Count Your Telangiectasias (5.29.2026) Save

05/29/2026. This is the RheumNow podcast. Hi. I'm doctor Jack Cush, executive editor with roomnow.com. A lot to cover this week.

We're coming up on UR next week in London. We'll be there covering the meeting. Hope you'll be following us. You know, one way to follow us is through either the panel discussions and videos, read the articles, watch the tweets, or do the quizzes. You know, we do a quiz every Saturday.

And, last quiz, you know, didn't do so good, if you ask me. A lot of people miss these two questions on lupus. True or false? An NIH lupus study said fatigue was found to correlate with disease activity. And less than half of you got that right.

The right answer is false. It didn't correlate with disease activity. It's sort of like non lupus features that, drove fatigue. Another question on a very popular topic, and that is hydroxychloroquine blood levels. When monitoring, hydroxychloroquine blood levels, the whole blood level that is associated with higher SLE flares and hospitalizations was less than seven fifty ngmL.

Really good article was written about that. This past week we had a really good article by Shivani Garg and Don Thomas on why you should be doing hydroxychloroquine blood levels. You might want to check that out. So, let's start with a study from the VA administration who looked at, RA patients and the influence of RA on cancer treated with immune checkpoint inhibitors. We know immune checkpoint inhibitors give us IR immune related adverse events, IRAEs, but that's not the point here.

This is, popular, immunotherapy being used to treat all kinds of cancers. What happens if you have RA on top of that? Do they have worse outcome? And the study of three zero one patients compared to a large non RA population showed no increased risk in all cause mortality. Death was death rates were similar and less than one percent.

Cause of death was the same. Infections were rare, less actually infections were less than one percent. The death rate I think was around thirty percent in the time that they followed up. So RA didn't, you know, your RA patients who need these therapies can go ahead and get these therapies. A Korean, study looked at fracture rates in RA.

We know it's increased, and that's what they found, a sixty eight percent increase in fractures in RA population compared to non RA based on claims data. Turns out that being treated with aggressive therapies, biologics or targeted synthetics did not change that result. That merits further investigation. Head scratcher for me is why seropositives had more fractures than did seronegative, and these were significant. Overall, a nineteen percent increase.

Vertebral, a forty percent increase. Hip fractures, a fifty five percent increase. You know, RA, seronegative, seropositive, my lecture on that is that they are both bad, but they do have different outcomes, do they not, in in other ways? I don't know why that happened, I think it's interesting. Another RA study looked at holding methotrexate when you're going to vaccinate.

This is a study of two fifty patients receiving the Prevnar thirteen, PCV thirteen vaccine, and either they continued the methotrexate or they held it for a month. As you know, the research by Park et al first showed that you could hold methotrexate for two weeks and they do great. Methotrexate really hampers vaccine responses. Big time. Methotrexate and Rituximab.

So you need to plan around that. Then Park's follow-up study, also a great study, showed you can only hold methotrexate for one dose, one week. This study must have been done before those were published, but nonetheless two forty nine patients, and then they held methotrexate for four weeks. They proved that holding it for four weeks gave the best humoral responses, but then in this study they had an extension of one year, where they're holding the methotrexate for four weeks, well, it was going to hurt the patient. You know, they were gonna flare or do worse, and turns out they did not.

Hold the methotrexate one week, two if you must, you don't need to hold it for four. A study of JAK inhibitors in Still's disease with macrophage activation, I've talked about that before. We don't have a lot of data, so there was I found it interesting that there was a small series of seven patients treated with ruxolitinib Jakafi usually used for myelofibrosis and other indications, not indicated in rheumatology. Nonetheless, it was used in seven patients, one and a half to 11 years of age, male female equal. Five of the seven had complete remission, the other two partial remission, two relapsed when they stopped the steroids.

Looks good, think about it, when you don't know what to do when systemic JIA is complicated by MAS. Hopkins looked at, the safety features of hydroxychloroquine and used in their cohort of one hundred and six chronic LEDLE, discoid LE patients, five year outcomes. In their cohort, the patients who were treated with hydroxychloroquine, compared to those who were not, had less hyperlipidemia, less peripheral arterial disease, less angina, and less coronary artery disease. They followed that up with a TriNetX large EMR analysis showing basically the same results in DLE, hydroxychloroquine associated with significantly less hypertension, hyperlipidemia, diabetes, coronary artery disease and stroke. Again, everyone should in lupus, there's got be on Plaquenil.

But really, everyone in RA should be on hydroxychloroquine as well. I know you could probably find some old videos that I did where I was sort of, you know, saying don't use hydroxychloroquine as your sole drug, your only drug, your first drug. I think it's an add on drug that has tremendous value, especially in RA, especially in lupus. A study of extracellular traps. Anti neutrophil extracellular traps, or NETs, was studied in three forty nine autoimmune patients, R A S L E and scleroderma.

NETs were found antibodies to NETs were found in thirty seven percent. NETs, by the way, are sort of the phenomena involved in the LE cell. You know, grabbing a nucleus and engulfing it. That's all NET driven, okay? Nets were found in over a third of lupus patients, but the important thing here is that when they were there, it was associated with higher rates of antiphospholipid syndrome, arterial thrombosis.

What about if it was found in RA? It was found in forty percent of RA where it was associated with higher levels of ACPA or more ACPA positivity. Both those findings were significant. A retrospective study of hydroxychloroquine and leflunomide in Sjogren's. Oh boy, this is, you know, great excitement for the rheumatology community.

It's called the REPURPOSE II study. The problem with this study is it's only like, you know, a few patients. You know, twenty five in each group. Actually, I'm sorry, this is a phase two trial of patients who were treated with hydroxychloroquine and leflunomide versus just, I think, one of those in patients with active Sjogren's, and it was shown to be effective. So but there's plenty of studies that show that DMARDs don't work, including hydroxychloroquine.

Does not work in Sjogren's. This is a small study. I wouldn't change my treatment because of it. We need better drugs, we need better treatments. That's coming up.

We've got a lot of good studies that are in play right now that look very promising. I like this study about Sjogren's syndrome not Sjogren's syndrome scleroderma and how you can maybe assess patients with scleroderma. A retrospective international study looked at telangiectasia count, either done by the physician or done by the patient. And this has been out there a while, that you can count the telangiectasias on the face and on the hands and arms. And in this study, the counts associated were clearly associated, significantly associated with pulmonary artery hypertension and digital ulcers.

Then, more importantly, maybe that Well, I mean moderately important, was a moderate agreement between MD telangiectasia counts and patient telangiectasia counts. The kappa statistic there is a point six So, not too bad, moderate agreement. But, you know, I, on all my scleroderma patients, I do a modified Rodnan Skin score. I score skin tightness in, I think it's 18 areas from the fingers down to the toes bilaterally, and I record that at every visit, just like I record, you know, a C die or a gas score at every visit in RA. Maybe we should be doing telangiectasia counts.

It's pretty simple. They're easy to spot, right? On, again, face, hands and forearms. And their categories were none, one to six, seven to five or greater than 15. Sounds like greater than 15 may not be a good thing.

Another study in autoimmune disease looked at adverse drug events. And you know what? It's high in autoimmune disease. Which one which of our autoimmune disease had the greatest number of one or more adverse drug events, a study of ten thousand patients, actually it was systemic sclerosis, thirty six percent. Contributors to adverse drug events were polypharmacy.

Yeah, polypharmacy, I'm going talk about that later. And interestingly, you would think that, well, there are autoimmune patients, there are a lot of aggressive medicines, you know, bad things happen. Turns out that there were more adverse drug events from non autoimmune drugs, not from DMARDs and steroids. A lot of them were from antacids and, you know, H2 blockers, for the stomach. Acetaminophen, and other pain medicines, and medicines for depression and anxiety were more likely to give adverse drug events.

Now this may next one may be the goofy study of the week. I don't know what to make out of it. It's a very large biobank study. Four hundred and eighty thousand people looked at the influence of mobile phone use on rheumatoid arthritis. So, they followed these people over thirteen years.

In this four eighty k population study, it was six thousand new RA cases. And yes, cell phone use was associated with an increase in incident RA hazard ratio of one point one four. That was significant. That's a fourteen percent increase. And it was eight percent if you used it your cell phone only thirty minutes or more week.

Turns out that going hands free and using a speakerphone was not associated with it. Now am I gonna say that cell phone is gonna cause RA? You know, no. Cell phones have been around a long time. I don't think we're seeing more RA because of all the cell phone use.

But this is a much talked about association. Other studies have been done looking at the effects of maybe radiation, five gs mobile phones, on things like cancer and chronic diseases not necessarily autoimmune, and they mainly debunked that possibility. I put it out there to let you know, well, there is a study, you know, but I think we need more research on this to know how to handle this or, whether this is something worth counseling your patients on. I think you should spend your time counseling patients on weight loss, smoking cessation, healthier lifestyles, if you want to avoid RA, that might be the way to go. A population study again, this time from The UK Clinical Practice Research Datalink.

It's a very large study from which a lot of good population studies are drawn. They looked at five point two million pregnancies, two point five million births, and they found that amongst our autoimmune patients there's a lot of problems. But we know that, but I thought I would delineate those for you and what they found. I thought the surprising one that there was an increased relative risk of miscarriage in Sjogren's. I didn't know that.

I know plenty about pregnancy and RA and lupus and other inflammatory conditions. I wouldn't consider Sjogren's autoimmune. I don't know if I consider it inflammatory because anti inflammatory therapy doesn't work. Pure and simple. But a sixty six percent increase.

C sections are increased in IBD twenty seven percent, small for gestational age, increase two and a half fold in lupus, as was preterm birth fifty three percent increase. Stillbirth increased in lupus this has all been reported before, and more anxiety and depression in lupus patients during pregnancy. So, again, another quiz question that I put out this week, that a lot of you didn't get right. And it said, you know, according to, no, after treating an infection, after treating which infection can you safely resume anti TNF therapy? And the right choice here that most people didn't get right was zoster.

The bottom line is that you can't resume TNF inhibitors with either an invasive fungal infection, histo and cocci, or invasive candidiasis, not oral candidiasis. And you can't resume TNFs with atypical mycobacterial infections or NTMs, nontuberculous mycobacterial, because you never fully eradicate you treat those, they get better, that's great, but you never fully eradicate that. And if you give back the TNF inhibitor, they're gonna break down more granulomas, they're gonna again recur. So you never do that. You should also never do that with BCG, right?

Especially if had, a recurrence of TB from BCG. The one that you can restart is herpes zoster. That's, many people, when they get zoster on TNF, they stop the TNF, they treat the zoster, and they restart the TNF. And there are studies to show that that's there's no further recurrence. Why they got it on a TNF?

Well, they got RA. They're old enough. They're on other drugs and steroids. They're probably they may also be on JAK inhibitors. That drives zoster use.

So, and then there was a comment about, well, vagal nerve stimulation would be good here. Well, no. Vagal nerve stimulation would not be an alternative in someone with an infection. Vagal nerve stimulation works by the cholinergic reflex and whatnot, but by basically inhibiting TNF as its main mechanism. It's got a lot of number of different mechanisms, but I think the main mechanism is TNF inhibition.

You'd still get the same issue as if you restarted, you know, etanercept. That was, an erroneous comment that came across, from this. Last report from, doctor Yazdani and colleagues, looked at polypharmacy in lupus. This is a population based study from Atlanta of four fifty one verified SLE patients, and they showed that half of their patients had polypharmacy. I've talked about polypharmacy.

I worry about polypharmacy. I think you should too. Polypharmacy is bad if your patient is on 10 drugs or more. I call that the 10 run rule. If you're playing softball, if If you get 10 runs ahead to quit the game, let's go have a beer.

Right? If you get if your patient's on 10 drugs, your patient's in big trouble, and you're adding to it as a prescriber of medicines. In in this, I think it's a validated number, of five or more drugs you're guilty of polypharmacy. And they showed an age relationship. And as the age went up, the risk of polypharmacy went up, and it was over fifteen percent in those 60.

Most of their patients were women, most of their patients were African American. So the, I'm sorry, The number of polypharmacy was sixty eight percent over age 60. It was fifteen percent in young lupus. So it increases with age, and especially with older age. It increases with higher disease activity compared to lower 66 versus 46.

It increases with those who have SLD related damage versus those without sixty nine percent versus forty two percent. It's higher with longer disease duration. That makes sense, right? So and and and more immunosuppressives you are, more likely you are to have polypharmacy. If you're on three or more immunosuppressives, like hydroxychloroquine, etc, eighty percent incidence of polypharmacy.

If you're on zero or only one immunosuppressive, only about thirty eight percent polypharmacy. The other important thing on this study was, okay, yeah, most patients were on, you know, eighty percent were on hydroxychloroquine and forty four percent were on corticosteroids. Turns out that most of the polypharmacy was contributed by non lupus medicine. Antihypertensives in two thirds. Non opioid pain relievers fifty two percent.

Allergy drugs twenty two percent. Depressants twenty two percent. Gastric reflux medicines twenty two percent. This is a big problem. So patients come to you, you know, you're a homeopath, you're a believer in, you know, FDA approved drugs, and that's what you do often.

The problem is patients who are sick go to more doctors. The more doctors they go to, the more prescriptions they go. And that's kind of your you got a problem, I got a drug. But when they're in a polypharmacy situation, the outcomes are bad. There's more hospitalizations, there's more deaths.

I mean, they did not look at that in this cohort study. But there are other studies I've talked about before. So your job is identify polypharmacy, and if you're gonna prescribe a drug, you gotta stop a drug. If you can't stop a drug, then don't prescribe a drug. If you gotta prescribe a drug and one needs to be stopped, you gotta call the guy started the antidepressant, or their drug for asthma, or whatever.

Again, it's, it's, I think, really our responsibility to make sure that the things we do are safe for our patients. Alright. So that's it for this week on the podcast. Next week, be there, be square. Our coverage of EULAR twenty twenty six from London will start on Wednesday.

Every Saturday, you know, you get you get that that, Room IQ quiz in your inbox. We'll be expanding the number of quiz questions. Usually, we do about seven questions. It'll probably be, like, up to 20 questions during, ULAAR. And that's a good way to also catch up on what you may have list at, list missed at EULAR.

Again, by taking the quiz, you learn the point. You learn in the true false questions, you learn in the multiple choice questions, and there's a link that you can further research on if you like. That's it for the podcast. Take care. Talk next week.