The RheumNow Week In Review 2 June 2017 Save

Hey now, I'm Jack Cush, executive editor of roomnow.com. It's the 06/02/2017 and this is the RoomNow we can review. This week on our report we're gonna feature some information about the Brits and their new gout guidelines and then two crazy reports about nutraceuticals and dietary fiber and osteoarthritis of the knee. Sounds goofy, but it's in the news. At the top of the news is a report about CAMS, that's complementary and alternative medicines, and a study, I think it was in China actually, of one hundred and eight patients with early RA, and looked at their use of CAMS.

Forty one percent of patients used CAMS, and what they found interestingly was that those who did use CAMS were more likely to have a delay in DMART initiation. Sounds like they were relying on natural therapies to treat what is obviously a systemic disease and may need DMARTs. More importantly, the patients who used CAM also had higher disease activity scores that also was involved in, those delaying the onset of DMARDs. It turned out the thing that was most predictive of an earlier use of DMARD initiation was higher HAC scores, health assessment questionnaires, or functional scores. Again, this is a separate kind of patient, a different kind of patient, one that needs to be counseled about the appropriate use of CAMS.

A study of axial spondyloarthritis patients looked at whether or not the nonsteroidals would have an effect. You know, it's thought that nonsteroidals are just symptomatic therapy, but there is some data in the spondylitis world that they may actually have some disease modification effects. This small study looked at specifically MRI findings in thirty three patients who were treated with nonsteroidals only and had axial spondyloarthritis. What they did see was that there was MRI evidence of less sacroiliitis in those who responded, and they had reasonable responses according to ASAS response criteria, that those who responded to just on steroidals that the MRI is improved as far as sacroiliitis, and also the bone marrow edema scores also approved as determined by MRI suggesting that when you control the disease, get all the good things that go along with that including, things that happen at the biologic level and the radiographic level and whatnot. So, I don't think that this is proof that nonsteroidals are, disease modifying, but I think that it is proof that if you do well with simple therapies, that's good enough.

A scleroderma lung study, we know because it looked at things like looked specifically at whether or not mycophenolate or cyclophosphamide were, important in reducing the damage done to the lungs in patients with scleroderma. As a sub analysis of the scleroderma lung study one and two, where they use either cyclophosphamide or mycophenolate with a placebo arm, they did show that there was significant reductions in skin thickness scores when you were on either one of those therapies and that neither was actually better than the other, but that both were superior to placebo. Again, this also maybe the weakest score you can do in scleroderma trials. What I learned a long time ago from Ginny Steen and Tom Medsker was that everybody gets better as far as their skin scores, but this was a placebo controlled trial and showed that the skin scores did get better with more aggressive therapy. Important to note nonetheless.

There was an interesting report about a rare methotrexate induced skin necrosis, and it was described in the same way as there were there are descriptions out there about Stevens Johnson syndrome and toxic epidermal necrolysis syndrome all being drug related. Here they relate, this necrotizing skin lesion, event, a rare event to methotrexate. It really is the same patients who have methotrexate toxicity. They tend to have renal insufficiency, they get severe mucositis, but in this case, they were getting skin necrosis with skin ulcerations, erosions, also with oral ulcers. The risk factors were those who had cytopenias and had renal insufficiency and were over age 60, and were not on folic acid.

The interesting thing about these patients, should this be seen, a seventeen percent mortality, very scary. Vindicate, a mnemonic. Do you like mnemonics? I find them bothersome and I find people who study by mnemonics a bit idiotic, but nonetheless, you know, a good mnemonic is worth remembering. Is this one worth remembering?

Vindicate, a mnemonic for avascular necrosis causes. V for vascular, I for infection, and N for infection, guess. D for drugs, I for inflammation, C for congenital causes, A for autoimmune, T for trauma, and lastly, E for endocrine. Congratulations on new mnemonic. A nice study looked at the cohort of women who, had rheumatoid arthritis and were becoming pregnant.

They studied them during their, preconception phase, and looked at what happened when they went from pre pregnancy to the third trimester as far as gene expression. And while they looked at many different genes, they did find a significant increase in type one interferon gene expression. And the question is whether or not that is associated with some of the things that we see later in pregnancy, including maybe better outcomes. But it turns out that they didn't do those correlations, and the best you're going get out of this is that that's one of the immunologic things that happen as a result of pregnancy that you get this more of a type one interferon gene activity. So again, that might be important to know for those of you doing pregnancy and RA research.

A nice survey looked at adult rheumatologists and whether or not they cared for kids, and they found that twenty three percent of adult rheumatologists claim to take care of pediatric cases, those with JIA, While ninety four percent of patients were patients, of the doctors, the rheumatologists were comfortable, diagnosing JIA, lesser, only two thirds or three quarters of patients were actually comfortable treating. I do a lot of surveys. Usually on surveys people give you the best version of themselves so these numbers are probably inflated. Doubt that ninety percent or more are comfortable and I doubt that three quarters of you are comfortable managing the condition. It is surprising though that there is a large number of rheumatologists who do take care of children or adolescents in one way or another, and there surely is a regional and geographic shortage of pediatric rheumatology care.

This is a challenge for the discipline overall. The good news, has been the release of the new British Society of Rheumatology, guidelines on the treatment of gout. They had a guideline I think in 2007 and they called for a new one because obviously a lot more, new therapies, some, new information, the rise of gout, in society. It's affected The UK as much as in The United States. In The UK it's about two point five percent to three percent of the population has gout and in The United States eight point three million people have gout.

So for a number of reasons they came up with pretty extensive guidelines with evidence based opinions. There's a multidisciplinary panel and they reviewed the literature and they came up with a number of factors. I'll leave you with two which I think are important. Number one, they strongly endorsed, as does the ACR, and you are the concept of treat the target, that this should be advocated for and that there should be a target of six and that you get there by any means. They also are a little bit more proactive than other guidelines in stating that early on patients should receive, urate lowering therapy, ULT, meaning that as soon as you have multiple attacks you should be on it.

And what they're noting in there is that there's a tremendous underutilization and misuse of allopurinol and other urate lowering therapies, that they're often reserved for patients with end stage and severe disease, and they're not often being given or maintained in patients with relatively early gout. So they make a big pitch for that. Worthwhile It's guideline, we reviewed it and high points in about a full page article on RheumNow. You should look at it and see if you agree with how they recommend gout be managed. An interesting report comes out as sub analysis of the RACAT study that tells us that you should be using triple DMARR therapy before you use aggressive biologics, specifically the comparative group being those on etanercept and methotrexate.

There are two triple DMARD versus biologic trials out there, the TIER study, which was done in early RA, and the RACAT study, which was done in established RA. And they both say the same thing, that it's more effective to use the cheaper regimen, the triple DMARG regimen, rather than to immediately switch to the biologic etanercept in this case plus methotrexate in those patients who fail methotrexate alone. In this specific analysis, they looked at the number of qualities, the quality adjusted life years, and the cost of care, and they could not justify the, more aggressive therapy, the more expensive therapy as being cost effective, not when they looked at all patients overall. If they did large sub analyses and found some subsets of very aggressive patients that could be predicted at the outset, you might make a case for it, but either way it's very clear that our most aggressive therapies still are our most expensive and maybe not the most cost effective, which is why we have to jump through the hoops we do when we want to use a biologic. So more information on triple D Mart therapy.

Lastly, there's two interesting reports about osteoarthritis of the knee. One comes from David Felsen and his coworkers which looked at, whether or not fiber intake may be associated with, better outcomes in osteoarthritis. And they looked at patients based on their dietary intakes and they looked at those who had symptomatic OA and those who had radiographic OA. What they showed was those who had a high fiber intake, a high amount of fiber intake, were significantly much less likely to have symptomatic OA, but not necessarily less radiographic OA. So it's not clear why the distinction, it's not even clear why fiber in the diet would lead to less symptomatic OA.

It could be that fiber in the diet may be anti inflammatory. A high amount of fiber in the diet may reflect a dietary practice which is advantageous to weight loss and to better joint health, but it's really not clear. But nonetheless, high fiber, who knew? And then lastly, there's another report about chondroitin in osteoarthritis of the knee. As you know, it's often combined with glucosamine as a combined product.

That was the subject of the GATE study, the glucosamine arthritis intervention trial that I was a part of and published in New England Journal over ten, fifteen years ago. In this, and one of the arms in that trial was a controvitin only trial, and there it did not show to be effective. There have been numerous trials that have shown very mixed results, and it seems that, when this author, Register, and this particular formulation of Congerodin has been used in trials, the results have been always positive. And while that may be, you know, again, I think there was six zero three patients in this trial that it's called the concept trial. Patients were randomized to receive either placebo or Celebrex two hundred milligrams a day or, eight hundred milligrams a day of chondroitin sulfate, and they showed that the chondroitin sulfate was equal to celecoxib in the clinical outcomes and that that was superior to placebo.

But their main outcomes were a visual analog scale pain score and a functional, score as well, and they showed both of those to be significantly higher, but truly the magnitude of difference between active treatment groups and the placebo group was not very large. Again, result should be viewed with some degree of skepticism as, when these authors report these results they always look good, when others it doesn't quite look as good. These results need to be repeated, need to be repeated with other products and by other investigators to make chondroitin sulfate a recommendation. Now I have one major rule with regard to nutraceuticals, and that is the more it costs, the less it works. If it's cheap and patients think it works, knock yourself out.

It does have a heparin like effect, so it shouldn't be given to patients who are at risk for bleeding or those who are on blood thinners, but you know I don't see any damage being done with chondroitin sulfate. I am also not very sure of the potential benefits, but this is a large trial. It merits consideration and discussion. It also merits reinvestigation. That's it for this week at roomnow.com.

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