Bah Humbug Vitamin D (12.20.2024) Save

It's 12/20/2024. Ho ho ho, and this is the RheumNow podcast. Hi. I'm Jack Cush, executive editor of rheumnow.com. RheumNow live is coming up February eighth and ninth, just what, eight weeks away or something like that.

Actually, less than that. Check out the agenda. It's incredible. I'll talk about it at the end of the program. We've got a number of interesting reports at the end of the year here that I thought that we should be covering.

Nail fold capillaroscopy, do you do it? I do. I don't just do it in scleroderma and suspected scleroderma. I like to do it in autoimmune disease in general. And I've always been very impressed by the abnormalities on nail fold capillaroscopy in patients with polymyositis, but especially dermatomyositis.

I put up a report this week of seventy six DM patients, and when they underwent nail fold video capillaroscopy, which is obviously a lot better than the tools that I use. I use cheap tools, but nonetheless, I think very good tools. They found seventy four percent of patients had abnormal nail fold capillaroscopy, diminished density, abnormal morphology. And the patients with dermatomyositis and abnormal nail fold capillaroscopy were more likely to have, more Raynaud's and maybe, more likely to develop ILD. I think it's a severity marker, and I think it's worth looking at.

And of course, you get the hint when you look at these patients and they have periungal erythema or those desquamative changes of inflammation and periungal distribution. I think it's worth doing. A review of sarcoidosis this week came out showing that, rheumatic manifestations of sarcoidosis found in a range of, ten to forty percent includes bone lesions, acute arthritis, chronic arthritis. Chronic arthritis usually involving the ankle, and tarsus. Axial disease, dactylitis, we've talked about before, and sarcoid myopathy.

Things to consider when a, faced with those diagnoses that sarcoidosis could be in the differential diagnosis. Do a chest X-ray, single best test. ACE levels, not a great test unless they have abnormal lung involvement. Do the chest X-ray. That's actually where you're gonna find your clues as to sarcoidosis, and then maybe following through on biopsy.

We've talked in the past about, the percentage of patients with IBD who may have occult spondyloarthritis, and that ranges from like eight to really about fifteen percent. This particular study looked at, IBD patients who underwent, magnetic resonance, enterography, MRE, where they're looking at the gut but in doing the gut with MR, they can also get a good look at the SI and pelvis. So they can find occult sacroiliitis, if you will. So in these ninety five patients, they found by observation and clinical disease. Only six point three percent, six out of ninety five developed IBD.

So it's a low number if you wait for the clinical manifestations. It's a higher number if you go searching for it with camera studies and not camera studies, but by doing x rays and doing more extensive analysis. But again, that seems about right compared to what's been described before. The interesting thing was that finding sacroiliitis on MR studies did not increase the odds of the patient having, spondylitis. Turns out that IBD arthritis in general, which is often peripheral not axial, but could be axial, was gonna be most closely linked to having arthralgia, an eighty four fold increase odds, right?

But also maybe the more predictive feature was extra intestinal manifestations, things like pyoderma and other things that go along with IBD. So keep that in mind if you're thinking about the possibility of enteropathic related arthritis or maybe even a called sacroiliitis. Rheumatologists love RUPES. I'm not sure it really exists. I've had a few patients with RUPES.

This is a particular study of forty one patients that were compared to a hundred and sixty SLE and seven zero nine RA patients. Turns out RUPES patients are more likely to be diagnosed at a younger age than RA but older than lupus. So younger than 60 and older than 20, and that's significant. The majority of these patients probably have more of a lupus, onset of symptoms more so than RA, but it's not that far behind. What distinguishes the RUPES patients was they were more likely to have ILD, hypergammaglobulinemia, and lab abnormalities, but seldom ever develop renal or CNS manifestations.

Now if that helps you in your diagnosis of RUPES, God bless. I'm not so sure, I'm searching for RUPES that hard these days, but it does show up, right? And my advice, this is not part of the study, it's a lot like overlap syndrome. You don't treat the label, there's no specific drug, you treat the dominant manifestations. If it's an overlap of myositis and rheumatoid arthritis, you're gonna treat the myositis if that's the dominant manifestation.

And most likely they'll take care of the RA, right? Same thing for you know, ILD and and and lupus and scleroderma. Well, you're probably gonna and that combination sounds more like an ILD scleroderma thing. So treat the dominant manifestation when treating RUPES and you'll be doing fine. I don't know if this is groundbreaking news, but the US Preventative Task Force always comes up with new recommendations on what should be used.

And it came out this week with an opinion against the routine use of vitamin D, with or without calcium, for the primary prevention of fractures or the primary prevention of falls in either men 60 or postmenopausal women. So again, just because you're postmenopausal or 60, doesn't mean that you get vitamin D or calcium because it's gonna prevent fractures. In fact, the evidence for that is none. Nil, zero, zilch, nada. So there may be other reasons why you might wanna use vitamin D or calcium, but obviously those are gonna go in high risk individuals, right, who either by DEXA or their history might merit the use of vitamin D with or without calcium.

But a priori just because of age, no, it has no, beneficial effect on either fracture prevention, or fall prevention. But we do know in this age group, that fragility fractures are in fact going up and they are associated with higher morbidity. So it is important to look for risk factors and then do the right thing. But age alone is not the risk factor. So let's talk about vasculitis.

I think I've got two interesting things here about vasculitis I can talk about. One is this data about will being on steroids affect biopsy results for vasculitis? And this particular study, this was a study from Tokyo, one hundred and twenty six patients who had suspected ANCA associated, either small or medium sized vessel ANCA associated vasculitis and the diagnostic test was a quadricep muscle biopsy. Of one hundred and twenty six, seventy one were positive and diagnosed with ANCA associated vasculitis. The biopsy yield was the same if the patients were not on steroids or on steroids.

That the biopsy positivity rate was fifty nine percent for people off steroids and fifty three percent for people on steroids, not significantly different. So being on steroids is not necessarily a hindrance to the utility of that test. It looks like fifty to sixty percent of patients, that could be a diagnostic test and should be considered. I think that's useful clinical information. The other vasculitis report was down here at the bottom about avacopan.

I got this from one of my colleagues on LinkedIn, sent me this report. As you know, the C5a receptor antagonist avacopan is used in ANCA associated vasculitis to treat GPA, MPA, hopefully to steroid spare. The main warning in the package insert based on the clinical trials is for liver side effects. The clinical trials used for registration, abnormal LFTs were seen in, twelve to thirteen percent of individuals and four percent discontinued, the study drug avacopan because of liver problems. Well, there was a report this week in Japanese literature of twenty two patients with ANCA associated vasculitis, and avacopan, related, hepatic injury.

That was seen in nine out of the twenty two cases they reported. It's kind of a high number. It's forty percent or something like that. But nonetheless, I think it's worth looking for this if you're gonna use a vacapam. Again, nine patients had liver injury.

It was severe with an elevated total bilirubin and only four of those nine. And one patient died from a rare syndrome called vanishing bile duct syndrome. Hard to know if that's associated with, avacopan. I doubt it based on one case report. But nonetheless, the concern about hepatotoxicity with this agent should be, on your mind if you're gonna go that route.

And I think we should be using steroid sparing drugs as much as possible. An interesting report, from Italy on initial use of methotrexate in patients with chronic inflammatory arthritis, two forty two patients, over half of them with RA, a third with PSA, sixteen percent with undifferentiated arthritis. Overall survival of methotrexate was best in, RA and PSA and roughly equal. It was about sixty percent at two years, forty percent at four years, twenty percent at, ninety six months. Survival was not very good with undifferentiated arthritis and that may relate to the diagnosis more so than the drug in those patients, right?

Meaning that undifferentiated arthritis becomes something else or becomes nothing else, and so the drug is stopped or drugs are changed. But again, these methotrexate durability numbers are a little bit lower than what's been described in the past, you know, five year numbers of, you know, fifty to seventy percent. This is sixty percent at two years, forty percent at and, you know, I think that this may relate to one, mixing populations, and two, we have a lot of other drugs these days. And methotrexate isn't always our first drug, but in this study, it was the first drug. So I think it's encouraging, and supportive data of what you expect out of methotrexate in your patients with inflammatory arthritis.

A recent report showed the potential biomarker value of serum IL-forty levels in RA showing it could distinguish, RA from OASLE and controls that it did correlate not with disease activity, but with RA autoantibodies, coagulation factors, and, was decreased in patients on TNF inhibitor treatment. IL-forty was I think described in 2017 to B cell associated, cytokine. It is involved in neutrophil function, extracellular traps thought to be important in early RA, you know, in the development of autoantibodies and progression maybe from preclinical disease to manifest disease. It seems in multiple studies to behave like a biomarker, to some extent. Now, will it really be for it has to be tested that way for me to go that way.

But, again, it's prevalence, and how much it stands out seems to me like it may very well also be a future, therapeutic target in clinical trials, but that hasn't happened as of yet. A study out there about axial SpA, an international study, it's called the International Map of Axial SpA. It's a survey of 5,500 plus patients, 3,200 in Europe, seven seventy in The USA. Mean age is 44 years. The important thing here is that this is a cross sectional assessment of over 5,500 patients.

The mean I score, 5.4 active, SPA is a FASD I have four or greater. Seventy five percent had a FASD I have greater than four. The mean bad diet was 5.4. We're not doing that good at managing SPA. What's the deal?

The numbers were highest in South Africa, eighty seven percent had active disease, and sixty eight percent in Asia. I didn't see any exact reports for The UK, Australia or The United States. But nonetheless, and not surprising, active disease in these patients was associated with, functional limitations, spinal stiffness, and difficulty finding a job due to spondylitis. Yes, we can do better. Last report is about tocilizumab efficacy in giant cell arteritis.

As you know, it's approved based on the GIACTA study. I don't think we're using enough, tocilizumab in managing GCA. And, maybe it's gonna take other drugs getting approved for GCA before we start jumping on that bandwagon and quickly moving on from steroids because the data is we tend to overuse steroids here. But what they did in this particular study of four seventy one patients in Spain with GCA who were treated with tocilizumab is that they looked at their vascular phenotypes. What was the vasculature involved?

And it turns out that the biggest group is as you would expect, cranial giant cell arteritis, right? Forty six percent. The least common was the extracranial GCA, that's only seventeen percent, less than one in five, and half being cranial. And there are other one third, 37% were mixed, cranial and extracranial. So we do know the extracranial patients tend to be younger, maybe by about five years, sixty six versus seventy one percent.

And it had a longer delay to the diagnosis, maybe as long as six months longer. So, the systemic manifestations were, and ischemic manifestations were more common with, cranial giant cell arteritis. But the important point is that all these patients, how do they respond to tocilizumab? At one month, half the patients with cranial disease had responded and were in remission. It was forty three percent for extracranial and forty seven percent for mixed.

By twenty four months, they were all doing very well at two years, seventy nine, eighty one, eighty nine percent, they're all doing great in remission. If you look at another measure of remission, EULAR remission, the numbers are about the same. We're getting better responses seen with the cranial GCA at one month, thirty five percent, the other ones were about twenty seven, twenty eight percent. But at twenty four months, seventy plus percent were in EULAR remission. So these drugs work and they work without regard for the vascular bed affected.

And that's something to keep in mind when managing your patients with giant cell arteritis. I wanna, give you a preview, check out, go to roomnow.live and look at the agenda, click on the top, and pull down the agenda and see our speakers is a great program. I mean, I know it's my program and Cavanaugh's program, but where are you gonna hear, a lecture on how to manage morphia and linear scleroderma? Do you really know? Have you ever heard a great lecture on that?

We've got a great lecture from Heidi Jacoby from UT Southwest who's gonna talk about that. We have a section on JAK inhibitors. John Giles talking about the end of the oral surveillance study. What do we now know three years later? Madeline Feldman is talking about when generics, hit the jacks, tofacitinib is gonna become in generics in not too distant future.

We're gonna talk about TIC inhibitors from Joe Marola and where they fit. And Christina Charles Schulman is gonna talk about JAK inhibitors in dermatomyositis. Oh my goodness. The spondylitis pod, two hours on spondylitis, Desiree Vanderheide, Catherine Bayquell, Jennifer Sal from California talking about hidradenitis suppurativa, and then a panel discussion. I don't think you're gonna top this.

We got a great lecture on EGPA, imaging and vasculitis and management of PMR, all the best speakers in the business. Roomnow. Live, check out the agenda, I think you're gonna like it. We'll see you in Dallas on February eighth and ninth. Have a great Christmas.

We'll talk again in the new year. Ho, ho, ho.