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Hi everyone. It's July 24, 2026. This is the RheumNow podcast and I'm Jack Cush with RheumNow. A number of uh popular things this week. I think the big hit this week was fibromyalgia. We'll talk about that. We had a really stellar Tuesday night rheumatology webinar that I'll talk about briefly, and uh a few great articles during our gout campaign that we'll also cover in this podcast.
A few um news items rather than journal reports. Uh the uh European Union this week approved narendum alas. It's uh trade name is Jessade um from BI, was approved in the EU for use in idiopathic pulmonary fibrosis and progressive pulmonary fibrosis, IPF and PPF. Uh nerendum alas, uh as you know, was approved in October and December of 2025 for those same indications by the FDA for use in the United States. Are you using these drugs? We had a big long campaign on ILD in September where we discussed this in great length. This is an easier drug to use than nintedanib, uh and certainly the uh prevalence of our patients calls for some of these drugs. Will you be using them? Will you be partnering with pulmonary to use them? Again, the experts say that we can use them. We don't need to necessarily partner. I think it's a major advance.
Um, Lancet Rheumatology has thrown another log on the fire that is avacopan. Um, again, they wrote a really good editorial that I point you to that it's a full read. It's in Lancet Rheumatology. It points out what are the problems. It sort of reviews the recent history on this if you're not up to date about why avacopan may be in trouble. Avacopan, now currently owned by Amgen, um has been called out by the FDA, also by the EMA in Europe, and also by Japanese regulators. All of them basically calling for the drug to be withdrawn. Um and it explains why, but it also is a balanced piece and says, you know what, there's in postmarketing experience, there's good data about its efficacy in real world studies. It's been shown to lower steroid use, um and the issue of hepatotoxicity um may be overstated since most of that seems to have occurred in Japanese populations. So it's a nice read. I would point you to it. I think it's worth reading.
Uh a report on lupus looked at um the risk of MI in lupus patients by looking at it from a standpoint of an MI population. So this is a large UK study of MI patients, almost 800,000 of them, and in that study 0.1% of those patients had SLE, 715, when compared to the non-SLE patients um not surprisingly the SLE patients were uh younger and more female, but if you
but if you were a lupus and you had an MI you had a significantly higher risk of all cause mortality, a 62% higher risk, and within the first 30 days, and even going out to 5 years the hazard ratio is still 1.84.
And this jives with other past reports saying that a mortality rate in a lupus patient with an MI really goes up acutely in the post-MI era right afterwards. So the interesting thing about this data, them having a higher mortality, this is despite the patients being younger and overall having less traditional cardiovascular risk factors and co-morbidities.
So, again, this underscores that paradigm that we should really be looking to get our patients off of steroids or as low as steroids as possible and better managing their inflammatory disease in a number of different ways.
Uh, a few reports on scleroderma this week. EUSTAR, as you know, is a European large prospective study of systemic sclerosis patients. In this sub-study they actually looked at the efficacy and safety — more the safety than efficacy — of JAK inhibitors in scleroderma. And they, in their database of like 19,000 patients, I think they only had 38 on JAK inhibitors and they matched them up with scleroderma patients who were treated with either mycophenolate, methotrexate, or rituximab — 180 in those groups. In all these groups they were relatively matched as far as their profiles and their demographics; one-third of all these patients had diffuse cutaneous disease and two-thirds had limited disease.
Limited number of adverse events — 23 adverse events in almost a thousand patient years on JAK inhibitors — and the efficacy of JAK inhibitors was equal to the other drugs. None of them really stood out. Things that you would look to as efficacy would be things like their skin fibrosis scores. In fact, it improved a little bit on the JAK inhibitor with a modified Rodnan skin score dropping almost two points. Patients on JAK inhibitors had improvement in swollen joint counts and their lung function as measured by FVC remained stable during the period of observation. Overall about 39% stopped the drug, meaning 61% stayed on it, and that was also on par.
The one point that I saw that I thought was interesting is very few of those patients had calcinosis going in and none of them progressed, but there were no new cases of calcinosis in this cohort, and I'm wondering if that might be one of the hidden advantages of
JAK inhibitor therapy. We talked a few years ago about — I think it was early reports showing that tofacitinib looked very good in a somewhat controlled trial of systemic sclerosis. I think this needs to be investigated more thoroughly.
I like this report about malnutrition in scleroderma. Obviously GI disease is common in systemic sclerosis and the measure of malnutrition in those patients is their BMI. In a cohort of 450 systemic sclerosis patients followed for over 5 years, they found that lower BMIs were not uncommon, and they were associated with several findings: one, pseudo-obstruction; two, a smaller oral aperture; and three, a higher medsger vascular severity score. The BMI — the mean for the total population was I think 25, 26 — generally didn't change, but in many of the patients in whom the BMI was lower it did tend to have a downward trend over time that was not significant.
The point of this report might be you should be using BMI as a vital sign in patients with systemic sclerosis. We often don't pay attention to weight and BMI — you probably should, for a lot of different reasons, especially a condition like this. And I don't know about you, but I've always used the patient's weight as a primary outcome variable. Patients with heart failure, you know, that were on diuretics and afterload reducers and whatnot — their weight was gigantically important. Why is it not so for scleroderma?
Two reports on Still's disease. One looked at the efficacy of biologics versus traditional DMARDs — biologics being IL-1 and IL-6 inhibitors, DMARDs being methotrexate, calcineurin inhibitors, and JAK inhibitors — 126 patients, one-third from Germany, one-third from Shanghai. Biologics had more sustained event-free remissions and event-free states; those were highly significant. They were also more likely to have their steroids discontinued when compared to the patients that were on the oral DMARDs and calcineurin inhibitors. And again, this is in line with both the ACR and EULAR guidelines that say first and primarily your treatment approach to systemic JIA is a biologic — an IL-1 and IL-6 inhibitor. It's more important than steroids, it's more important than methotrexate, and really that needs to be paramount.
I got a question from one of our colleagues — in her country they don't have IL-18 inhibitors, and the patient wouldn't take anakinra, or couldn't — actually couldn't take
or couldn't actually couldn't take anakinra and didn't want to take shots yet it was newly diagnosed systemic JIA adult um so what are you going to do um I I think that in such patients methotrexate starting with steroids methotrexate and then um probably adding a JAK inhibitor now that's not in the guidelines anywhere, but you don't have any choices if you can't use a cytokine inhibitor as per the guidelines.
Another study comes uh from China looking at uh lung disease. Um I put this out there although I kind of have a problem with it. 209 patients with AOSD, adult onset Still's disease, they identify 23% of those people as having lung disease by chest X-ray. Now that's about right. You know, if you look at large, as I have looked at large cohorts of patients, how many are going to have pneumonitis? It's about 20%.
Um, they're not really answering the question of this issue of chronic lung disease in Still's patients. But anyway, as identified by X-ray, um, 23% had AOSD lung disease. And of those patients, um, 69% of them were asymptomatic.
They noted that the risk factors for lung disease in Still's were pleuritis. That's kind of a duh, isn't it? Is it not? Uh, MAS uh with a 2.6 hazard ratio and uh disease relapses. Again, um a twofold or higher uh risk. Um they talk about imaging patterns. I don't think this made a lot of sense because they were all over the map on this. Exudative pattern, interstitial pattern, suspected pulmonary hypertension that goes along with the chronic lung issue in Still's. It's not one disorder. It's not even a narrow set of disorders. It's like a little bit of this, a little bit of that, some proteinaceous alveolosis, and you know, come on. Uh uh and and the studies of an HLA association have not worked out. Um, I do think this happens. I've seen a lot of Still's patients, uh, and I can tell you about four or five out of the over hundred that I've seen that had chronic lung disease. And you wonder, was it related to them getting an IL-1 inhibitor or an IL-6 inhibitor, but again, it's very uncommon as per EULAR guidelines, you should be looking for this um, and have a low threshold for doing imaging for that.
A meta-analysis of 51 studies shows that guess what we rheumatologists are not that good at vaccination. Um influenza vaccination rates uh were 50% in RA, 42% in lupus, 43 in spondylitis, 53 in PsA, pneumococcal even worse. Um 37% 30% 39% and 41% in those same four disorders.
By the way, um I may chastise you here, but you're no worse than your internist but you're no worse than your
internist colleagues who are also not good at doing vaccinations in their non-rheumatology patients. So, but clearly there's a greater need in your patients.
This is obviously not as much an issue in older patients and patients with comorbidities who are more likely to actually get vaccination. But this is to serve as a reminder that something that we really need to pay attention to. And again, you're probably the people who will be driving this.
A study of cancer — and how you treat patients with cancer and inflammatory arthritis disorder. This is like a 9-year study. 148 inflammatory arthritis patients, 43 with SpA, 35 with PsA, and 50 with RA, had a prior cancer, followed for almost 60 months. And 19% had a cancer recurrence.
When they did their comparisons, the post-cancer exposure to either biologic or targeted synthetic did not increase the progression of cancer or recurrence of cancer after they adjusted for age and comorbidities. And again, this goes along with the guidelines. Your patient's got a cancer, especially if it's a solid cancer, treat them as if they don't have the cancer. Treat the disease as you would and pay no attention to the cancer. You take care of the arthritis, let the oncologist take care of the cancer.
As you know, we have a gout campaign going on the month of July. It's been really exciting. I think we've seen some really interesting articles, really high read rates on why do gout flares start at night, gout in minority populations by Hyon Choi, the kidney and gout by Professor Johnson who's a nephrologist, and Joshua Baker writing about uric acid — should it be lower? Yes, it should. And he tells you the evidence for that.
If you didn't see this week's Tuesday night rheumatology webinar, it was just stellar. Lisa Stamp, Ted Mikuls, Angelo Gaffo, and Michael Pillinger — a master class on gout management. The title was upgrading and maximizing your use of classic gout drugs. Mainly we talked about urate lowering therapy and colchicine and the pitfalls of prescribing. It's a podcast, it's a video, it's 58 minutes long. Check it out.
Other reports this week on gout: SGLT2 inhibitors reduce not only the occurrence of gout but the use of gout meds. A study of 26,000 gout patients with diabetes, most of which were older and most of which had a lot of polypharmacy — if they were treated with an SGLT2 inhibitor versus a DPP-4 inhibitor, they had less allopurinol starts
had less allopurinol starts — 38% less. They were also used less — 38% less. They were also used less steroids, less non-steroidals, less colchicine, and less diuretics — between a 15 and 22% reduction.
And I bring this up because of all the diabetes medicines that are getting play in rheumatology, mainly talking about GLP-1 agonists, the SGLT2 inhibitors are far far more effective in gout prevention and gout better outcomes than are the GLP-1 agonists in gout. And that's a slam dunk — been seen in multiple studies.
A UK primary care database study of almost 21 years looked at the potential benefit of being on colchicine. So these are gout patients — 31,000 patients — who started on colchicine as a new prescription compared to the same number who did not start on colchicine. They were older, at a BMI of 30, followed for four and a half years, and colchicine had a 12% significantly lower — 12% lower risk of arthroplasty.
I think it was in the 5-year period — that was overall. If you just looked at patients who had gout and hip or knee OA and went on colchicine, it was a 23% lower risk of future arthroplasty. So is there something unique about colchicine? Well, it's anti-inflammatory — in controlling inflammation it might lessen the progression of degenerative joint disease. Again, since this is an observational study, I don't think you can get too much into how did that happen or what the explanation might be.
Two reports this week on allopurinol hypersensitivity — the actual risk of severe allergic reactions, toxic epidermal necrolysis, Stevens-Johnson syndrome, severe cutaneous adverse reactions — SCARs is what they call them — is 0.4 to 2%. It may be higher and maybe up to 10% in people with chronic kidney disease.
The report that we put up was the testing for HLA-B*5801 dramatically increases the risk of this. It's over 100-fold increased risk — odds ratio 117 in this one particular report.
Another report from Hopkins looked at 16 patients who had allopurinol-induced severe cutaneous adverse reactions and showed that it was not just HLA-B*5801 — which in their study gave a 208-fold higher risk of these reactions — but also HLA-A*3402, which gave almost a 21-fold higher risk.
So HLA-B*5801 explains about 2/3 of these bad reactions that occur in the United States, and there are not many of them to be honest. But if you had testing for the second class one allele, you now cover about 80% of cases. So you might add that to your list — again, patients who are from Han Chinese or Southeast Asian backgrounds should be tested for HLA-B*5801. And then
African-Americans B5801. Um, and then African-Americans are at higher risk in the United States, are at higher risk in the United States, but not everybody does it. And the but not everybody does it. And the question is, how often will you get question is, how often will you get burned? And in in a career, in a burned? And in in a career, in a lifetime, maybe only once, but when lifetime, maybe only once, but when it happens, there's a risk of death. it happens, there's a risk of death. It's kind of ugly. If you've been It's kind of ugly. If you've been following our website, we have some following our website, we have some quotes and factoids about gout. I'm quotes and factoids about gout. I'm going to put two up here for you here. going to put two up here for you here.
Being on low-dose aspirin either 81 or Being on low-dose aspirin either 81 or 325 milligrams increases the risk of 325 milligrams increases the risk of gout by 81%. gout by 81%.
81% almost a doubling of risk. However, 81% almost a doubling of risk. However, if you're on allopurinol or urate if you're on allopurinol or urate lowering therapy, you don't have to lowering therapy, you don't have to worry about that. There is no higher worry about that. There is no higher risk. That's important. Again, ULT is risk. That's important. Again, ULT is protected and you could be on background protected and you could be on background 81 milligrams a day assuming someone 81 milligrams a day assuming someone needs to be on that. And then the other needs to be on that. And then the other fact that we put up I think a few days fact that we put up I think a few days ago is uh 40% of acute acute gout ago is uh 40% of acute acute gout attacks have a normal uric acid. You attacks have a normal uric acid. You know that because we see that um the know that because we see that um the other 40% number is that 40% of acute other 40% number is that 40% of acute gout patients and attacks are not tested gout patients and attacks are not tested for a uric acid level. for a uric acid level.
Wow. And I'm going to throw in the other Wow. And I'm going to throw in the other 40% number that you all know which is 40% number that you all know which is only 40% of people who go on urate urate only 40% of people who go on urate urate lowering therapy achieve their target of lowering therapy achieve their target of six or less in uric acid and that's six or less in uric acid and that's especially so in primary care but even especially so in primary care but even in rheumatology 40%. Only 40%. So that in rheumatology 40%. Only 40%. So that 40% number is something that should 40% number is something that should bother all of us who manage gout.
Um a great report uh written up by uh Chio great report uh written up by uh Chio Yokose from the Mass General Brigham Yokose from the Mass General Brigham uh on evidence-based dietary uh on evidence-based dietary recommendations. It's a nice read. Um recommendations. It's a nice read. Um she talks about, you know, yes, we she talks about, you know, yes, we should all be on low-purine diets, but should all be on low-purine diets, but the hazard of that is you'll be on an the hazard of that is you'll be on an unhealthy diet and you won't — you no unhealthy diet and you won't — you no purines means no protein, which means purines means no protein, which means you're going to get high fructose things you're going to get high fructose things and things that are bad for gout. and things that are bad for gout.
We do know that you need to be on high We do know that you need to be on high protein and gout patients have diabetes and protein and gout patients have diabetes and diabetics need to be on high protein diabetics need to be on high protein diets. Um but and again you know Atkins diets. Um but and again you know Atkins diets which is a high protein diet has diets which is a high protein diet has been associated with some severe been associated with some severe worsening of gout. So there's a little worsening of gout. So there's a little bit of a conundrum there. The diets that bit of a conundrum there. The diets that are generally recommended are the DASH are generally recommended are the DASH diet which was originally developed or diet which was originally developed or best tested for hypertension management. best tested for hypertension management. As you know anti-inflammatory and As you know anti-inflammatory and Mediterranean diets work here. And the Mediterranean diets work here. And the other question she gets into is shellfish other question she gets into is shellfish and seafood. Um, and the point and seafood. Um, and the point there is that um, I used to say, you there is that um, I used to say, you know, that seafood recommendation know, that seafood recommendation doesn't really count cuz I — it does — I doesn't really count cuz I — it does — I have never seen it. And I got I got
have never seen it. And I got booed off stage in New England when I brought that up because they see it all the time. Not a lot of shellfish in Dallas, Texas where I live. So yes, seafood and especially shellfish is a big problem for a lot of patients. But if the patient is to be well controlled on urate lowering therapy, you could reintroduce the use of shellfish without hazard and without risk. And of course, she makes the important point of dietary counseling for these patients. Look for a card on my website called GoutTop that you can print out and give to patients. It's got all this information about diet on there that you might want to impart upon them.
A great article this week also by another person from MGH, Sarah Terkeltaub, talking about new thinking on calcium pyrophosphate deposition disease, which affects 8 to 10 million Americans. She begins by going over the fact that the classification and nomenclature has changed. We don't really talk about pseudogout anymore. That's the old term.
Now, if you look at this great figure she has in the article, it's a big Venn diagram with overlapping circles. The biggest circle being OA patients with CPPD. Then there are two medium-sized circles of either acute calcium pyrophosphate arthritis or chronic calcium pyrophosphate arthritis, and then a smaller circle for the crowned dens syndrome where there's calcification at C1-C2. Again, chondrocalcinosis is still in there for X-ray only evidence.
She talks about imaging — that CPPD is really a crystal identification disorder, but that's not always possible, and when not possible, imaging might supplant crystal identification, with ultrasonography and CT having greater sensitivity than the conventional radiograph and showing chondrocalcinosis.
As you know, management is acute steroids or colchicine, chronic IL-6. There are no FDA approved therapies, but there are trials — three trials that are in progress right now, including one with an IL-6 inhibitor. But she says there's evidence for, although not well controlled, for hydroxychloroquine, methotrexate, IL-1 inhibitors, and/or IL-6 inhibitors in patients, I assume, with chronic CPPD arthritis.
Lastly, fibromyalgia. Oh my goodness, I put this up. It's a review article in New England Journal from last week from David Williams and Daniel Clauw, where they review the diagnosis and management of fibromyalgia. And my apologies for quoting them and rewriting their article in a more dense
easier to read in a more dense, easier to read fashion, but even mine is a little bit long. Again, fibromyalgia affects up to 6% of the US population. It is a widespread pain disorder where fatigue and sleep problems, along with memory problems, are a gigantic problem. It is a hypersensitivity disorder. It's a centrally mediated hypersensitivity to external sensory stimuli that leads to pain, brain fog, fatigue, mood changes, etc.
The diagnosis is clinical — labs, imaging tests, not really. There's no immunologic tests, sorry. And the thoughts that this is a small fiber autonomic neuropathy, or that it's an autoimmune disease — the autoimmune disease is not well substantiated. Again, we do know it's centrally mediated, we do know there's a hyperresponsiveness.
They are rightly so big on treatment of sleep — that's where all the great gains in therapy are coming from. And they're strongly in favor of stretching therapies, tai chi, qigong, yoga, and then also cognitive behavioral therapy.
So again, when it comes to treatment, the tenets are education, self-care, focusing on sleep, focusing on movement and stretching, and behavioral means. And they're very big about CBT, cognitive behavioral therapy, to help both sleep and/or pain, but probably more so for sleep.
They do say that the drugs that are out there and approved that you use all the time — analgesics, muscle relaxants, tricyclics, gabapentinoids, and SNRIs — modest effects if anything. And then when they do work, they work because of their control on sleep, which again underscores the importance of sleep.
A few new things that I didn't know about. Well, I know about the new sublingual cyclobenzaprine that's FDA approved. I was not aware of a study of combination therapy outperforming monotherapy. Gabapentinoids at bedtime plus an SNRI during the daytime had 68% improvement in global pain compared to 42% for duloxetine, or 39% for pregabalin, versus 18% for placebo.
That's significant, and those are 6-week results. Obviously NSAIDs and opioids really don't do anything here and should be avoided.
They expressed some enthusiasm — and let me underscore the word "some" — for low-dose naltrexone as an emerging, unrecognized option, but we need studies on that. And there is good data about transcranial stimulation, TENS, maybe gabapentinoids, and THC — it's unclear though where those stand at this point.
Anyway, watch for our content on gout this month.
this month that it's going to wrap up next week. Next week our TNR Tuesday rheumatology is going to be on advanced therapies. Um Herb Baraf, um uh Naomi Schlesinger. Um oh my goodness. Um a few others I now I'm blanking on. I should have looked them up, but it's a stellar lineup.
Um, and we're going to talk about uh the uricase drugs, the use of cytokine inhibitors, um, drugs that are coming down uh the development pipeline. Um, I think it's going to be another exciting session that you'll want to tune into.
That's it for this week on the podcast. We'll talk next week. Take care.
A few um news items rather than journal reports. Uh the uh European Union this week approved narendum alas. It's uh trade name is Jessade um from BI, was approved in the EU for use in idiopathic pulmonary fibrosis and progressive pulmonary fibrosis, IPF and PPF. Uh nerendum alas, uh as you know, was approved in October and December of 2025 for those same indications by the FDA for use in the United States. Are you using these drugs? We had a big long campaign on ILD in September where we discussed this in great length. This is an easier drug to use than nintedanib, uh and certainly the uh prevalence of our patients calls for some of these drugs. Will you be using them? Will you be partnering with pulmonary to use them? Again, the experts say that we can use them. We don't need to necessarily partner. I think it's a major advance.
Um, Lancet Rheumatology has thrown another log on the fire that is avacopan. Um, again, they wrote a really good editorial that I point you to that it's a full read. It's in Lancet Rheumatology. It points out what are the problems. It sort of reviews the recent history on this if you're not up to date about why avacopan may be in trouble. Avacopan, now currently owned by Amgen, um has been called out by the FDA, also by the EMA in Europe, and also by Japanese regulators. All of them basically calling for the drug to be withdrawn. Um and it explains why, but it also is a balanced piece and says, you know what, there's in postmarketing experience, there's good data about its efficacy in real world studies. It's been shown to lower steroid use, um and the issue of hepatotoxicity um may be overstated since most of that seems to have occurred in Japanese populations. So it's a nice read. I would point you to it. I think it's worth reading.
Uh a report on lupus looked at um the risk of MI in lupus patients by looking at it from a standpoint of an MI population. So this is a large UK study of MI patients, almost 800,000 of them, and in that study 0.1% of those patients had SLE, 715, when compared to the non-SLE patients um not surprisingly the SLE patients were uh younger and more female, but if you
but if you were a lupus and you had an MI you had a significantly higher risk of all cause mortality, a 62% higher risk, and within the first 30 days, and even going out to 5 years the hazard ratio is still 1.84.
And this jives with other past reports saying that a mortality rate in a lupus patient with an MI really goes up acutely in the post-MI era right afterwards. So the interesting thing about this data, them having a higher mortality, this is despite the patients being younger and overall having less traditional cardiovascular risk factors and co-morbidities.
So, again, this underscores that paradigm that we should really be looking to get our patients off of steroids or as low as steroids as possible and better managing their inflammatory disease in a number of different ways.
Uh, a few reports on scleroderma this week. EUSTAR, as you know, is a European large prospective study of systemic sclerosis patients. In this sub-study they actually looked at the efficacy and safety — more the safety than efficacy — of JAK inhibitors in scleroderma. And they, in their database of like 19,000 patients, I think they only had 38 on JAK inhibitors and they matched them up with scleroderma patients who were treated with either mycophenolate, methotrexate, or rituximab — 180 in those groups. In all these groups they were relatively matched as far as their profiles and their demographics; one-third of all these patients had diffuse cutaneous disease and two-thirds had limited disease.
Limited number of adverse events — 23 adverse events in almost a thousand patient years on JAK inhibitors — and the efficacy of JAK inhibitors was equal to the other drugs. None of them really stood out. Things that you would look to as efficacy would be things like their skin fibrosis scores. In fact, it improved a little bit on the JAK inhibitor with a modified Rodnan skin score dropping almost two points. Patients on JAK inhibitors had improvement in swollen joint counts and their lung function as measured by FVC remained stable during the period of observation. Overall about 39% stopped the drug, meaning 61% stayed on it, and that was also on par.
The one point that I saw that I thought was interesting is very few of those patients had calcinosis going in and none of them progressed, but there were no new cases of calcinosis in this cohort, and I'm wondering if that might be one of the hidden advantages of
JAK inhibitor therapy. We talked a few years ago about — I think it was early reports showing that tofacitinib looked very good in a somewhat controlled trial of systemic sclerosis. I think this needs to be investigated more thoroughly.
I like this report about malnutrition in scleroderma. Obviously GI disease is common in systemic sclerosis and the measure of malnutrition in those patients is their BMI. In a cohort of 450 systemic sclerosis patients followed for over 5 years, they found that lower BMIs were not uncommon, and they were associated with several findings: one, pseudo-obstruction; two, a smaller oral aperture; and three, a higher medsger vascular severity score. The BMI — the mean for the total population was I think 25, 26 — generally didn't change, but in many of the patients in whom the BMI was lower it did tend to have a downward trend over time that was not significant.
The point of this report might be you should be using BMI as a vital sign in patients with systemic sclerosis. We often don't pay attention to weight and BMI — you probably should, for a lot of different reasons, especially a condition like this. And I don't know about you, but I've always used the patient's weight as a primary outcome variable. Patients with heart failure, you know, that were on diuretics and afterload reducers and whatnot — their weight was gigantically important. Why is it not so for scleroderma?
Two reports on Still's disease. One looked at the efficacy of biologics versus traditional DMARDs — biologics being IL-1 and IL-6 inhibitors, DMARDs being methotrexate, calcineurin inhibitors, and JAK inhibitors — 126 patients, one-third from Germany, one-third from Shanghai. Biologics had more sustained event-free remissions and event-free states; those were highly significant. They were also more likely to have their steroids discontinued when compared to the patients that were on the oral DMARDs and calcineurin inhibitors. And again, this is in line with both the ACR and EULAR guidelines that say first and primarily your treatment approach to systemic JIA is a biologic — an IL-1 and IL-6 inhibitor. It's more important than steroids, it's more important than methotrexate, and really that needs to be paramount.
I got a question from one of our colleagues — in her country they don't have IL-18 inhibitors, and the patient wouldn't take anakinra, or couldn't — actually couldn't take
or couldn't actually couldn't take anakinra and didn't want to take shots yet it was newly diagnosed systemic JIA adult um so what are you going to do um I I think that in such patients methotrexate starting with steroids methotrexate and then um probably adding a JAK inhibitor now that's not in the guidelines anywhere, but you don't have any choices if you can't use a cytokine inhibitor as per the guidelines.
Another study comes uh from China looking at uh lung disease. Um I put this out there although I kind of have a problem with it. 209 patients with AOSD, adult onset Still's disease, they identify 23% of those people as having lung disease by chest X-ray. Now that's about right. You know, if you look at large, as I have looked at large cohorts of patients, how many are going to have pneumonitis? It's about 20%.
Um, they're not really answering the question of this issue of chronic lung disease in Still's patients. But anyway, as identified by X-ray, um, 23% had AOSD lung disease. And of those patients, um, 69% of them were asymptomatic.
They noted that the risk factors for lung disease in Still's were pleuritis. That's kind of a duh, isn't it? Is it not? Uh, MAS uh with a 2.6 hazard ratio and uh disease relapses. Again, um a twofold or higher uh risk. Um they talk about imaging patterns. I don't think this made a lot of sense because they were all over the map on this. Exudative pattern, interstitial pattern, suspected pulmonary hypertension that goes along with the chronic lung issue in Still's. It's not one disorder. It's not even a narrow set of disorders. It's like a little bit of this, a little bit of that, some proteinaceous alveolosis, and you know, come on. Uh uh and and the studies of an HLA association have not worked out. Um, I do think this happens. I've seen a lot of Still's patients, uh, and I can tell you about four or five out of the over hundred that I've seen that had chronic lung disease. And you wonder, was it related to them getting an IL-1 inhibitor or an IL-6 inhibitor, but again, it's very uncommon as per EULAR guidelines, you should be looking for this um, and have a low threshold for doing imaging for that.
A meta-analysis of 51 studies shows that guess what we rheumatologists are not that good at vaccination. Um influenza vaccination rates uh were 50% in RA, 42% in lupus, 43 in spondylitis, 53 in PsA, pneumococcal even worse. Um 37% 30% 39% and 41% in those same four disorders.
By the way, um I may chastise you here, but you're no worse than your internist but you're no worse than your
internist colleagues who are also not good at doing vaccinations in their non-rheumatology patients. So, but clearly there's a greater need in your patients.
This is obviously not as much an issue in older patients and patients with comorbidities who are more likely to actually get vaccination. But this is to serve as a reminder that something that we really need to pay attention to. And again, you're probably the people who will be driving this.
A study of cancer — and how you treat patients with cancer and inflammatory arthritis disorder. This is like a 9-year study. 148 inflammatory arthritis patients, 43 with SpA, 35 with PsA, and 50 with RA, had a prior cancer, followed for almost 60 months. And 19% had a cancer recurrence.
When they did their comparisons, the post-cancer exposure to either biologic or targeted synthetic did not increase the progression of cancer or recurrence of cancer after they adjusted for age and comorbidities. And again, this goes along with the guidelines. Your patient's got a cancer, especially if it's a solid cancer, treat them as if they don't have the cancer. Treat the disease as you would and pay no attention to the cancer. You take care of the arthritis, let the oncologist take care of the cancer.
As you know, we have a gout campaign going on the month of July. It's been really exciting. I think we've seen some really interesting articles, really high read rates on why do gout flares start at night, gout in minority populations by Hyon Choi, the kidney and gout by Professor Johnson who's a nephrologist, and Joshua Baker writing about uric acid — should it be lower? Yes, it should. And he tells you the evidence for that.
If you didn't see this week's Tuesday night rheumatology webinar, it was just stellar. Lisa Stamp, Ted Mikuls, Angelo Gaffo, and Michael Pillinger — a master class on gout management. The title was upgrading and maximizing your use of classic gout drugs. Mainly we talked about urate lowering therapy and colchicine and the pitfalls of prescribing. It's a podcast, it's a video, it's 58 minutes long. Check it out.
Other reports this week on gout: SGLT2 inhibitors reduce not only the occurrence of gout but the use of gout meds. A study of 26,000 gout patients with diabetes, most of which were older and most of which had a lot of polypharmacy — if they were treated with an SGLT2 inhibitor versus a DPP-4 inhibitor, they had less allopurinol starts
had less allopurinol starts — 38% less. They were also used less — 38% less. They were also used less steroids, less non-steroidals, less colchicine, and less diuretics — between a 15 and 22% reduction.
And I bring this up because of all the diabetes medicines that are getting play in rheumatology, mainly talking about GLP-1 agonists, the SGLT2 inhibitors are far far more effective in gout prevention and gout better outcomes than are the GLP-1 agonists in gout. And that's a slam dunk — been seen in multiple studies.
A UK primary care database study of almost 21 years looked at the potential benefit of being on colchicine. So these are gout patients — 31,000 patients — who started on colchicine as a new prescription compared to the same number who did not start on colchicine. They were older, at a BMI of 30, followed for four and a half years, and colchicine had a 12% significantly lower — 12% lower risk of arthroplasty.
I think it was in the 5-year period — that was overall. If you just looked at patients who had gout and hip or knee OA and went on colchicine, it was a 23% lower risk of future arthroplasty. So is there something unique about colchicine? Well, it's anti-inflammatory — in controlling inflammation it might lessen the progression of degenerative joint disease. Again, since this is an observational study, I don't think you can get too much into how did that happen or what the explanation might be.
Two reports this week on allopurinol hypersensitivity — the actual risk of severe allergic reactions, toxic epidermal necrolysis, Stevens-Johnson syndrome, severe cutaneous adverse reactions — SCARs is what they call them — is 0.4 to 2%. It may be higher and maybe up to 10% in people with chronic kidney disease.
The report that we put up was the testing for HLA-B*5801 dramatically increases the risk of this. It's over 100-fold increased risk — odds ratio 117 in this one particular report.
Another report from Hopkins looked at 16 patients who had allopurinol-induced severe cutaneous adverse reactions and showed that it was not just HLA-B*5801 — which in their study gave a 208-fold higher risk of these reactions — but also HLA-A*3402, which gave almost a 21-fold higher risk.
So HLA-B*5801 explains about 2/3 of these bad reactions that occur in the United States, and there are not many of them to be honest. But if you had testing for the second class one allele, you now cover about 80% of cases. So you might add that to your list — again, patients who are from Han Chinese or Southeast Asian backgrounds should be tested for HLA-B*5801. And then
African-Americans B5801. Um, and then African-Americans are at higher risk in the United States, are at higher risk in the United States, but not everybody does it. And the but not everybody does it. And the question is, how often will you get question is, how often will you get burned? And in in a career, in a burned? And in in a career, in a lifetime, maybe only once, but when lifetime, maybe only once, but when it happens, there's a risk of death. it happens, there's a risk of death. It's kind of ugly. If you've been It's kind of ugly. If you've been following our website, we have some following our website, we have some quotes and factoids about gout. I'm quotes and factoids about gout. I'm going to put two up here for you here. going to put two up here for you here.
Being on low-dose aspirin either 81 or Being on low-dose aspirin either 81 or 325 milligrams increases the risk of 325 milligrams increases the risk of gout by 81%. gout by 81%.
81% almost a doubling of risk. However, 81% almost a doubling of risk. However, if you're on allopurinol or urate if you're on allopurinol or urate lowering therapy, you don't have to lowering therapy, you don't have to worry about that. There is no higher worry about that. There is no higher risk. That's important. Again, ULT is risk. That's important. Again, ULT is protected and you could be on background protected and you could be on background 81 milligrams a day assuming someone 81 milligrams a day assuming someone needs to be on that. And then the other needs to be on that. And then the other fact that we put up I think a few days fact that we put up I think a few days ago is uh 40% of acute acute gout ago is uh 40% of acute acute gout attacks have a normal uric acid. You attacks have a normal uric acid. You know that because we see that um the know that because we see that um the other 40% number is that 40% of acute other 40% number is that 40% of acute gout patients and attacks are not tested gout patients and attacks are not tested for a uric acid level. for a uric acid level.
Wow. And I'm going to throw in the other Wow. And I'm going to throw in the other 40% number that you all know which is 40% number that you all know which is only 40% of people who go on urate urate only 40% of people who go on urate urate lowering therapy achieve their target of lowering therapy achieve their target of six or less in uric acid and that's six or less in uric acid and that's especially so in primary care but even especially so in primary care but even in rheumatology 40%. Only 40%. So that in rheumatology 40%. Only 40%. So that 40% number is something that should 40% number is something that should bother all of us who manage gout.
Um a great report uh written up by uh Chio great report uh written up by uh Chio Yokose from the Mass General Brigham Yokose from the Mass General Brigham uh on evidence-based dietary uh on evidence-based dietary recommendations. It's a nice read. Um recommendations. It's a nice read. Um she talks about, you know, yes, we she talks about, you know, yes, we should all be on low-purine diets, but should all be on low-purine diets, but the hazard of that is you'll be on an the hazard of that is you'll be on an unhealthy diet and you won't — you no unhealthy diet and you won't — you no purines means no protein, which means purines means no protein, which means you're going to get high fructose things you're going to get high fructose things and things that are bad for gout. and things that are bad for gout.
We do know that you need to be on high We do know that you need to be on high protein and gout patients have diabetes and protein and gout patients have diabetes and diabetics need to be on high protein diabetics need to be on high protein diets. Um but and again you know Atkins diets. Um but and again you know Atkins diets which is a high protein diet has diets which is a high protein diet has been associated with some severe been associated with some severe worsening of gout. So there's a little worsening of gout. So there's a little bit of a conundrum there. The diets that bit of a conundrum there. The diets that are generally recommended are the DASH are generally recommended are the DASH diet which was originally developed or diet which was originally developed or best tested for hypertension management. best tested for hypertension management. As you know anti-inflammatory and As you know anti-inflammatory and Mediterranean diets work here. And the Mediterranean diets work here. And the other question she gets into is shellfish other question she gets into is shellfish and seafood. Um, and the point and seafood. Um, and the point there is that um, I used to say, you there is that um, I used to say, you know, that seafood recommendation know, that seafood recommendation doesn't really count cuz I — it does — I doesn't really count cuz I — it does — I have never seen it. And I got I got
have never seen it. And I got booed off stage in New England when I brought that up because they see it all the time. Not a lot of shellfish in Dallas, Texas where I live. So yes, seafood and especially shellfish is a big problem for a lot of patients. But if the patient is to be well controlled on urate lowering therapy, you could reintroduce the use of shellfish without hazard and without risk. And of course, she makes the important point of dietary counseling for these patients. Look for a card on my website called GoutTop that you can print out and give to patients. It's got all this information about diet on there that you might want to impart upon them.
A great article this week also by another person from MGH, Sarah Terkeltaub, talking about new thinking on calcium pyrophosphate deposition disease, which affects 8 to 10 million Americans. She begins by going over the fact that the classification and nomenclature has changed. We don't really talk about pseudogout anymore. That's the old term.
Now, if you look at this great figure she has in the article, it's a big Venn diagram with overlapping circles. The biggest circle being OA patients with CPPD. Then there are two medium-sized circles of either acute calcium pyrophosphate arthritis or chronic calcium pyrophosphate arthritis, and then a smaller circle for the crowned dens syndrome where there's calcification at C1-C2. Again, chondrocalcinosis is still in there for X-ray only evidence.
She talks about imaging — that CPPD is really a crystal identification disorder, but that's not always possible, and when not possible, imaging might supplant crystal identification, with ultrasonography and CT having greater sensitivity than the conventional radiograph and showing chondrocalcinosis.
As you know, management is acute steroids or colchicine, chronic IL-6. There are no FDA approved therapies, but there are trials — three trials that are in progress right now, including one with an IL-6 inhibitor. But she says there's evidence for, although not well controlled, for hydroxychloroquine, methotrexate, IL-1 inhibitors, and/or IL-6 inhibitors in patients, I assume, with chronic CPPD arthritis.
Lastly, fibromyalgia. Oh my goodness, I put this up. It's a review article in New England Journal from last week from David Williams and Daniel Clauw, where they review the diagnosis and management of fibromyalgia. And my apologies for quoting them and rewriting their article in a more dense
easier to read in a more dense, easier to read fashion, but even mine is a little bit long. Again, fibromyalgia affects up to 6% of the US population. It is a widespread pain disorder where fatigue and sleep problems, along with memory problems, are a gigantic problem. It is a hypersensitivity disorder. It's a centrally mediated hypersensitivity to external sensory stimuli that leads to pain, brain fog, fatigue, mood changes, etc.
The diagnosis is clinical — labs, imaging tests, not really. There's no immunologic tests, sorry. And the thoughts that this is a small fiber autonomic neuropathy, or that it's an autoimmune disease — the autoimmune disease is not well substantiated. Again, we do know it's centrally mediated, we do know there's a hyperresponsiveness.
They are rightly so big on treatment of sleep — that's where all the great gains in therapy are coming from. And they're strongly in favor of stretching therapies, tai chi, qigong, yoga, and then also cognitive behavioral therapy.
So again, when it comes to treatment, the tenets are education, self-care, focusing on sleep, focusing on movement and stretching, and behavioral means. And they're very big about CBT, cognitive behavioral therapy, to help both sleep and/or pain, but probably more so for sleep.
They do say that the drugs that are out there and approved that you use all the time — analgesics, muscle relaxants, tricyclics, gabapentinoids, and SNRIs — modest effects if anything. And then when they do work, they work because of their control on sleep, which again underscores the importance of sleep.
A few new things that I didn't know about. Well, I know about the new sublingual cyclobenzaprine that's FDA approved. I was not aware of a study of combination therapy outperforming monotherapy. Gabapentinoids at bedtime plus an SNRI during the daytime had 68% improvement in global pain compared to 42% for duloxetine, or 39% for pregabalin, versus 18% for placebo.
That's significant, and those are 6-week results. Obviously NSAIDs and opioids really don't do anything here and should be avoided.
They expressed some enthusiasm — and let me underscore the word "some" — for low-dose naltrexone as an emerging, unrecognized option, but we need studies on that. And there is good data about transcranial stimulation, TENS, maybe gabapentinoids, and THC — it's unclear though where those stand at this point.
Anyway, watch for our content on gout this month.
this month that it's going to wrap up next week. Next week our TNR Tuesday rheumatology is going to be on advanced therapies. Um Herb Baraf, um uh Naomi Schlesinger. Um oh my goodness. Um a few others I now I'm blanking on. I should have looked them up, but it's a stellar lineup.
Um, and we're going to talk about uh the uricase drugs, the use of cytokine inhibitors, um, drugs that are coming down uh the development pipeline. Um, I think it's going to be another exciting session that you'll want to tune into.
That's it for this week on the podcast. We'll talk next week. Take care.
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