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Top Four and More (4.10.2026)

Apr 10, 2026 3:15 pm
Dr. Jack Cush reviews the news and journal reports from RheumNow.com this week - including his top four favorite subjects.
Transcription
It's 04/10/2026, and this is the RheumNow podcast. This week on the podcast, my top four. The first three are top because they're public health problems. The fourth is a Jack Cush problem. Let's begin with CDC releasing some statistics this week about obesity in The United States, mainly looking at adults over age 20.

What's that number? What do you think it is? Of course, we know that each decade, each year, obesity goes up. There's an obesity epidemic in The United States. The number right now as of 2023 according to NHANES, that's sort of their annual survey statistics tool, was forty point three percent.

About ten percent of that's severe obesity, thirty two percent they're overweight by BMI. So these are studies where they are looking at BMI and whatnot. This is the public health challenge. This is why I've been presenting, a lot of obesity data, a lot of GLP one data. I think it certainly is a big issue, for all healthcare providers, especially those of us in rheumatology.

Another big concern of mine is that of mental health and depression. It is a major problem throughout healthcare. It is a major problem for our patients with our disorders, especially when we're trying to get optimal responses, and we are impaired by problems of depression, anxiety, bipolar disease. A UK study called the Our Future Health Study of one point five million in The UK found that affective disorders was significantly higher in autoimmune patients compared to the general population. Twenty nine percent versus eighteen percent.

That's an odds ratio of one point eight six. Again, these affective disorders are depression, bipolar anxiety. Using common tools like the PHQ-nine for depression, the GAD-seven for anxiety, these are tools that we could be using in practice. And it was very high, but then after adjustments for income and pain, it came down a little bit, but it's still there. The point is, what are you doing about it?

How is this coloring your practice? You should include a PHQ-nine in your survey tools, or a PHQ-two. PHQ-nine, nine questions. The PHQ-two, two questions. Or use my survey form that just ask the question, do you have depression?

And then you know whether you need to deal with it, look at it, compare it to what responses are, what the problems are. Big big issue. The other big issue from almost a over a decade now has been the opioid addiction problem in The United States. The good news is that between 2015 and twenty twenty three, long term opioid use has declined significantly. And as of 2023, there's about four plus million in The United States who are taking long term opioids.

It's still a problem, don't you think? I mean, the number is down, and, problems with the fentanyl and whatnot have gone down, and deaths have gone down in more recent years. But this still is a problem and we also published that during the same period gabapentin use has gone up. And there are a lot of warnings about gabapentin, there's a lot of concern that gabapentin is not effective. I do use gabapentin, I do use it as an adjunct modifier of pain responses, I do use it as a sleep aid and a fibromyalgia drug, but the evidence for it is really not that strong.

And why am I using it? Well, I don't have a lot of other great options, do I? This still is a public health problem. Problem number four is Still's disease. Yeah, it's a Jack Cush problem.

You know, I went into rheumatology because of systemic JIA and two incredible cases that I saw during my second year of residency, and have been devoted to it ever since, and hence you have to hear me talk about it a lot. I think it's not a bad thing. Still's disease always seems to come up. There was a recent article about machine learning to predict the horrible complication of Still's disease in both kids and adults. That complication being macrophage activation syndrome.

You don't want to miss it because Still's disease kills no one, unless you kill them with steroids and too much steroids, and you don't do that. The evidence says that, that you don't do that. But macrophage activation, which happens in twenty twenty five percent of kids and up to thirty seven percent of adults, is deadly, especially if not caught early. This machine learning application was applied to three twelve patients with adult Still's disease. The XGB Boost model gave you the five best predictors of developing MAS, and that would be very high ferritin, splenomegaly, very high platelets, cholesterol sed rate.

The AUC on that is eighty four percent, sensitivity eighty two percent, specificity seventy one percent. Let's look at that, and I would tell you the big predictors of macrophage activation, MAS, is ferritin hyperferonemia. You think ferritin is a good diagnostic test for Still's. It's not. It's only elevated in fifty percent, but extreme ferritins when you see it, uh-oh, holy crap, this could be MAS.

That's what you especially when they previously had very high white counts, and now the white count's turning and going down. When the white count goes down, the LFTs go up, the ferritin goes up, the CRP goes way up, IL-six levels go way up, and sed rate goes way down. It's a paradoxical picture from that usually seen with just active systemic stills. So this is very good. They have in here platelets and sed rate as being predictive, and they really mean low sed rate.

Platelet is just another acute phase reactant, just like ferritin. Cholesterol is curious on here. I don't know why it's on here. If you look at the data, low cholesterol in HLH, the hemophagocytic syndrome, is a poor indicator of survival. Low cholesterol.

And it's that sort of a cholesterol paradox with inflammation, high inflammation, low cholesterol kind of picture. Except in this paper it looked like high cholesterol. And in other papers it's HDL that predicts mortality. Don't be doing cholesterols and stills. I don't know what the hell you're doing if you're doing that.

It's really not that helpful, even though this paper said it was. Let's move on. Itch is a common problem with scleroderma. I wrote about this this week because I see it and I often don't know what to do about it. What the paper was mainly about, and this was a study of two thousand, one hundred and seventy three systemic sclerosis patients, and they were followed serially.

They had over 20,000 assessments, including 20,000 itch assessments. Who does itch assessments? 87 of these patients were female, the mean age was 55, forty percent of the patients had diffuse systemic sclerosis, which means sixty percent did not, and itch was seen in about forty percent of the patients. Was actually seen in about thirty five percent of patients, all the subgroups. It was moderate in severity, four out of ten in severity, and it was seen throughout the disease course.

What I had previously thought was that itch was a sign of rapidly progressing skin involvement and the scleroderma with, you know, thickening of the dermis with collagen and whatnot, and it was those changes and stretching of the dermis that led to the itch sensation. Turns out that, no, this is seen at all different phases of disease, and in up to thirty five percent of patients. The management is still problematic. I, you know, I send them to my dermatologist. Itch medicine is often not very effective.

Skin smoothing medicines and use of whatever you can to control the progression of scleroderma are the main things that are recommended. A study of mucocutaneous disease in lupus comes from the Asia Pacific lupus cohort, but has over four thousand one hundred SLE patients, and they defined, mucocutaneous disease as oral ulcers, rashes, malar rash, I think even Raynaud's. And anyway, it turns out that How many people do you think in their four thousand lupus patients in their cohort had mucocutaneous disease? It was only thirty six percent. I would have guessed like forty to fifty percent, but it was only thirty six percent.

Number one, about a third of them had rash, and that would be all kinds of rash, including malar rash. Alopecia, one in six. Mucosal ulceration, one in twelve patients. And overall, about fifteen-sixteen percent had persistent mucocutaneous disease. The disease associations with mucocutaneous disease included being Caucasian smoking, abnormal serologies, cutaneous vasculitis, myositis, serositis, nephritis, and psychiatric and brain manifestations of lupus.

All associated with skin disease. So, again, that's the I think that sort of coincides with what I see. I think though that finding, you know, we often think that mucocutaneous disease is on that spectrum of mild lupus white people, skin and joint disease and whatnot. This says though it does associate with more severe aspects of disease including nephritis, serositis, vasculitis and myositis, and that you should be looking for that. Speaking of myositis, a study from the Johns Hopkins myositis study group, which is, you know, Lisa Stein, Christopher and all their colleagues do great work there, their study of six thirty seven dermatomyositis looked at the issue of flares of dermatomyositis.

They found that flares were associated with objective measures of dermatomyositis disease activity, meaning if you're active you're more likely to have flares. Yes, a sort of duh statement. But what were the manifestations? Mainly rash, seventy six percent, muscle weakness, fifty eight percent, respiratory findings, symptoms and imaging abnormalities in nineteen percent, and arthritis in twelve percent as the basis for flares. And again, these patients all had met criteria for flares that they also looked at.

The interesting, they had many interesting points on this paper that you should look at, that two-five percent of patients who had flares were going to be diagnosed with cancer within the next twenty four months. It's a low number, but maybe that's a relevant number to you. Next week on RheumNow, I've got some really interesting data about the IMAX criteria for screening for cancer in myositis, dermatomyositis patients. A few good studies published about this recently, look for that on Monday. A five year Italian study of hospitalized autoimmune patients between 2018 and 2023 found that, and there was four thousand eight hundred patients, and they looked at what their cancer risk was amongst these almost four thousand nine hundred immune mediated disorder patients compared to over three hundred zero non IMID patients.

And IMID patients, immune mediated inflammatory disorders, had significantly higher risk of cancers, about a thirty two percent higher risk, odds ratio of one point three two, mainly in the first year of diagnosis. That as you follow those people longer, going out to five plus years, it went from one point eight three odds ratio down to one point two at five years or beyond. And of course the cancers that these patients had are the ones we've talked about before: more lung and bladder, more lymphoma, leukemia and melanoma, and they did include skin cancer, but I'm sure skin cancer would have been increased, in there as well. A nice report about AAV, ANCA associated vasculitis patients, two thousand eight hundred. How many do you think developed Pneumocystis, PJP infections?

You know, those are patients where maybe prophylaxis is most, appropriate, and the number was six point two percent. The people more likely to develop PJP, were being older, having higher max doses of glucocorticoids total cumulative doses as well. Rituximab, Citoxan, cyclophosphamide, were all predictors, as was being on PJP prophylaxis, which was actually proof that they had the problem. Those predictors had a fairly good concordance rate at two months and also at one year, so those should be things that where you really should strongly think about the use of PJP prophylaxis. In the first year it was estimated that the monthly risk was about one percent, and in the cohort they identified with these criteria thirty four potentially preventable cases of PJP if prophylaxis were applied.

I like this study about polymyalgia rheumatica, it was a study of two fifty seven patients from one center with PMR. They looked at, you know, the ones that were referred versus the ones that were not referred and then diagnosed. So like a hundred and fifty two, I think, or fifty four were diagnosed by them, ninety eight were referred by GPs, and when they compared the referrals, that GP referrals were mainly for diagnostic, more so for diagnostic uncertainty, fifty one percent, and less so for relapse of disease, twenty seven percent, or recurrence of disease, eleven percent. When they looked at the diagnostic accuracy, or the inverse of that, which were patients who were wrongly diagnosed, PMR diagnostic accuracy was better in rheumatologists than primary care eighty three percent versus sixty two percent. But congratulations to primary care doctors for being right sixty two percent of the time, and then referring the other ones for what was probably another diagnosis.

So, again, a good strong relationship between you and the primary care base that refers to you would be Why don't you get an email list of your primary care base, you can get it from your hospital system, and send them all a letter about the people that you want to see, who you'll see with expediency. Guess what? You'll start getting the patients that you really want to see. We tend to be quite passive about what comes to us. Speaking of comparisons, who's better at managing rheumatoid arthritis?

Orthopedist or rheumatologist? That seems like a no brainer, right? Well, not necessarily in Japan. They did a study there called the ANSWER Study, where they looked at seven thousand two hundred RA patients who were being managed by either orthopedists or rheumatologists. Turns out in Japan this is very common.

Orthopedists will commonly manage them, not surgically manage them, medically manage them. And in this cohort of seven thousand two hundred, five thousand four hundred were managed by rheumatologists, eighteen hundred by the orthopedist, and what were the difference? And again, these are patients that were being treated with either JAK inhibitors or biologics, right? So, the orthopedist, the RA patients they managed tended to have a longer diagnosis, more disease duration. They were more seropositive, had more functional impairment, they gave them more intra articular steroids, they had and they also used more methotrexate, steroids and TNF inhibitors compared to the other drugs.

They these patients also had less comorbidity and which were probably then being managed by the rheumatologists, and they were less likely to use oral steroids than the rheumatologists. The rheumatologists were more likely to use IL-six inhibitors and abatacept. And guess what? In the end, who came out better? Who managed them better?

They were exactly the same. They were exactly the same, Which is a testimony to the strength of knowledge and practice by orthopedists in Japan. I think they're all operating off of the same info set and guideline list, and good things can happen when that happens. A study from China, from Beijing, was published in the Mayo Clinic proceedings this past week, and I found it interesting it's a direct head to head study of tofacitinib versus methotrexate. An open label, randomized, active control study of one hundred and sixteen DMAR naive RA patients.

Think about that: they're all DMAR naive, 116 of them, you know, 58 or whatever that is get one or the other, and everyone gets a single intramuscular injection of I think it was beta methicillin. At three months tofacitinib responses were better than methotrexate. How do they measure response? A greater than 50% reduction in SDI, the simplified disease activity index, that was 94% improved on TOFA and seventy five percent improved on methotrexate. Similarly, C.

Dye and -twenty eight CRP outcomes favored tofacitinib. And here's a really interesting point: Tofacitinib was more cost effective than methotrexate. Well, that's obviously a function of, Beijing and China, where tofacitinib is not on patent, it's about to go off patent, and this is sort of a big issue for you, is it not? It's gonna go off patent here in The United States, it's gonna get cheaper. And what will be the cost differences between methotrexate and a JAK inhibitor?

And will that change what your first line therapy is? Remember, every guideline says first line methotrexate. It's the anchor drug according to the ACR. I think that could change when tofacitinib and other JAK inhibitors get cheap. Three more reports that we wrote about, I wrote of a review.

Lancet published a review on Vexus syndrome. As soon as I published it, it went boom, right to the top, as most read article. As you know, Vexus is an X linked autoinflammatory disorder caused by a somatic mutation of the UBA1 gene, leading to all kinds of hemopoetic and immunologic, problems that lead to what has, prior to its identification, led to treatment refractory systemic, inflammatory disorders that often were confused with relapsing polychondritis, sweet syndrome, ANCA vasculitis, maybe Still's disease, but again it's important that we now have a way of diagnosing this. It is diagnosed by doing genetic testing. How common is this disorder?

It is seen in one in four thousand men over the age of 50, so it's rare. But it's even more rare, six times more rare, in one in twenty six thousand women over the age of 50. And again, it's been confused, lot of different diagnoses. The review is a good one, our review of it was a good one. The main treatments of this right now seem to be steroids, IL-six inhibitors or JAK inhibitors, but there is no diagnostic criteria that are universally agreed upon.

Having an awareness, and knowing when to do the test makes it sort of, an achievable diagnosis in many. And when I lecture in front of large groups of audiences, there's, you know, I don't know, twenty-twenty five percent of rheumatologists have made that diagnosis. That's impressive. I like to review this week on, calcinosis cutis in systemic sclerosis. When we see it, it's ugly, we don't really know how to treat it.

I have written about it, talked about it before. The universally agreed upon treatment for problematic calcinosis is surgery. There really is no drug that works. This is a study from the U Star database of over seven thousand systemic sclerosis patients, and while there were many predictors mainly being that of worse disease, Patients who had calcinosis cutis became patients who were more likely to have higher Rodnan Skin scores, meaning more severe disease. Telangiectasias, digital ischemia and ulcers, advanced capillaroscopy changes, tendon friction rubs, GI involvement, pulmonary arterial hypertension, synovitis and renal crisis.

It's a bad news finding in systemic sclerosis. Last report was comes from JAMA, and it was an interesting report of six about rotator cuff findings on MRI and how important they are, and they basically said they're incidental no matter what you think. A cross sectional study of the general population in Finland, six zero two people undergoing bilateral shoulder MRI for some sort of shoulder pain, found that MRI abnormalities were seen in everyone. Like ninety six percent of people over the age of 40 who had MRIs had rotator cuff abnormalities, regardless of whether excuse me, these six zero two did not have symptoms. Some did, some didn't.

So regardless of symptoms, the MRI positivity meant nothing. So, six zero two, five ninety five had abnormalities. What were the abnormalities? A quarter had tendinopathy, sixty two percent had partial tears, eleven percent had full thickness tears. And these were all findings that were worse in an older and older population.

And that's kind of the problem, isn't it? Who are you ordering MRI of the shoulder in? Your older RA, your older PSA, your older OA patients. It means nothing! If you started doing MRIs on everybody, you see the same findings.

The question is: you do the MRI to make the diagnosis that's going to lead to better treatment or surgery. The predictors of surgery and benefit of surgery is acute rotator cuff tears, often with a pop, right? Often in younger people surgery more likely happen in people who have physical demands where they need their shoulders and need to fix this problem. Successive surgery is based on tendon quality, low amount of fatty infiltration gives you better outcomes, and the size of the tear, meaning small tears repair much more easily and have less failure in the future. I'm going to think twice about ordering MRI and instead assuming everybody all my RA patients 50 with shoulder pain probably have rotator cuff disease.

Let's do some physical therapy, let's get better control of their RA. Think about it. Let's talk next week here on the podcast. Take care.

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