RheumNow Week In Review How Not To Treat Hand OA %288.24.18%29 Save
RheumNow Week In Review How Not To Treat Hand OA %288.24.18%29 by Dr. Cush
Transcription
It's the 08/24/2018. This is the RheumNow we can review. Hi. I'm doctor Jack Cush, executive editor of roomnow.com, and this week, we're gonna begin with a clinical challenge. It's Tuesday, a good clinic day for you.
It's the morning session, and your third patient shows up, a new patient. And, basically, it's an adult, let's say 30, 40, 50 years old, doesn't really matter, who has an acute asymmetric oligoarticular inflammatory arthritis. Meaning there's a few swollen joints here. They're definitely swollen. There's no doubt about it.
You have no labs. You have no other information. You wanna be profound and teach those residents and fellows what this is, and you expound the following differential diagnosis. What is your differential diagnosis? Well, you're gonna tell me that at the end of this report.
In the meantime, let's cover some of the news from the past week at roomnow.com. Let's begin with a comparative study of women and pregnancy and the effects of arthritis on untoward outcomes including preterm delivery. This particular study is a study of five hundred or almost six seventy patients with rheumatoid arthritis, 170 patients with JIA, and these were compared to women who don't have arthritis, about five sixty four, and the outcome here is preterm birth. In a single setter study, what they showed was having either rheumatoid arthritis or juvenile idiopathic arthritis was associated with nearly a twofold increase in preterm birth. Not a horrible outcome, but nonetheless an adverse pregnancy outcome that has significant consequences and should be avoided if at all possible.
What they did show in their sub analysis of this is the risk of preterm delivery was most attached to or linked to disease activity and steroid use. Steroid use is probably a marker or a surrogate marker for uncontrolled disease. Again, is yet another study that shows it's not the drugs, it's the disease activity that determines the outcome in pregnancy amongst our patients who have inflammatory arthritis, rheumatic disease, and yes, even lupus and other autoimmune conditions. We must control activity first. An interesting study comes as an outgrowth or a sub analysis of the METiOR study.
May sound familiar, the METiOR study was a study published in 2013 in the New England Journal. It was a study of about three fifty mild to moderate osteoarthritis of the knee patients who had a meniscal tear. And they were then randomized to either receive meniscal surgery, menisectomies or partial menisectomies or physical therapy. The outcome of that particular study was that it didn't matter that physical therapy was almost as good as surgery. However, of those people who did have physical therapy, there was thirty percent who within six months went on to receive subsequent surgery.
So the takeaway from the METEOR study is that if you have early OA and you have a meniscal tear, that is probably smarter to do physical therapy first and that having physical therapy does not impair the outcomes later on. Interesting and sort of landmark study in the orthopedic world. In this particular study that looked at some of the data that was acquired in that analysis, they looked at two twenty one patients and specifically looked at what the association was between having knee synovitis or knee effusions on what happened to cartilage over time. And what they showed quite interestingly was that if you had either large degrees of effusion or synovitis and it was sustained, that this was associated with greater degrees of cartilage thinning over an eighteen month period. It sort of proves what we've always said that inflammation drives cartilage loss, inflammation is not a good thing for any joint, that even patients with OA, need to be treated probably more aggressively if they have effusions and if they have detectable synovitis.
I think a very important study. Another important study is a negative study and I didn't even put the study in the tweet or in the news release that we had on this but it's a 200 patient study from Netherlands. It's on the use of hydroxychloroquine in osteoarthritis of the hands. It's Mika Haase's group. It's another one of many very well done studies showing don't don't use hydroxychloroquine or DMARDs in people who have hand OA.
The studies are uniformly negative. It's a gigantic waste of time. I had a few comments from people saying, you know, my experience, I use a little sulfasalazine or I use a little methotrexate. Sorry folks, not proven, a gigantic waste of time. I don't really have a great solution as well.
So that's, you know, great for me to tell you, please don't use it and the evidence argues against it. But on the other hand, what do you do? Well, my best solution for hand o a, inflammatory or not, erosive or not, is to use simple analgesics, acetaminophen, somewhere between two thousand and four thousand milligrams of long acting acetaminophen a day. I combine it with a little bit of low dose prednisone, something I learned from Ted Pincus. It seems to go a long way, not just in RA, but even in some cases of OA, two point five milligrams a day.
Hand, physical therapy, there are reports suggesting that you can do localized injections of DIPs and PIPs. God help you if you know how to do it or if you have an ultrasound, congratulations, you might be able to do it. I also like to use cohesive tape. Cohesive tape is that stretchy tape that you patients get when they're having their blood drawn. It's also called co band.
It looks something like this. You can buy for about a buck a roll. Two inch tape covers both the DIP and the PIP and patients can immobilize those joints when they're particularly active. I tell patients keep reusing the tape, have it on there for ten to fourteen days. That's my best regimen.
If you've got another one, please write us, write an article, do research, we really need help in treating osteoarthritis of the hand. An interesting lupus study, a multinational lupus study of over 1,500 patients looked at the consequences of having renal disease on at least financial expenditures to manage lupus. In this particular study that was over seven years long, they showed that patients who had proteinuria were likely to have a fourfold higher amount of cost of total care, going up from 20,000 if you didn't have proteinuria to over 84,000 if you did have proteinuria. Similarly, and to a much greater degree, if you had a GFR of less than 30 cc's per minute, and meaning you had more than moderate, CKD, that those patients with renal failure actually incurred a 15 fold higher rate of cost going up from less than $20,000 to more than $310,000 in an eighteen month period. So again, actually this is really sort of important data.
I think it tells you the importance of managing renal disease in patients with lupus, which means we must manage blood pressure and be vigilant in monitoring for such outcomes. Whether you do that on your own or with a nephrologist is up to your own level of expertise. A study from Romania looked at the incidence of TB amongst patients taking TNF inhibitors. Specifically, looked over five hundred patients who had, taken TNF inhibitors for either rheumatoid arthritis, psoriatic arthritis or ankylosing spondylitis. In Romania, the background population risk of TB is ninety seven cases per one hundred thousand, individuals.
That's about 20 times higher than is seen in United States, Canada, The UK for instance, where the rates are roughly three to five cases per 100,000. So it's 20 times higher in the general population. What happens if you're an RA patient and you're you tend to have a LTBI, latent tuberculosis? Well, they measured TB and latent TB either by tuberculin skin test greater than five millimeters or greater or 10 millimeters greater or QuantiFERON. Regardless of the method, the rates of TB, LTBI that is, were significantly higher.
Five milliliters, it was thirteen hundred and forty eight. 10 millimeters, it was eight sixty two. Just a quantifier on being positive, it was five forty. This means that having a positive PPD was six to 14 fold higher if you were taking a TNF inhibitor with rheumatoid arthritis or another inflammatory disease. Again, this backs up the data that Kevin Winthrop has shown us from the CDC and other places where if you take a TNF inhibitor on top of the disease, can get as much as a nine fold or higher increased rate of LTBI.
An interesting study comes looking at acute coronary syndrome patients and the influence of hyperesthymia. This is a study of almost 28,000 individuals followed in two very large studies and it showed that amongst these patients, forty six percent had hyperuricemia and not all these people, actually very few of that group actually had gout. So what were the consequences of having hyperuricemia? Well, showed uric acid levels above six was significantly showed with a greater risk of cardiovascular events, and that was not linked to having gout. So again, hyperuricemia is a bad player in vascular disease and cardiac outcomes, and it's become a more and more of an issue in the cardiology world, not just in the gout and rheumatology world.
Another difficult disease to manage is systemic sclerosis. I found an interesting study that we put up this week, which was about the outcomes of systemic sclerosis patients who are hospitalized. Specifically, this looked at a nationwide database of almost fifty thousand scleroderma hospitalizations and took the subset of those about nine to ten thousand individuals and looked at the outcomes. They showed that number one, the rate of death was five percent. Not good, but not bad compared to some of the lupus studies where, mortal outcomes are much higher in lupus patients who get hospitalized.
This was high, but not that high. Turns out of those who died, and those, I'm sorry, those who were hospitalized and who died, the leading cause was infection. Infection accounted for seventeen percent of the hospitalizations and as much as thirty three percent of the overall deaths amongst systemic sclerosis patients. Mortality was closely linked not just to infection, but also to having acute renal failure and also to aspiration. The total length of stay and costs were linked to other things including pulmonary fibrosis, myositis, renal disease and bowel obstruction.
So as we know, the complications of systemic sclerosis can be really serious and really have dastardly outcomes. We know in this nationwide study, I think that these data say that we need to be vigilant in keeping our patients out of the hospital and maybe keep bigger eye open for managing infections as a way of keeping patients out of the hospital. Interesting study is an in vitro ex vivo study looking at temporal artery biopsies in temporal artery tissue explants and taking PBMCs from patients who had temporal arteritis and what the role of IL-twelve and 23 was. Well, the bottom line was IL-twelve and 23 was found in a temporal artery biopsies by immunohistochemical staining that they found that when they, used IL IL 12, or IL 23 on PBMCs in culture, they increased the amount of pro inflammatory cytokines, Th one and Th two side, Th 17 cytokines. So IL six, twenty two, gamma interferon in IL eight when you gave IL 12, you gave IL 23, there was a lot more IL six, twenty two, IL 17 a and IL 17 f suggesting that these two, cytokines play an important role in large vessel vasculitis, and may be an important target.
Well, we know that actually this has been studied. Carol Langford had a small study, but controlled study showing this does work, albeit not quite as effectively, maybe at the same degree in another unrelated study looking at IL-six inhibition, with tocilizumab, using abatacep to inhibit IL-twelve and twenty three was actually, not, I'm sorry, IL-twelve twenty three is another drug as we know for, it's Stelara and that actually hasn't been studied. Abatacept has been studied, and was not quite as effective as tocilizumab. So maybe we need to have some studies looking at either IL-twelve twenty three inhibitors, or maybe IL-twenty three inhibitors by themselves or IL-twelve by itself. We'll see on down the line.
You may want to look at some of our blogs from this week, a nice blog about no show rates in clinic from Rachel Tate. And I wrote a blog about the, dead word cemetery in rheumatology, which has got a lot of comments, including the ultimate fate of terms like connective tissue disease, rheumatism, CREST syndrome and MCTD. Let's go to the answer that we pose at the top of this report. A patient who presents with acute asymmetric oligoarticular inflammatory arthritis, what's the differential diagnosis? Here they are.
Psoriatic arthritis, spondyloarthritis, reactive arthritis, IBD associated arthritis, sarcoidosis, fungal infection, TB infection, undifferentiated arthritis, CPPD, even RA, chlamydia, Lyme, and acute gonococcal infection. If you've got others, send them my way. That's it for this week on RheumNow. You can go to the website to find these citations and read up more about these interesting reports. Tell your brother, your mother, your undertaker, the candlestick maker about RheumNow.
Tell them to register. We'll send them good news every week or every day about rheumatology. No nonsense, just education and important news for the care and practice of rheumatology. See you next week. Bye.
It's the morning session, and your third patient shows up, a new patient. And, basically, it's an adult, let's say 30, 40, 50 years old, doesn't really matter, who has an acute asymmetric oligoarticular inflammatory arthritis. Meaning there's a few swollen joints here. They're definitely swollen. There's no doubt about it.
You have no labs. You have no other information. You wanna be profound and teach those residents and fellows what this is, and you expound the following differential diagnosis. What is your differential diagnosis? Well, you're gonna tell me that at the end of this report.
In the meantime, let's cover some of the news from the past week at roomnow.com. Let's begin with a comparative study of women and pregnancy and the effects of arthritis on untoward outcomes including preterm delivery. This particular study is a study of five hundred or almost six seventy patients with rheumatoid arthritis, 170 patients with JIA, and these were compared to women who don't have arthritis, about five sixty four, and the outcome here is preterm birth. In a single setter study, what they showed was having either rheumatoid arthritis or juvenile idiopathic arthritis was associated with nearly a twofold increase in preterm birth. Not a horrible outcome, but nonetheless an adverse pregnancy outcome that has significant consequences and should be avoided if at all possible.
What they did show in their sub analysis of this is the risk of preterm delivery was most attached to or linked to disease activity and steroid use. Steroid use is probably a marker or a surrogate marker for uncontrolled disease. Again, is yet another study that shows it's not the drugs, it's the disease activity that determines the outcome in pregnancy amongst our patients who have inflammatory arthritis, rheumatic disease, and yes, even lupus and other autoimmune conditions. We must control activity first. An interesting study comes as an outgrowth or a sub analysis of the METiOR study.
May sound familiar, the METiOR study was a study published in 2013 in the New England Journal. It was a study of about three fifty mild to moderate osteoarthritis of the knee patients who had a meniscal tear. And they were then randomized to either receive meniscal surgery, menisectomies or partial menisectomies or physical therapy. The outcome of that particular study was that it didn't matter that physical therapy was almost as good as surgery. However, of those people who did have physical therapy, there was thirty percent who within six months went on to receive subsequent surgery.
So the takeaway from the METEOR study is that if you have early OA and you have a meniscal tear, that is probably smarter to do physical therapy first and that having physical therapy does not impair the outcomes later on. Interesting and sort of landmark study in the orthopedic world. In this particular study that looked at some of the data that was acquired in that analysis, they looked at two twenty one patients and specifically looked at what the association was between having knee synovitis or knee effusions on what happened to cartilage over time. And what they showed quite interestingly was that if you had either large degrees of effusion or synovitis and it was sustained, that this was associated with greater degrees of cartilage thinning over an eighteen month period. It sort of proves what we've always said that inflammation drives cartilage loss, inflammation is not a good thing for any joint, that even patients with OA, need to be treated probably more aggressively if they have effusions and if they have detectable synovitis.
I think a very important study. Another important study is a negative study and I didn't even put the study in the tweet or in the news release that we had on this but it's a 200 patient study from Netherlands. It's on the use of hydroxychloroquine in osteoarthritis of the hands. It's Mika Haase's group. It's another one of many very well done studies showing don't don't use hydroxychloroquine or DMARDs in people who have hand OA.
The studies are uniformly negative. It's a gigantic waste of time. I had a few comments from people saying, you know, my experience, I use a little sulfasalazine or I use a little methotrexate. Sorry folks, not proven, a gigantic waste of time. I don't really have a great solution as well.
So that's, you know, great for me to tell you, please don't use it and the evidence argues against it. But on the other hand, what do you do? Well, my best solution for hand o a, inflammatory or not, erosive or not, is to use simple analgesics, acetaminophen, somewhere between two thousand and four thousand milligrams of long acting acetaminophen a day. I combine it with a little bit of low dose prednisone, something I learned from Ted Pincus. It seems to go a long way, not just in RA, but even in some cases of OA, two point five milligrams a day.
Hand, physical therapy, there are reports suggesting that you can do localized injections of DIPs and PIPs. God help you if you know how to do it or if you have an ultrasound, congratulations, you might be able to do it. I also like to use cohesive tape. Cohesive tape is that stretchy tape that you patients get when they're having their blood drawn. It's also called co band.
It looks something like this. You can buy for about a buck a roll. Two inch tape covers both the DIP and the PIP and patients can immobilize those joints when they're particularly active. I tell patients keep reusing the tape, have it on there for ten to fourteen days. That's my best regimen.
If you've got another one, please write us, write an article, do research, we really need help in treating osteoarthritis of the hand. An interesting lupus study, a multinational lupus study of over 1,500 patients looked at the consequences of having renal disease on at least financial expenditures to manage lupus. In this particular study that was over seven years long, they showed that patients who had proteinuria were likely to have a fourfold higher amount of cost of total care, going up from 20,000 if you didn't have proteinuria to over 84,000 if you did have proteinuria. Similarly, and to a much greater degree, if you had a GFR of less than 30 cc's per minute, and meaning you had more than moderate, CKD, that those patients with renal failure actually incurred a 15 fold higher rate of cost going up from less than $20,000 to more than $310,000 in an eighteen month period. So again, actually this is really sort of important data.
I think it tells you the importance of managing renal disease in patients with lupus, which means we must manage blood pressure and be vigilant in monitoring for such outcomes. Whether you do that on your own or with a nephrologist is up to your own level of expertise. A study from Romania looked at the incidence of TB amongst patients taking TNF inhibitors. Specifically, looked over five hundred patients who had, taken TNF inhibitors for either rheumatoid arthritis, psoriatic arthritis or ankylosing spondylitis. In Romania, the background population risk of TB is ninety seven cases per one hundred thousand, individuals.
That's about 20 times higher than is seen in United States, Canada, The UK for instance, where the rates are roughly three to five cases per 100,000. So it's 20 times higher in the general population. What happens if you're an RA patient and you're you tend to have a LTBI, latent tuberculosis? Well, they measured TB and latent TB either by tuberculin skin test greater than five millimeters or greater or 10 millimeters greater or QuantiFERON. Regardless of the method, the rates of TB, LTBI that is, were significantly higher.
Five milliliters, it was thirteen hundred and forty eight. 10 millimeters, it was eight sixty two. Just a quantifier on being positive, it was five forty. This means that having a positive PPD was six to 14 fold higher if you were taking a TNF inhibitor with rheumatoid arthritis or another inflammatory disease. Again, this backs up the data that Kevin Winthrop has shown us from the CDC and other places where if you take a TNF inhibitor on top of the disease, can get as much as a nine fold or higher increased rate of LTBI.
An interesting study comes looking at acute coronary syndrome patients and the influence of hyperesthymia. This is a study of almost 28,000 individuals followed in two very large studies and it showed that amongst these patients, forty six percent had hyperuricemia and not all these people, actually very few of that group actually had gout. So what were the consequences of having hyperuricemia? Well, showed uric acid levels above six was significantly showed with a greater risk of cardiovascular events, and that was not linked to having gout. So again, hyperuricemia is a bad player in vascular disease and cardiac outcomes, and it's become a more and more of an issue in the cardiology world, not just in the gout and rheumatology world.
Another difficult disease to manage is systemic sclerosis. I found an interesting study that we put up this week, which was about the outcomes of systemic sclerosis patients who are hospitalized. Specifically, this looked at a nationwide database of almost fifty thousand scleroderma hospitalizations and took the subset of those about nine to ten thousand individuals and looked at the outcomes. They showed that number one, the rate of death was five percent. Not good, but not bad compared to some of the lupus studies where, mortal outcomes are much higher in lupus patients who get hospitalized.
This was high, but not that high. Turns out of those who died, and those, I'm sorry, those who were hospitalized and who died, the leading cause was infection. Infection accounted for seventeen percent of the hospitalizations and as much as thirty three percent of the overall deaths amongst systemic sclerosis patients. Mortality was closely linked not just to infection, but also to having acute renal failure and also to aspiration. The total length of stay and costs were linked to other things including pulmonary fibrosis, myositis, renal disease and bowel obstruction.
So as we know, the complications of systemic sclerosis can be really serious and really have dastardly outcomes. We know in this nationwide study, I think that these data say that we need to be vigilant in keeping our patients out of the hospital and maybe keep bigger eye open for managing infections as a way of keeping patients out of the hospital. Interesting study is an in vitro ex vivo study looking at temporal artery biopsies in temporal artery tissue explants and taking PBMCs from patients who had temporal arteritis and what the role of IL-twelve and 23 was. Well, the bottom line was IL-twelve and 23 was found in a temporal artery biopsies by immunohistochemical staining that they found that when they, used IL IL 12, or IL 23 on PBMCs in culture, they increased the amount of pro inflammatory cytokines, Th one and Th two side, Th 17 cytokines. So IL six, twenty two, gamma interferon in IL eight when you gave IL 12, you gave IL 23, there was a lot more IL six, twenty two, IL 17 a and IL 17 f suggesting that these two, cytokines play an important role in large vessel vasculitis, and may be an important target.
Well, we know that actually this has been studied. Carol Langford had a small study, but controlled study showing this does work, albeit not quite as effectively, maybe at the same degree in another unrelated study looking at IL-six inhibition, with tocilizumab, using abatacep to inhibit IL-twelve and twenty three was actually, not, I'm sorry, IL-twelve twenty three is another drug as we know for, it's Stelara and that actually hasn't been studied. Abatacept has been studied, and was not quite as effective as tocilizumab. So maybe we need to have some studies looking at either IL-twelve twenty three inhibitors, or maybe IL-twenty three inhibitors by themselves or IL-twelve by itself. We'll see on down the line.
You may want to look at some of our blogs from this week, a nice blog about no show rates in clinic from Rachel Tate. And I wrote a blog about the, dead word cemetery in rheumatology, which has got a lot of comments, including the ultimate fate of terms like connective tissue disease, rheumatism, CREST syndrome and MCTD. Let's go to the answer that we pose at the top of this report. A patient who presents with acute asymmetric oligoarticular inflammatory arthritis, what's the differential diagnosis? Here they are.
Psoriatic arthritis, spondyloarthritis, reactive arthritis, IBD associated arthritis, sarcoidosis, fungal infection, TB infection, undifferentiated arthritis, CPPD, even RA, chlamydia, Lyme, and acute gonococcal infection. If you've got others, send them my way. That's it for this week on RheumNow. You can go to the website to find these citations and read up more about these interesting reports. Tell your brother, your mother, your undertaker, the candlestick maker about RheumNow.
Tell them to register. We'll send them good news every week or every day about rheumatology. No nonsense, just education and important news for the care and practice of rheumatology. See you next week. Bye.
If you are a health practitioner, you may Login/Register to comment.
Due to the nature of these comment forums, only health practitioners are allowed to comment at this time.