RheumNow Podcast Richer Or Poorer (5.17.19) Save
RheumNow Podcast Richer Or Poorer (5.17.19) by Dr. Cush
Transcription
It's the 05/17/2019. This is the RheumNow podcast. I'm Doctor. Jack Cush, executive editor of roomnow.com. It's been said that I've been poor and I've been rich and rich is better.
I think Mae West said it, I think Cher said it. It's attributed to a lot of other people. What they forgot to leave out was if you're rich, you'll live longer and that's our top story. A study from Norway, a public health study, looked at a large percentage of the population and compared those who were in the top 1% richest and top 1% poorest and there are striking differences in life expectancy. In fact, fourteen years longer for men, eight years longer for women when you look at those who are richer.
So money may not buy you love, but it'll buy you a few years. This was not just seen in Norway study, it was also sort of replicated in an earlier study from The United States. I don't know what this means for arthritis patients but you might advise your patients to work on their income. A nice study comes out of Otis looking at the risk of pregnancy outcomes in patients who have psoriatic arthritis and ankylosing spondylitis. We know a fair amount about what happens in pregnancy in RA, namely that not everybody goes into remission and that there's a substantial number, as many as half of patients, who will have difficulties during their pregnancy with their RA.
And it's the mother's health and maternal disease activity that actually determines more of the fetal outcome than does any medicine. This is also important in other inflammatory arthritities such as PSA and AS. A fairly large study, looked at two cohorts, followed them forward, looked at activity and showed that PSA and AS patients have a significant risk of adverse pregnancy outcomes, including preterm delivery where there's an increased adjusted relative risk of one point eight higher or eighty percent higher in PSA and three eighty percent higher, three point eight two in ankylosing spondylitis. Similarly, a higher rate of cesarean sections with a sixty three percent higher risk in psoriatic arthritis and a five hundred or five point eight two relative risk in patients with ankylosing spondylitis. Turns out that the use of steroids in such patients also increases the risk of these adverse outcomes for the mother.
So, again, we do need to worry about, disease activity, and our first order of business should be controlling this activity before our patients get pregnant or as they go into pregnancy. A nice bit of information comes from a large nationwide, actually worldwide study, looked at many, many studies and specifically looking at the use of, natural dietary supplements, meaning homeopathic, nutraceuticals, these sort of things. The worldwide use of these natural dietary supplements is seen in almost fifty percent of RA patients, the number was forty seven percent specifically, and did not vary according to where they looked around the world in these many different studies that they found. While patients or those reporting said that half the patients responded, there was also issues of adverse events, thirteen percent, and the real problem was that only thirty percent of the patients had informed their physicians they were taking natural dietary supplements. I think that's something we need to worry about, something we need to ask about because patients may be relying on those agents for efficacy.
They think they're just as good as the prescription drug and may be safer because those don't come with an eight page handout from the pharmacy. CMV infection, you know, this comes up sometimes in our patients. Our patients are immunosuppressed, they're on steroids, you hear about rare bizarre cases of patients who are hospitalized. A nice review of 14 patients who had CMV infection in autoimmune disease found that the vast majority of them had fever, undiagnosed fever, many of them were in the hospital. Thirteen of the fourteen were on steroids before or during the hospitalization and eight of them had co infections.
The real problem here is that four of them died, four out of fourteen, not a good number, and they tended to have long hospitalization stays which had bad outcomes probably because they were not easily diagnosed. This may be one of the infections that our patients may be at risk for, especially if they're on steroids. Low back pain is highly prevalent in our society, just a number that comes from a recent Annals of Internal Medicine article from May 14 that amongst US workers twenty six percent have chronic low back pain and that five point six percent it is severe low back pain. Those are numbers that will bring you business and that will be difficult to manage. There is this problem of, statin induced myopathy.
They are HMGCR positive, they have a necrotizing myopathy, and you can withdraw therapy and they may get better, but some of them go on to have chronic courses and the question is how are those patients going to be managed. A review of the PCSK9 inhibitors. PCSK9 inhibitors includes drugs like Repatha. These are newer agents designed for refractory, difficult to treat, hyperlipidemias. They work by, inhibiting the LDL receptor and lowering therefore LDL levels along with other, lipids, and they're highly effective.
Sort of a small study that looked at a number of patients who were given these PCSK9 inhibitors, for their hyperlipidemia shows number one that they don't have worsening of their CK and myopathies. These are patients who have, by the way, myopathy from statins, so that's good but also their CK is actually lowered, although not significantly from a mean of nine fifty six to four nineteen, and more importantly that their, HMGCR antibody titers decreased and that two out of the eight showed significant improvement in their myositis. So this may be an alternative for patients who have difficult myopathy and may also have statin related issues where you can't use the statins, this may be a compelling choice. You know there is also a problem in managing GCA patients who can't take steroids. They're elderly, they may have comorbidities, they may have diabetes, steroids can be difficult to tolerate.
We're often looking for a steroid sparing agent to use in these patients and there's been a number of studies, often many of them not well done using methotrexate with mixed results. A recent report looked at eighty three patients on methotrexate on a mean dose of thirteen point five milligrams per week and eighty three who did not receive methotrexate. This is open label real world patients. Bottom line is that those who are on low dose methotrexate showed less relapse rates and that was significant, almost a sixty eight percent reduction in relapse rates but no change in steroid use. So I think that what we hear from the people who look at this data and report on this is that we need studies studies like this but we really need well designed studies, especially ones that are going to use serious doses of methotrexate, more like fifteen to twenty five milligrams per week as opposed to many of these studies which are hampered by this one low doses, but in this case low dose seem to be good enough.
So I have a bevy of studies on gout to discuss I think are really interesting. Number one, dual energy CT scans, these beautiful pictures of urate deposition disease with total body urate stores that are surprising and shocking and whatnot, this is a test that's actually becoming more widely available and if you talk to your radiology department you'll be surprised they can do it. You know, the pictures show you more than what you expect. The question is how good are they in diagnosing gout? I don't think it takes the place of clinical diagnosis with laboratory and crystal identification, but this may be important in management or diagnosis on patients.
It turns out in a review of the literature, 10 studies that they looked at, the sensitivity is good, it's eighty one percent. The specificity is great at ninety one percent. When they applied this to patients with earlier disease, not quite so good. The sensitivity dropped significantly down to fifty five percent, although specificity remained high suggesting that dual energy CT or deck scanning is most valuable in patients who have established gout. A large Medicare analysis looked at gout patients specifically looking at the issue of chronic pain and finds a twofold increase in chronic pain in gout patients.
This may not be surprising to you, maybe it is. Gout tends to be an episodic disease and pain tends to be an episodic issue, but to have a two fold increase is substantial and given the fact that it's like over nine million patients in The United States, think the number is nine point three million new estimates, and that's like what, that's eight times more than rheumatoid arthritis. Pain is a big issue and what is also seen from these studies is that the use of urate lowering therapies such as febuxostat or allopurinol was associated with significant reduction in chronic pain where the hazard ratio dropped to zero point seven two or a twenty eight percent drop in pain when those were being used. So the big goal in gout is what? A serum uric acid level of six or less if you have to topaceous gout five or less.
You know, this was a big issue between the American College of Physicians who says you don't need to monitor your rate levels and they didn't buy into Treat to Target in their guidelines. Of course, we as rheumatologists do monitor uric acid levels and believe in Treat to Target and its benefits. An interesting study is in the literature about eighty seven patients who were followed and looks at what happens to their images both on x-ray and on CT, when they were given a treat to target regimen. Half were given a treat to target regimen, the other half were not after two years. Actually, was no real difference in x-ray scores or joint space narrowing scores on plain x-ray, but CT erosion scores were significantly decreased in patients who are on the T2T regimen, and also they actually had lower total urate volumes as measured by again dual energy CT scans suggesting that there's a systemic reduction in urate levels when you do a better reduction in systemic urate levels when you do T2T.
Lastly, one of my pet peeves: Does gout happen in RA patients? There's an inverse relationship with it, meaning that someone has RA really shouldn't have gout and someone's gout really shouldn't have RA and that's generally true but yet we see consults and diagnoses all the time of patients who are diagnosed with you know everything spondylitis, vasculitis, gout, RA and lupus and you know that these are all inaccurate diagnoses. You often see RA and gout on the same page together and you've got to assume that most of those are inaccurate and I've often said that it's one or the other. If you can't get it from the history, do a, you know, serologies and a uric acid and that'll help you figure it out. But there is a small percentage of patients with RA who have gout and this is drawn from a number of basically inferential sources and indirect ways.
VA prospective study on rheumatoid arthritis has actually looked at this. It's a large study of almost 2,000 patients with RA and when they looked at their records they found that seventeen percent of their RA patients had hyperuricemia. Secondly, that six point one had a diagnosis of gout. Now I'm sure these were based on, you know, administrative records reviews, claims data, looking at ICD-ten, ICD-nine codes, So these were not necessarily verified diagnosis of gout, but you know, gout in a VA clinic is probably pretty accurate. So that shows you the magnitude of the problem and it does exist and it can be hard to manage such patients.
Often you don't know what you're managing one way or the other. I have a few that are taking your rate lowering therapy in addition to their standard rheumatoid therapies. I'll give you one sort of pearl and that is leflinamide is an effective DMARD that is approved for use in rheumatoid arthritis. It's never really been studied in gout, but it is a urate lowering drug. It actually has the ability to drop, urate levels by as much as 20 in patients who aren't receiving other urate lowering therapies.
One of my other pet peeves: methotrexate and lung disease. Does methotrexate make rheumatoid lung disease worse? Now, let's be clear, methotrexate causes an acute hypersensitivity pneumonitis acute onset, shortness of breath, white out in both lungs, hypoxia, stop methotrexate, give them steroids, they get better, everyone's wonderful, happy go home. That's quite different than RA lung, severe disease, long standing disease, seropositive disease, nodular disease, and a slow insidious decline in lung function with an interstitial lung disease and labs and PFTs that reflect that. Of course your pulmonary colleagues are telling your patients not to take methotrexate if they have ILD and that makes no sense because you need methotrexate to do your best combination therapy.
So this was looked at actually by a UK study group. They looked at two, large cohorts of early RA in Wales and Ireland, and assessed them for whether or they had ILD. As a few thousand patients, found amongst them ninety two eligible patients who had ILD. About a third of them were given methotrexate during their course of management and two thirds of them were not. The bottom line was when they looked at the risks associated with methotrexate and incident ILD it was not significantly increased.
The odds ratio was zero point eight five and it crossed over one, in the confidence intervals. Moreover, the use of methotrexate was associated with a reduced risk of developing ILD or, and if it did happen, a delayed risk. That's kind of surprising. Our last report I'm not going to talk much about and that's generic price fixing that came up this week in many big articles in New York Times and Reuters and Wall Street Journal. I'll refer you to our website and the link that we have, you can read the article which gives you a good synopsis.
Should really should look at the sixty Minutes piece on television, one of the links we have in there. It's really eye opening. You know, you've seen this for a long while. Plaquenil used to be a cheap drug, nonsteroidals used to be cheap drugs, they're not anymore. I once went to get a prescription for sixty pills of prednisone which used to cost about 3 or $4 and they wanted to charge me $60.
I said, Excuse me, I'm a rheumatologist. I know what I'm paying for here. Well, that's actually what happened. So there is an issue of price fixing that seems to be apparent from the records provided both in the written reports and the TV reports. It again is eye opening.
Take a look at it. Hopefully with all that's going on with the price of drugs, the price of expensive drugs, the rebate system and now generic price fixing falling under the radar of the current administration, we'll start to see some new rules, some more fair treatment for our patients, and ultimately better outcomes for those who have arthritis. Tune in next week, we'll see you, take care.
I think Mae West said it, I think Cher said it. It's attributed to a lot of other people. What they forgot to leave out was if you're rich, you'll live longer and that's our top story. A study from Norway, a public health study, looked at a large percentage of the population and compared those who were in the top 1% richest and top 1% poorest and there are striking differences in life expectancy. In fact, fourteen years longer for men, eight years longer for women when you look at those who are richer.
So money may not buy you love, but it'll buy you a few years. This was not just seen in Norway study, it was also sort of replicated in an earlier study from The United States. I don't know what this means for arthritis patients but you might advise your patients to work on their income. A nice study comes out of Otis looking at the risk of pregnancy outcomes in patients who have psoriatic arthritis and ankylosing spondylitis. We know a fair amount about what happens in pregnancy in RA, namely that not everybody goes into remission and that there's a substantial number, as many as half of patients, who will have difficulties during their pregnancy with their RA.
And it's the mother's health and maternal disease activity that actually determines more of the fetal outcome than does any medicine. This is also important in other inflammatory arthritities such as PSA and AS. A fairly large study, looked at two cohorts, followed them forward, looked at activity and showed that PSA and AS patients have a significant risk of adverse pregnancy outcomes, including preterm delivery where there's an increased adjusted relative risk of one point eight higher or eighty percent higher in PSA and three eighty percent higher, three point eight two in ankylosing spondylitis. Similarly, a higher rate of cesarean sections with a sixty three percent higher risk in psoriatic arthritis and a five hundred or five point eight two relative risk in patients with ankylosing spondylitis. Turns out that the use of steroids in such patients also increases the risk of these adverse outcomes for the mother.
So, again, we do need to worry about, disease activity, and our first order of business should be controlling this activity before our patients get pregnant or as they go into pregnancy. A nice bit of information comes from a large nationwide, actually worldwide study, looked at many, many studies and specifically looking at the use of, natural dietary supplements, meaning homeopathic, nutraceuticals, these sort of things. The worldwide use of these natural dietary supplements is seen in almost fifty percent of RA patients, the number was forty seven percent specifically, and did not vary according to where they looked around the world in these many different studies that they found. While patients or those reporting said that half the patients responded, there was also issues of adverse events, thirteen percent, and the real problem was that only thirty percent of the patients had informed their physicians they were taking natural dietary supplements. I think that's something we need to worry about, something we need to ask about because patients may be relying on those agents for efficacy.
They think they're just as good as the prescription drug and may be safer because those don't come with an eight page handout from the pharmacy. CMV infection, you know, this comes up sometimes in our patients. Our patients are immunosuppressed, they're on steroids, you hear about rare bizarre cases of patients who are hospitalized. A nice review of 14 patients who had CMV infection in autoimmune disease found that the vast majority of them had fever, undiagnosed fever, many of them were in the hospital. Thirteen of the fourteen were on steroids before or during the hospitalization and eight of them had co infections.
The real problem here is that four of them died, four out of fourteen, not a good number, and they tended to have long hospitalization stays which had bad outcomes probably because they were not easily diagnosed. This may be one of the infections that our patients may be at risk for, especially if they're on steroids. Low back pain is highly prevalent in our society, just a number that comes from a recent Annals of Internal Medicine article from May 14 that amongst US workers twenty six percent have chronic low back pain and that five point six percent it is severe low back pain. Those are numbers that will bring you business and that will be difficult to manage. There is this problem of, statin induced myopathy.
They are HMGCR positive, they have a necrotizing myopathy, and you can withdraw therapy and they may get better, but some of them go on to have chronic courses and the question is how are those patients going to be managed. A review of the PCSK9 inhibitors. PCSK9 inhibitors includes drugs like Repatha. These are newer agents designed for refractory, difficult to treat, hyperlipidemias. They work by, inhibiting the LDL receptor and lowering therefore LDL levels along with other, lipids, and they're highly effective.
Sort of a small study that looked at a number of patients who were given these PCSK9 inhibitors, for their hyperlipidemia shows number one that they don't have worsening of their CK and myopathies. These are patients who have, by the way, myopathy from statins, so that's good but also their CK is actually lowered, although not significantly from a mean of nine fifty six to four nineteen, and more importantly that their, HMGCR antibody titers decreased and that two out of the eight showed significant improvement in their myositis. So this may be an alternative for patients who have difficult myopathy and may also have statin related issues where you can't use the statins, this may be a compelling choice. You know there is also a problem in managing GCA patients who can't take steroids. They're elderly, they may have comorbidities, they may have diabetes, steroids can be difficult to tolerate.
We're often looking for a steroid sparing agent to use in these patients and there's been a number of studies, often many of them not well done using methotrexate with mixed results. A recent report looked at eighty three patients on methotrexate on a mean dose of thirteen point five milligrams per week and eighty three who did not receive methotrexate. This is open label real world patients. Bottom line is that those who are on low dose methotrexate showed less relapse rates and that was significant, almost a sixty eight percent reduction in relapse rates but no change in steroid use. So I think that what we hear from the people who look at this data and report on this is that we need studies studies like this but we really need well designed studies, especially ones that are going to use serious doses of methotrexate, more like fifteen to twenty five milligrams per week as opposed to many of these studies which are hampered by this one low doses, but in this case low dose seem to be good enough.
So I have a bevy of studies on gout to discuss I think are really interesting. Number one, dual energy CT scans, these beautiful pictures of urate deposition disease with total body urate stores that are surprising and shocking and whatnot, this is a test that's actually becoming more widely available and if you talk to your radiology department you'll be surprised they can do it. You know, the pictures show you more than what you expect. The question is how good are they in diagnosing gout? I don't think it takes the place of clinical diagnosis with laboratory and crystal identification, but this may be important in management or diagnosis on patients.
It turns out in a review of the literature, 10 studies that they looked at, the sensitivity is good, it's eighty one percent. The specificity is great at ninety one percent. When they applied this to patients with earlier disease, not quite so good. The sensitivity dropped significantly down to fifty five percent, although specificity remained high suggesting that dual energy CT or deck scanning is most valuable in patients who have established gout. A large Medicare analysis looked at gout patients specifically looking at the issue of chronic pain and finds a twofold increase in chronic pain in gout patients.
This may not be surprising to you, maybe it is. Gout tends to be an episodic disease and pain tends to be an episodic issue, but to have a two fold increase is substantial and given the fact that it's like over nine million patients in The United States, think the number is nine point three million new estimates, and that's like what, that's eight times more than rheumatoid arthritis. Pain is a big issue and what is also seen from these studies is that the use of urate lowering therapies such as febuxostat or allopurinol was associated with significant reduction in chronic pain where the hazard ratio dropped to zero point seven two or a twenty eight percent drop in pain when those were being used. So the big goal in gout is what? A serum uric acid level of six or less if you have to topaceous gout five or less.
You know, this was a big issue between the American College of Physicians who says you don't need to monitor your rate levels and they didn't buy into Treat to Target in their guidelines. Of course, we as rheumatologists do monitor uric acid levels and believe in Treat to Target and its benefits. An interesting study is in the literature about eighty seven patients who were followed and looks at what happens to their images both on x-ray and on CT, when they were given a treat to target regimen. Half were given a treat to target regimen, the other half were not after two years. Actually, was no real difference in x-ray scores or joint space narrowing scores on plain x-ray, but CT erosion scores were significantly decreased in patients who are on the T2T regimen, and also they actually had lower total urate volumes as measured by again dual energy CT scans suggesting that there's a systemic reduction in urate levels when you do a better reduction in systemic urate levels when you do T2T.
Lastly, one of my pet peeves: Does gout happen in RA patients? There's an inverse relationship with it, meaning that someone has RA really shouldn't have gout and someone's gout really shouldn't have RA and that's generally true but yet we see consults and diagnoses all the time of patients who are diagnosed with you know everything spondylitis, vasculitis, gout, RA and lupus and you know that these are all inaccurate diagnoses. You often see RA and gout on the same page together and you've got to assume that most of those are inaccurate and I've often said that it's one or the other. If you can't get it from the history, do a, you know, serologies and a uric acid and that'll help you figure it out. But there is a small percentage of patients with RA who have gout and this is drawn from a number of basically inferential sources and indirect ways.
VA prospective study on rheumatoid arthritis has actually looked at this. It's a large study of almost 2,000 patients with RA and when they looked at their records they found that seventeen percent of their RA patients had hyperuricemia. Secondly, that six point one had a diagnosis of gout. Now I'm sure these were based on, you know, administrative records reviews, claims data, looking at ICD-ten, ICD-nine codes, So these were not necessarily verified diagnosis of gout, but you know, gout in a VA clinic is probably pretty accurate. So that shows you the magnitude of the problem and it does exist and it can be hard to manage such patients.
Often you don't know what you're managing one way or the other. I have a few that are taking your rate lowering therapy in addition to their standard rheumatoid therapies. I'll give you one sort of pearl and that is leflinamide is an effective DMARD that is approved for use in rheumatoid arthritis. It's never really been studied in gout, but it is a urate lowering drug. It actually has the ability to drop, urate levels by as much as 20 in patients who aren't receiving other urate lowering therapies.
One of my other pet peeves: methotrexate and lung disease. Does methotrexate make rheumatoid lung disease worse? Now, let's be clear, methotrexate causes an acute hypersensitivity pneumonitis acute onset, shortness of breath, white out in both lungs, hypoxia, stop methotrexate, give them steroids, they get better, everyone's wonderful, happy go home. That's quite different than RA lung, severe disease, long standing disease, seropositive disease, nodular disease, and a slow insidious decline in lung function with an interstitial lung disease and labs and PFTs that reflect that. Of course your pulmonary colleagues are telling your patients not to take methotrexate if they have ILD and that makes no sense because you need methotrexate to do your best combination therapy.
So this was looked at actually by a UK study group. They looked at two, large cohorts of early RA in Wales and Ireland, and assessed them for whether or they had ILD. As a few thousand patients, found amongst them ninety two eligible patients who had ILD. About a third of them were given methotrexate during their course of management and two thirds of them were not. The bottom line was when they looked at the risks associated with methotrexate and incident ILD it was not significantly increased.
The odds ratio was zero point eight five and it crossed over one, in the confidence intervals. Moreover, the use of methotrexate was associated with a reduced risk of developing ILD or, and if it did happen, a delayed risk. That's kind of surprising. Our last report I'm not going to talk much about and that's generic price fixing that came up this week in many big articles in New York Times and Reuters and Wall Street Journal. I'll refer you to our website and the link that we have, you can read the article which gives you a good synopsis.
Should really should look at the sixty Minutes piece on television, one of the links we have in there. It's really eye opening. You know, you've seen this for a long while. Plaquenil used to be a cheap drug, nonsteroidals used to be cheap drugs, they're not anymore. I once went to get a prescription for sixty pills of prednisone which used to cost about 3 or $4 and they wanted to charge me $60.
I said, Excuse me, I'm a rheumatologist. I know what I'm paying for here. Well, that's actually what happened. So there is an issue of price fixing that seems to be apparent from the records provided both in the written reports and the TV reports. It again is eye opening.
Take a look at it. Hopefully with all that's going on with the price of drugs, the price of expensive drugs, the rebate system and now generic price fixing falling under the radar of the current administration, we'll start to see some new rules, some more fair treatment for our patients, and ultimately better outcomes for those who have arthritis. Tune in next week, we'll see you, take care.



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