Vitamin D Headlines (5.9.2025) Save

It's 05/10/2025. This is the RheumNow podcast. Hi, I'm Doctor. Jack Cush, executive editor of roomnow.com. This week, I'm gonna talk about triple positivity.

I'm gonna say some things I never thought I'd say about a true underlying pathogenesis to CRPS. Oh my goodness. And now I'm really gonna go out on a limb and say something nice about vitamin D. I think you've heard me go off on vitamin D in the past.

Great rheumatologists go to great rheumatology meetings. Now for the first time ever, RheumNow live on demand is available. We'll have more coming up after today's podcast.

Let's get into the news. You know, this is the first full week of our lupus campaign called Lupus Unlocked You Have the Keys to Mastery. So, have a lot of lupus content, but before we get into that, we had a lot of other news on the website this week. I want to start with congratulations Doctor. Virginia Pasquale, a good friend, great mentor, exemplary pediatric rheumatologist and scientist who's been elected to the American Academy of Arts and Sciences.

She's now at the Weill Cornell School of Medicine doing translational research as only she can. Congratulations to Virginia. Interesting meta analysis of vasculitis and interstitial lung disease, eight studies, six fifty patients shows these patients have significant mortality and the mortality is related to age, having a past history of smoking, a UIP pattern, history of exacerbations and being the micro and the microscopic polyangiitis type. Again, ILD when it happens on any of our diseases is just ups the odds on bad outcomes. An international committee called the IMAX Group, International Myositis Assessment and Clinical Studies Group, God bless you for the work that you do.

They had a consensus study as only they could and came away with the research that says the new preferred term, I didn't know if this was an issue, but now it's clear for the antisynthetase syndrome is the antisynthetase syndrome and the preferred abbreviation for the antisynthetase syndrome is A SIS. A capital S, lowercase y, capital S. This was chosen over S and I can't imagine why. So, ASUS is the abbreviation, antisynthetase is the syndrome. A microbiome study on patients with complex regional pain syndromes.

These are difficult to manage pain patients. I don't think we understand the pathogenesis of this. They did a 16S RNA amplification to look at the taxa in the stool samples of 53 patients compared to 52 controlled and showed a clear cut difference in microbiome and also in short chain fatty acid levels between CRPS and controls with over ninety percent accuracy. I can't make anything of this other than it's a head scratcher and I think it's great when you can find data like this. I think it needs to be looked at by others and delved into in a high volume research, even randomized control way with a lot of blinding.

But if this is true, imagine, you know, you can't treat their pain, they're refractory, I don't know where to start, I don't know when to end, but if you could manipulate the microbiome, wow, that would be incredible. An eye opener, and I think you probably know this, what do you do in patients who require lung transplant? Can you do lung transplant in patients with connective tissue disease? A study of forty two patients with long standing RA complicated by ILD, and the ILD complication actually started within a year in most of those patients. These patients were collected forty two over a sixteen year period.

The survival was not good. Although after transplant, the one year survival was eighty eight percent, the median survival was five point three years, which by the way, these numbers on survival are the same as lung transplants in other patients with connective tissue disease, and also in non connective tissue disease patients who require lung transplants. So, our patients do just as good as others, and hence, ILD in our patients with RA is not a contraindication to lung transplantation. You could say the same for other rheumatic diseases. The mortality overall was forty three percent.

It was higher in people who had the UIP pattern on CT scan. A single center study of almost 140 patients looked at the value of doing CARB P antibodies in addition to rheumatoid factor and ACBA, and they showed that patients who were triple positive had worse disease, they had worse activity. Significantly higher TJCs compared to single positivity. They also had higher pain scores, higher dash 28 CRPs, higher sed rates, higher ACPA levels, but lower rheumatoid factor and didn't matter if you were single, double or triple positive, it didn't make a difference in bone markers and also in bone erosions, but nonetheless, more severe disease. So, I don't routinely do CAR P antibodies.

You can do them. It performs just as well as ACPA, maybe not as well as ACPA, but the question is, do you get something more? And I don't believe that patients who are seronegative that you can do CARB P antibodies or 14,338 for that matter and find a whole bunch of people who are seropositive for those markers when they're negative for RF and ACPA, you'll find a few. But I think I would encourage each of you to find your own way here and to look at your own experience. An interesting case report, it's a case series, but I think it's interesting because of the claim.

Seven patients with established long standing RA refractory to disease with moderate severe RA and nodules who were started on either tofacitinib or upadacitinib. Five out of the seven had complete resolution of their nodules. But, and one other had reduced a reduction in nodule size, and these nodule changes took three to twelve months, generally six to twelve months for most of the patients on JAK inhibitor therapy. Could that be yet another benefit of JAK inhibition? I don't think that's been well studied in clinical trials and this case report, I think should lead people to go back and look at that data, if in fact it was studied.

But honestly, having done lots of RA clinical trials in the past, you know whether they have nodules going in, but you don't measure nodules during a trial. Because the question is, how do you measure them? You know, I squeezed them and they were this big when I started and they were this smaller when I ended. Again, nodule burden and quantifying it is a difficult thing to do. But I think it's really cool.

A Finnish birth cohort shows us something about the natural history of osteoarthritis of the knee. So, this is a birth cohort that started in 1986, and they followed these patients for many, many years. They were all obviously asymptomatic when they were enrolled, but early on, they developed cartilage defects at the patellofemoral joint fifty six percent, tibiofemoral joint twenty five percent. Again, they had some osteophytes that were seen in seventeen to twenty percent. Again, most of these patients who had these MRI only abnormalities had high BMI's and that might be the reason for it, but it was a pre antidated and predicted future knee OA tells you that this is a long standing process that starts on you.

I mean, knees, I ended up having knee replacement when I was 60. I blew out my knee playing football when I was 17. I continue to play sports on both knees that were damaged, you know, for the next ten, fifteen years. And I got pretty bad knee OA that required bilateral knee replacement and it changed my life and it was wonderful, but I'm sure I started my damage back when I was in my teens and it was probably from my activity, more so than anything else. Cool study that makes me eat pro.

It's reported in JAMA. It's called the delay study D LAY as in delay the onset of disease with multiple sclerosis. This is a high dose vitamin C trial, double blind, randomized, placebo controlled, where they get vitamin D3, a hundred thousand units given every two weeks for two years. And the patients that were enrolled were people who had sort of preclinical MS, what's called clinically isolated syndrome. And they basically found that disease activity over time was less than those on vitamin D sixty percent versus those on placebo seventy four percent that being significant, a thirty four percent reduction overall.

They had significantly better MRIs, they said significantly less cases of relapsing remitting MS in the end. The time to develop disease activity took longer on vitamin D, four thirty two days versus two twenty four days. Again, that being significant. This data kind of jives with Karen Costenbatter's data about vital preventing autoimmune disease, which I have some concerns about the methodologies, especially again, the VITAL study was given vitamin D to look at cancer and cardiovascular outcomes where it had no effect. But the secondary analysis that was done in the VITAL study showed it looks like it might've had some effect.

This is encouraging data. And, yes, I have some doubts about all the claims on vitamin D. I don't believe most of them. I think it's a marker for most of us who develop some kind of illness that's associated with everything, but not generally known that vitamin D supplementation prevents all the things that it's been linked to. Those are my gripes.

An interesting study from Michelle Petrie's group in arthritis care and research shows that patients who have very low or very high vitamin D, twenty five hydroxy vitamin D levels had worse and more adverse pregnancy outcomes. This includes miscarriages, preterm deliveries. Again, they were significantly increased in people with very low levels or people with very high levels, which is an odd thing. Anyway, the patients who had the lowest risk of these adverse pregnancy outcomes were those who had, and this is the recommended level to shoot for is forty to sixty nanograms per ml. So, you should be doing vitamin D levels at conception and maybe during pregnancy, if you'd like to maybe affect some of the outcomes here.

Another really cool study recently in New England Journal was on NASH or NAFLD, which is now called MASH, metabolic dysfunction associated steatohepatitis, double blind randomized placebo controlled trial, 1,100 patients, all with a BMI of thirty four to thirty five, and being at risk showed significant reductions in the risk and the outcomes of patients as far as their mesh. Another cool benefit to GLP-1s in the world of medicine. What about the SGLT2 inhibitors? An emulation trial was published this week about SGL-two inhibitors in patients with lupus. So, these are the sodium glucose transporter inhibitors.

This was a clinical trial emulation using insurance claims data, two thousand one hundred lupus patients versus two thousand one hundred controls, and they're all lupus patients, I guess, and they're either on diabetic medicines, the SGLT2 inhibitors or not, and guess what? They significantly reduce the risk of many cardio renal complications and serious outcomes that are seen in lupus. This includes acute kidney injury, chronic kidney disease, end stage renal disease, emergency room visits, heart failure, and even sepsis. Again, impressive. So, good news for your patients who have lupus and who require either an SGLT2 or GLP-one.

Janet Pope wrote an editorial for the journal and also for RheumNow during our lupus campaign asking the question, are emulation trials real or fake? And she kind of reviews the study and reviews that there are channeling biases associated with trying to model data after the trial you'd like to do, but can't do. So, you use existing, pre existing data and you retrospectively emulate that trial. She likes the results. She believes the results.

She wonders though about emulation trials, we'll be seeing a lot of them in the future. I think it's good to maybe review that. Again, this month is lupus month worldwide. There are a lot of good lupus conferences out there. The biggest one is in Toronto on the twentieth through twenty fourth.

I think that all the lupus mavens are going to be there. We have a campaign on RheumNow and a lot of lupus content being covered. Here's some of the reports this week, a retrospective study of one hundred and thirty one children with lupus, look specifically at lymphopenia. We know it's a criteria for the diagnostic criteria, but what is its value as an independent variable? In their one hundred and thirty one patients, was a little lymphopenia was found in fifty three percent, highly correlated with double stranded DNA antibody titers, highly correlated with disease activity with a correlation coefficient of 0.63.

That's pretty high. Lymphopenia was associated with more nephritis seventy two percent, more hypertension twenty four percent, more leukopenia that goes together thirty six percent and more neuropsychiatric lupus. So, I've always been a, to me, that's the hidden gem in diagnosing lupus. You know, they may not have leukopenia, but do the math and find they have lymphopenia, boom, you've got another criterion. Another lab test having significance in the world of lupus is procalcitonin.

I might have talked about this last week, I can't remember. But anyway, in this study of one hundred and sixteen juvenile lupus patients with had serious bacterial infections in seventeen percent, procalcitonin was a better predictor than other things that we look at, including Sedrate CRP, neutrophil lymphocyte ratio, platelet to lymphocyte ratio. An article this week appeared in the literature about whether you should be withdrawing steroids or immunosuppressive should you want to withdraw either. And in this study, it was basically a single center randomized controlled trial that looked to answer the question is withdrawing immunosuppressants, non inferior to withdrawing steroids. And in fact, it was non inferior.

So, isn't a preference of one over the other. Know you'd like this kind of paper as I would to tell us which one should I withdraw, which is the smarter regimen. I'm going to get to that in a second with another report, but this one says you have to choose and you have to choose based on you have to sort of individualize it to the patient, their situation, which drug they need better, which drug they hurt the most, they hate the most, etcetera. A great article this week by Mike Putman from the University of Wisconsin, where he talks about PJP prophylaxis and lupus. Should you do it or not?

He says, I'll pass, check it out. He'll give you a good history as to why he doesn't, and the rationale behind that. And I kind of agree with him. I don't put many of my patients on PJP prophylaxis. For me, it's usually ANCA associated vasculitis who are on multiple immunosuppressants and high dose steroids.

Those are ones that get highest risk and also patients on rituximab in general are at higher risk for PJP. Great blog by Doctor. David Pizzetsky from Duke. You know, I think one of our leaders in lupus, certainly incredibly well known for his research on serologies and double stranded DNA and title of his blog is From DNA to PGA. And he's talking about patient sort of outcomes.

In this blog, he gives you his history in getting into lupus and serologies, and then how you had to pivot and start talking about type two SLE. He's going to lecture on that at the lupus meeting coming up in a few weeks, where he and his coworkers at Duke came up with this idea that there's two types of lupus. One that's firmly rooted in inflammation, nephritis, anti double stranded DNA antibodies, that's type one. And then there's this other type of lupus, type two, characterized by pain, fatigue, mood disturbances, and brain fog, and that's the fibromyalgia of lupus or what he called lupus associated nocoplasticity. It's important to know because it clearly is going to change how you treat this.

Another great blog, an article by Guillermo Ruiz Irestorza from the University of Madrid. Guillermo does a great job of talking about when to start, how to follow and when to stop, and how to stop steroids in your lupus patients. I think it's a really good review article. He ends it with a few bullets like use hydroxychloroquine to basically help lower your needs for steroids, and everybody should be on hydroxychloroquine. Adjust the induction therapy you're going to use to the severity of the disease, also to limit your exposure to steroids.

Restrict your maintenance steroids prednisone to less than five milligrams per day, but he in fact would prefer less than two point five milligrams a day. If you're going to treat flares, moderate to severe flares, he recommends using methylprednisolone one hundred and twenty five to five hundred milligrams for three days as opposed to screwing around with higher doses of orals. He strongly recommends the use of immunosuppressives as a way of reducing the reliance on steroids. Consider methylprednisolone in people who are not responding to a higher dose of one week or more of prednisone like seven point five to ten milligrams, and then you should foresee the day when you're going to withdraw steroids. He says three to five years of being in remission.

Again, there are other studies saying lower amounts like two years, and then he does recommend that you stop the immunosuppressive drug before you stop. So, start prednisone withdrawal after stopping immunosuppressive drugs. So, immunosuppressive first, or we know first before you start playing with the prednisone, and then the taper is going to take you three to six months, but you need a plan on how to do that. Again, on our website, we feature a lot of lupus this month, including patriisms. These are famous things that the great Michele Petrie has said.

Here's a few: Hydroxychloroquine is lupus health insurance. Next, the P in prednisone stands for poison. Next, never argue with the chart, call the doctor to resolve an issue. And lastly, the diagnosis of lupus is not a gift, the patient has to earn it. We had a fabulous Tuesday night rheumatology this past week with Brad Rovan and Rich Furey talking about pivotal articles in lupus nephritis next week, upcoming Tuesday.

We have the world's leaders in cutaneous lupus, and this includes Doctor. Victoria Worth, Matilda Nicholas, Anthony Fernandez and Christopher Richardson. And they're going be talking about key issues in the diagnosis and management of cutaneous lupus. That's Tuesday night rheumatology, be there. Take care.

Room Now Live twenty twenty five has wrapped up, but you can still register for all the great content. Just go to roomnow.live. Roomnow.live is available to you on demand. You'll have comprehensive access to all the 2025 RoomNow live meeting content. This includes expert led lectures, multidisciplinary panel discussions, and focused step talks on rheumatology's hottest topics.

Plus there's our world class instructors including Drs. Jack Cush, Michele Petrie, Jeff Curtis, Desiree Vanderheide, and Alexis Hoggi. All sessions end with a thirty minute question and answer panel with the faculty. Register now. Head over to roomnow.live and start streaming today.