percent got it in the first year. That's pretty amazing. For those of you who are participating in that, that means you're being very aggressive. Congratulations, wonderful.

But 21 were late. If you were an early initiator, you had a twofold higher chance of achieving MDA, minimal disease activity, a superlative outcome in psoriatic arthritis. Likewise, you are going to have a significantly higher chance of significant reductions in your CDAI, the clinical disease activity index Joseph Smallin. So, while both people, whether you got early DMARDs or late DMARDs, everybody got better, but the benefits were greater when given earlier. Again, that kind of supports that whole idea of a therapeutic window of opportunity, right?

That's it for this week on the podcast. Hope you enjoyed it. Come back, Follow us next week on RheumNow. Take care of yourselves.