A detailed guide to Chronic Fatigue Syndrome (CFS), including its symptoms, causes, and effective treatment strategies to improve energy and well-being.
Researchers in the U.K. report that non-restorative sleep is the strongest, independent predictor of widespread pain onset among adults over the age of 50. According to the study published in Arthritis & Rheumatology (formerly Arthritis & Rheumatism), a journal of the American College of Rheumatology (ACR), anxiety, memory impairment, and poor physical health among older adults may also increase the risk of developing widespread pain.
Muscle, bone and nerve (musculoskeletal) pain is more prevalent as people age, with up to 80% of people 65 years of age and older experiencing daily pain. Widespread pain that affects multiple areas of the body — the hallmark feature of fibromyalgia — affects 15% of women and 10% of men over age 50 according to previous studies.
Led by Dr. John McBeth from the Arthritis Research UK Primary Care Centre, Keele University in Staffordshire, this newly published population-based prospective study identified factors that increase the risk of the development of widespread pain in older adults. The team collected data on pain, psychological and physical health, lifestyle and demographic information from 4326 adults over the age of 50 who were free of widespread pain at the start of the study (1562 subjects reported no pain and 2764 had some pain). These participants were followed up three years later for the development of widespread pain.
Results show that at follow-up, 800 (19%) reported new widespread pain. The development of new widespread pain was greater in those with some pain at the start of the study; 679 (25%) of those with some pain and 121 (8%) of those with no pain at the start developed new widespread pain at three year follow-up.
Analyses determined that pain status, anxiety, physical health-related quality of life, cognitive complaint and non-restorative sleep were associated with increased risk of widespread pain development, after adjusting for osteoarthritis (OA). Increasing age was associated with a decreased likelihood of the development of widespread pain.
“While OA is linked to new onset of widespread pain, our findings also found that poor sleep, cognition, and physical and psychological health may increase pain risk,” concludes Dr. McBeth. “Combined interventions that treat both site-specific and widespread pain are needed for older adults.”
Lupus patients have been waiting a while for some good news. Only one drug, belimumab (Benlysta), has been FDA-approved for lupus in more than 50 years — and that happened back in 2011. Since then, scientists have been trying to develop additional therapeutic agents (and failing for various reasons). But research presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals (ACR/ARP) Annual Meeting in Atlanta suggests that a new lupus medication, anifrolumab, might have the potential to get approved and make its way to market.
The manufacturer, AstraZeneca, is expected to file for FDAapproval in 2020. It’s hardly a slam dunk: The company conducted two phase 3 trials on anifrolumab, and one of them did not hit its primary endpoint, though secondary endpoints suggested that the drug had benefits. The second phase 3 study, which was presented for the first time at the recent ACR/ARP meeting, yielded more consistently positive results.
“I’m optimistic and hopeful that this drug will be approved,” says Chronicwoman medical advisor Vinicius Domingues, MD. “We have one [phase 3] study that was technically negative but with a lot of positives because of the secondary endpoints, plus a second [phase 3] study that was all positive. Patients should know that this is promising.”
The first phase 3 trial was called TULIP 1 (Treatment of Uncontrolled Lupus via the Interferon Pathway). Last August, AstraZeneca reported that anifrolumab failed to meet its primary target in TULIP 1, which was a “statistically-significant reduction in disease activity… as measured by the SLE Responder Index 4 (SRI4) at 12 months.”
SRI4 is a composite score that is often used to measure disease activity in patients with systemic lupus during clinical trials. According to SRI4, anifrolumab was as flop: Patients who added the drug to their treatment regimen did not, on average, fare better than those who added a placebo.
However, secondary endpoints in TULIP 1 found that anifrolumab beat the placebo. Those secondary endpoints included a different composite score of disease activity, called BICLA (British Isles Lupus Assessment Group-Based Composite Lupus Assessment), as well as reduced reliance on corticosteroid drugs.
The results of TULIP 1 appear in the journal Lancet Rheumatology and were discussed at the 2019 ACR/ARP meeting.
TULIP 2, the second phase III study of anifrolumab, used BICLA as its primary endpoint — and met it. TULIP 2, which was also presented at the 2019 ACR/ARP meeting, found that the drug beat the placebo as far as BICLA was concerned. It also determined that patients using it had greater improvements in skin disease and decreased use of corticosteroids.
While it’s true that researchers deliberately switched to a primary endpoint that they were likely to meet when moving from TULIP 1 to TULIP 2, there’s no clear consensus among rheumatologists that SRI4 is “better” than BICLA. In fact, a 2014 study compared these two outcome measures and determined that either one could “likely be an optimal primary endpoint” in a given clinical trial.
According to Northwestern University rheumatologist Michael Putman, MD, reporting on the trials for RheumNow, the SRI4 requires 100 percent improvement in some domains, “whereas with the BICLA you can get a little better across the board.” That might be part of why one endpoint seemed to work and the other didn’t, he said.
Anifrolumab is a monoclonal antibody that inhibits type 1 interferons, proteins that are involved in inflammation. Some lupus patients (but not all) have a “high interferon gene signature.” Scientists are simultaneously developing a test that can be used to identify those individuals. “It can be used to help predict who may or may not respond to this drug,” says Dr. Domingues. “This is an example of precision medicine, and it’s how cancer is being treated nowadays.”
“There has been a case building for many years about the importance of interferons in the pathogenesis of lupus,” Timothy Niewold, MD, Judith and Stewart Colton Professor of Medicine and Pathology and Director of the Colton Center for Autoimmunity at the New York University School of Medicine, told the ACR Daily News. “One of the most exciting recent developments is that drug companies have created agents to target the interferon pathway. It’s been a rocky road, but there have been some positive results.”
If anifrolumab gets the green light from the FDA, patients who haven’t responded well to other lupus treatments — especially those who have a high interferon gene signature — might benefit by including it in their current drug regimen, says Dr. Domingues. (The drug would be an add-on, not a replacement.)
If the drug eventually gets approved, label specifics such as recommended dosing and warnings about side effects would be revealed at that time. In the TULIP 2 study, participants in the treatment group used 300 mg of anifrolumab via infusion every four weeks. Serious adverse events were rare and occurred more frequently among those in the placebo group. The most common side effect experienced by those using anifrolumab was shingles, which occurred in 7 percent of anifrolumab users.
“Giant cell arteritis requires ongoing management, but it does not necessarily require continuous treatment.”
In 2017, tocilizumab (Actemra), a biologic drug that inhibits interleukin-6 (IL-6), was FDA-approved for giant cell arteritis — an inflammation of the lining of the arteries. At the time there was sufficient research showing that tocilizumab was better than prednisone (a steroid) for helping many patients reach remission in GCA. Yet it was unclear whether those who had reached remission should stop taking the drug or if they needed to continue using it.
Now a new study, presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals Annual Meeting in Atlanta, offers good news: A sizeable group of those who reached remission with tocilizumab were still in remission two years after stopping the drug.
The new study was an extension of an earlier 52-week study that led to tocilizumab’s FDA approval for giant cell arteritis. The drug is also approved for rheumatoid arthritis, juvenile idiopathic arthritis, and severe cytokine release syndrome.
More than 200 patients who had reached remission by using tocilizumab either once a week or every other week entered the post-marketing arm and were instructed to stop using the drug. According to their findings, 47 percent of those who had been previously taking tocilizumab weekly and 36 percent of those who had previously been taking it every other week remained in remission two years later.
Those who did experience flares were restarted on tocilizumab and/or given steroids. Those who resumed using tocilizumab (with or without a steroid) were once again able to reach remission.
“Giant cell arteritis requires ongoing management, but it does not necessarily require continuous treatment,” lead author John H. Stone, MD, MPH, told the ACR/ARP Daily News. “Patients should be started on tocilizumab as soon as they are diagnosed. The goal should be to get them off steroids as quickly as possible and maintain their response with tocilizumab.”
Some people with rheumatoid arthritis (RA) take a disease-modifying antirheumatic drug (DMARD) and/or a biologic and reach remission. Others try drug after drug after drug and never find one that’s effective — or that treats their symptoms without causing intolerable side effects. At the same time, other patients with active disease refuse to take the most powerful and effective medications on the market or can’t take them because of their medical history or personal risk factors that would make doing so dangerous.
While many scientists are continuing to explore better drug options, some are focused on developing new treatments that aren’t medications at all. One such experimental approach that’s gaining some traction is called vagus nerve stimulation, which entails using electrical impulses to stimulate the vagus nerve — the longest of the cranial nerves that stem from the brain.
The vagus nerve runs from the brain, through the face and neck, and down into the abdomen. It’s a key part of the autonomic nervous system, the division of your nervous system that controls functions you don’t have to think about, such as breathing, digesting food, and the beating of your heart. The vagus nerve is also the home of the inflammatory reflex, a pathway that appears to be crucial for detecting and modulating inflammation.
When something in your body gets injured or attacked by an invader (like a virus or bacteria), the vagus nerve helps decide how strong of an immune response the body should mount. When that response is appropriate, germs get killed off and injured tissue starts to heal. But when it’s too aggressive for the threat at hand — imagine trying to put out a small candle by holding it under a waterfall — you end up with chronic inflammation, which results in joint and tissue damage.
If you have an autoimmune condition, you already know that your immune system is far more revved up than it should be. In the case of RA, the immune system mistakenly tries to attack healthy tissue in the joints as well as in other organs. No one knows exactly what sets RA in motion, but experts do know that inflammatory substances called cytokines play an important role in causing tissue damage. Those cytokines include tumor necrosis factor (TNF) and interleukins (IL), among others.
Scientists now know that the vagus nerve has the power to reduce the production of them.
Vagus Nerve Stimulation vs. RA Medication: Same Targets, Different Approach
Many people with RA take drugs that target specific cytokines. Biologic medications such as etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade) target the ctytokine TNF, whereas anakinra (Kineret) targets IL-1 and tocilizumab (Actemra) and sarilumab (Kevzara) target IL-6.
But these drugs don’t work for everyone with RA. For these patients, stimulating the vagus nerve seems to be another way to reduce the production of cytokines that cause inflammation.
“The premise is that when you stimulate the vagus nerve it leads to the production of acetylcholine [a neurotransmitter], which binds to receptors on cells that secrete cytokines. When acetylcholine binds to those cytokine-producing cells, it inhibits them from producing TNF and interleukin-6,” says rheumatologist Mark Genovese, MD, a professor of medicine at Stanford University who conducted a pilot study on vagus nerve stimulation that was presented at the 2019 European Congress of Rheumatology (EULAR) conference.
In Genovese’s study, which was published as an abstract in the journal Annals of the Rheumatic Diseases, 14 people with RA who had tried and failed to respond to at least two medications had a small “MicroRegulator” — about the size of a nickel — implanted on the left side of the neck along the vagus nerve.
Although the primary goal of this small trial was to assess the safety of the device, half of patients who had impulses sent to the MicroRegulator once a day had significant improvements in their RA disease activity scores. A decrease in cytokine production was also measured.
A few adverse effects were reported, but all were temporary. Those included pain and swelling at the incision site as well as one patient who had temporary vocal cord paralysis.
Dr. Genovese is now helping SetPoint Medical, the company that is investigating vagus nerve science and sponsored the pilot study, design a much larger, multi-center clinical trial to learn more about whether vagus nerve stimulation can be used to treat RA, especially in people who don’t respond sufficiently to drugs.
Earlier studies, including another small trial that involved RA patients in Europe, similarly found that that implantable vagus nerve stimulator could be used to reduce TNF production and, in turn, inflammation.
While Dr. Genovese and SetPoint Medical are focused on implantable stimulators, other non-invasive approaches in this growing area of bioelectronic medicine are also being explored: One small study, published in the journal Bioelectronic Medicine this year, found that holding up a vibrational device to the ear could be used to stimulate the vagus nerve and inhibit the production of TNF, IL-1, and IL-6.
At the same time, researchers are trying to determine whether it’s possible to predict who is likely to respond well to RA medication and who’s apt to be a non-responder. One way to do that might be by testing vagal nerve tone: Low vagal tone has already been linked to more inflammation and a greater risk of autoimmune conditions.
Although more research is needed, RA patients with low vagal tone may turn out to be good candidates for vagus nerve stimulation. That’s the premise behind a medical device called ANS Neuroscan that’s being developed by Inmedix, says Vibeke Strand, MD, adjunct clinical professor in the division of immunology/rheumatology at Stanford University and a pharmaceutical and biotech consultant for companies including SetPoint Medical and Inmedix.
If ANS Neuroscan gets FDA clearance, rheumatologists might be able to use it as an in-office tool to help determine which patients are most likely to respond to biologics and who might fare better on an emerging therapy such as vagus nerve stimulation. This device provides information about vagal tone by measuring heart rate variability (as do electrocardiograms and a number of apps and gadgets like the Apple Watch).
Dr. Strand also notes that while patients who are found to have low vagal tone might very well benefit from vagus nerve stimulation, electrical impulses aren’t the only way to do it. You might be able to improve your vagal tone on your own by learning some specific breathing techniques or employing other mind-body strategies, though substantial training is likely to be involved.
“There’s a lot of stress associated with having rheumatoid arthritis, or any autoimmune disease, and that’s probably leading to some of the immune system over-activity and the autoimmune response” as modulated by the vagus nerve, says Dr. Strand.
The vagus nerve, she explains, is integral to the mind-body connection. It’s a major route by which messages travel between the brain and the gastrointestinal tract (gut-brain axis), which is why vagus nerve stimulation has also gained attention as a treatment for psychiatric and digestive disorders.
“The autonomic nervous system is part and parcel of our immune response,” says Dr. Strand. “It takes a little time for some people to wrap their heads around that.”
If ongoing and future studies are positive, vagus nerve stimulation might one day become a viable option for RA patients who don’t respond to medication, can’t take it, or don’t want to, says Dr. Strand. Some new research is also examining whether electrical nerve stimulators might be used in conjunction with drug therapies to boost their effectiveness, says Dr. Genovese.
While all this might sound a bit futuristic, vagus nerve stimulators are already on the market — just not yet for RA. Implantable stimulators have been FDA-approved for patients with drug treatment-resistant epilepsy and depression since 1997, and there’s an FDA-cleared non-invasive device aimed at people who get migraine attacks and cluster headaches. In addition to RA, vagus nerve stimulation is being investigated for a wide range of potential applications including inflammatory bowel disease, bipolar disorder, and Alzheimer’s disease.
Will rheumatoid arthritis patients soon be able to make use of a similarly FDA–approved implant or non-invasive device? Stay tuned, as the results of upcoming trials are expected in the near future.
The anti-malarial drug lowers cholesterol and blood sugar makes blood less sticky, which is good for reducing blood clots and heart attack risk.
If you take the anti-malarial drug hydroxychloroquine (Plaquenil) as part of your treatment for lupus or rheumatoid arthritis (RA), you may be getting cardiovascular protection as an added bonus.
That’s welcome news because it’s estimated that about half of lupus patients experience heart complications, and heart attacks occur at younger ages in lupus patients than in the general population. Even as young adults, black and Hispanic women with lupus often have plaque build-up in their arteries that hikes their risk of heart attack. And experts have long known that people with RA are more likely to develop heart disease, even if they don’t show signs of clogged arteries: inflammation from arthritis disease activity is thought to be the link.
Because hydroxychloroquine (HCQ) has been associated with lower levels of cholesterol, blood sugar, and the tendency of blood to clot — all cardiovascular risk factors — researchers looked at the association between HCQ use and the occurrence of heart attacks, strokes, and blood clots (in lungs or deep veins). The results were presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals annual meeting in Atlanta.
Using a health database that covers the entire population of British Columbia in Canada, researchers compared lupus and rheumatoid arthritis patients who had experienced a cardiovascular event with up to three matched patients who did not have a cardiovascular incident. Most of the patients were female (64 percent) and their average age was 74. In total, researchers studied 532 lupus cardiovascular cases and 1,249 controls, as well as 9,736 RA cardiovascular cases and 28,720 controls.
HCQ use was categorized by the most recent date covered by a prescription and divided into those currently using the medication (within last month), those who recently stopped using it (used within 30 to 365 days), those who stopped using HCQ more than a year previously, and those who had never taken it.
After controlling for such other factors as kidney disease and the use of glucocorticoids, disease-modifying anti-rheumatic drugs, and heart disease medication, lupus and RA patients currently using HCQ were 17 percent less likely to have a heart, stroke, or blood clot.
In contrast, those who had discontinued HCQ within the last year were 8 percent more likely to have one of the cardiovascular events.
When people stopped using HCQ more than a year ago, the risk of cardiovascular events was no different than those who had never been prescribed HCQ.
In another hydroxychloroquine study presented at the meeting, Johns Hopkins researchers looked at blood levels of HCQ in lupus patients who developed a blood clot (including heart attacks and clot-caused strokes). They found that patients with the highest levels of HCQ in their bloodstreams were the least likely to have developed a clot.
The researchers cautioned that following the suggestion of the American Academy of Ophthalmologists to reduce HCQ doses in an effort to prevent damage to the retina (which occurs in about one out of 5,000 patients taking HCQ for more than five years, according to Johns Hopkins), may also reduce or eliminate the benefit of HCQ in preventing blood clots.
If you’re taking hydroxychloroquine and are concerned about your dosage and how it may affect your heart disease risk or the odds of vision problems, talk to your rheumatologist and ophthalmologist to understand your risk factors and make the right decision for you.
Screening is important because silent hepatitis B and Cinfections can spring to life when you start biologics or new synthetic DMARDs.
Before you start taking a biologic drug or one of the new targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs), several screening tests are recommended. These include tests to see whether you have hepatitis B or C in your body that isn’t causing symptoms but might be reactivated after you start these powerful immune-suppressing drugs.
But there’s a big gap between what’s recommended and what’s really happening, as a new study reveals that fewer than one in four patients in a national registry received hepatitis screening before starting these medications.
“I think that we all believe that we are doing an excellent job taking care of our patients, but what we found is that there is a gap of care around screening for these infections,” Gabriela Schmajuk, MD, of the University of California, San Francisco, told Healio Rheumatology. Dr. Schmajuk was senior author of the new study, which was presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals Annual Meeting in Atlanta.
The researchers looked at electronic health records from 23,597 patients (average age 57, 72 percent female) being treated at 196 different practices participating in the Rheumatology Informatics System for Effectiveness national registry. Each received their first prescription for a biologic or new synthetic DMARD in 2017, with the majority (63 percent) starting a tumor necrosis factor inhibitor.
Prior to the first prescription, 77 percent were not screened for hepatitis B virus (HBV) and 86 percent were not screened for hepatitis C virus (HCV). Only 6 percent of patients were fully screened for HBV, including both HBV surface antigen and HBV core antibody, prior to their first prescription. Another 17 percent had received one of the tests. Only 14 percent of patients received complete testing for HCV prior to their first prescription.
Of the patients who were fully screened, 83% had screening completed before receiving their first prescription, and a total of 97% had completed screening within 60 days of receiving their prescription.
“We actually looked to see, among the patients who were screened, how many had a positive test, and we found a rate of about 2 to 3 percent, so it is not insignificant,” Dr. Schmajuk told Healio Rheumatology. “If we can prevent one of those people from reactivating, that is going to save all of the money that we spent in screening them.”
Reactivation of HBV may lead to a hepatitis flare, liver failure, and sometimes even death, so patients who screen positive for the virus are often treated with an antiviral medication to prevent reactivation and its complications. HCV reactivation can also lead to hepatitis, but it may not be as severe as that caused by HBV reactivation.
The researchers acknowledge that their data, which can only capture screening entered into electronic health records at the rheumatology practices, could be missing hepatitis screening that was only noted in writing in the patient chart or conducted elsewhere and faxed to the practice, not making it into the electronic record.
Pre-medication screening percentages differed wildly between practices, with 0 percent to 63 percent of patients screened for HBV and 0 percent to 80 percent of patients screened for HCV.
If you’re not sure whether you have been screened for hepatitis B or C and you’re starting a biologic medication make sure you ask your health care provider.
No one knows what causes fibromyalgia but some experts believe that stress may be a common trigger, especially in people who are susceptible to this chronic pain condition for physiological reasons. Now a new study adds support to the theory that psychological stress might increase the risk as well as lead to worse symptoms among those who have fibromyalgia.
Researchers at the Cleveland Clinic enrolled 593 fibromyalgia patients and surveyed them about their symptoms and history of abuse. Nearly 38 percent of fibromyalgia patients said that they had been physically and/or sexually abused at some point.
According to this study, patients who had a history of abuse were also more likely than those who had not been abused to report more severe fibromyalgia symptoms. Patients with a history of abuse had higher pain disability index scores, more generalized weakness, and had visited doctors more frequently.
Those who had been abused were also more apt to be seeing a psychiatrist and to have a drinking problem or a personal history of alcohol abuse.
“Our results suggest that stressors such as abuse have a wide range of detrimental effects on [fibromyalgia,]” the authors concluded. “We recommend that abuse should be inquired about in all patients evaluated for [fibromyalgia] as this may give more clarity to the nature and severity of the [fibromyalgia] presentation and prompt the need for psychological interventions.”
As the temperature increased, so did the risk of rash, joint inflammation, kidney problems, and other lupus symptoms.
Shifts in weather patterns have long been associated with a variety of health ailments, from seasonal allergies to migraine and joint pain. Now a new study suggests that changes in the outdoor environment may make people who have lupus more susceptible to flare-ups of specific symptoms.
The study, presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals Annual Meeting in Atlanta, analyzed data on 1,628 patients with lupus who had checkups between 1999 and 2017 as well as environmental and atmospheric data from the U.S. Environmental Protection Agency. The goal: to determine whether the environmental weather conditions 10 days before a checkup would correlate to changes in patient symptoms.
According to the authors, “there is a strong association between changes in atmospheric and environmental variables 10 days prior to patient visit and organ-specific lupus activity at the visit.”
Although they did not find a connection to systemic flares that impact all organs, they determined that certain environmental factors were strongly linked to flares of specific symptoms: As the temperature increased, so did the risk of rash, joint inflammation, kidney problems, serositis (inflammation of smooth tissue membranes), and hematologic problems such as anemia and low white blood cell count.
Windy conditions were also apt to lead to a spike in hematologic problems, plus an increase in neurological and pulmonary symptoms. Reports of joint inflammation and serositis increased in more humid weather, and an increase in air pollution (fine particulate matter) correlated to an uptick in rash, joint, serositis, and hematologic flares.
Although more research is needed to confirm the results, “these findings are the first step to vindicating the great majority of lupus patients who are convinced that their disease is influenced by weather changes and who inspired this research,” lead study author George Stojan, MD, assistant professor of medicine at Johns Hopkins Lupus Center, said in a press release.
Researchers hope that identifying the link between respiratory issues and RA will result in better ways to prevent or screen for rheumatoid arthritis in people with lung disease.
You may have already heard that people with rheumatoid arthritis (RA) are more likely to develop the serious lung disease chronic obstructive pulmonary disease (COPD), which makes it increasingly difficult to breathe. In 2017, Harvard researchers examined data from the huge Nurses’ Health Study and found that women with RA were about 68 percent more likely to develop COPD.
Now, some of the same research team has combined data on 205,153 participants in two waves of the Nurses’ Health Study and found that the connection also works the other way: After adjusting for age, women with COPD were almost 2.4 times as likely to develop RA and 2.7 times as likely to develop seropositive RA as women without lung disease.
The group also analyzed the risk after adjusting for smoking (a well-known risk factor for both conditions) and a variety of other lifestyle factors. The risk of RA for women with COPD was still increased by 89 percent and the risk of seropositive RA was still more than double, which suggests that the connection between the two disorders is at least partially independent of common lifestyle factors and needs further explanation.
The association of COPD with seropositive RA was most pronounced in the subgroup of women who were over 55 years old and were current or ex-smokers, who had 2.7 times the risk.
While the 2017 study found no increased risk of developing asthma in women who already have RA, the new study (which looked at 196,409 women) did identify a significant (but smaller) increase in the risk of RA among women who already have asthma. Women who reported asthma were 67 percent more likely to develop RA and 51 percent more likely to develop seropositive RA. The percentages were lower but still significant — 53 percent and 42 percent — after adjusting for smoking and other factors.
Just as rheumatologists have been advised to promptly investigate lung symptoms that occur in people with RA, the new study suggests that the possibility of RA should be on the minds of physicians when people with lung disease develop joint pain.
Further study may lead to the identification of overlapping factors that increase the risk of both lung and joint symptoms — perhaps common genes, autoimmune factors, or inflammation itself — and to underlying mechanisms that they may have in common.
In the study abstract, the researchers conclude that “identifying asthma and COPD patients as at-risk populations for RA can help develop prevention and screening strategies as well as provide insight into the role of chronic airway inflammation in RA pathogenesis.”
New data compares what happens when the dosage of DMARDs such as methotrexate is tapered or kept steady.
For most rheumatoid arthritis (RA) patients, sustained remission (inactive disease) is the goal of taking methotrexate or biologic DMARDS to manage their disease. However, what to do after reaching that goal hasn’t been clear. Should RA patients stick with the medication dose that’s working or gradually taper the dose — and thus lessen both the expense of the medication and possible side effects of these powerful RA medications?
Whether or not to taper is usually determined on an individual basis during discussions between individual patients and their doctors, based on shared decision-making around achieving and maintaining remission or low disease activity.
Now, there’s more data to help those discussions. It comes from a trial called ARTIC REWIND (Remission in Rheumatoid Arthritis: Assessing Withrawal of Disease-Modifying Antirheumatic Drugs in a Non-Inferiority Design) that enrolled patients who had been diagnosed with rheumatoid arthritis less than five years earlier and had no swollen joints for at least 12 months while taking a DMARD (about 80 percent on methotrexate). The researchers compared 78 people who were kept on their current DMARD dose with 77 who were moved to a half-dose of the same medication.
In the main finding, over the next 12 months, 6.4 percent of patients on the stable dose and 24.7 percent of patients moved to a half dose experienced a disease flare, defined as a combination of at least two swollen joints, a change in disease activity score, or both patient and physician agreeing that a clinically significant flare had occurred.
In other measures, 79.5 percent of patients continuing the stable DMARD dose had no progression of joint damage on imaging during the year, compared with 62.7 percent in the half-dose arm. Using Disease Activity Scores to define who was still in remission after a year, remission continued in 91.8 percent of patients on a stable dose and 85.1 percent of those moved to a half-dose.
More people (75) who continued on their prior dose experienced a drug side effect during the year, compared with 53 people who were moved to a half-dose. However, serious adverse events were more common in the tapered arm (four patients, including two serious infections) than in the stable-dose arm (two patients).
The researchers, primarily from Norway, concluded that continued DMARD therapy with stable doses led to significantly fewer disease activity flares and less frequent joint damage progression on imaging than tapered DMARD treatment.
The hard data should provide a helpful starting place for patients and rheumatologists to make decisions about tapering, which still need to take into account more subjective factors such as patients’ fears of RA disease progression and patients’ experiences with medication side effects.
