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.
Osteoarthritis is the most common and well-known type of arthritis. It’s largely a wear-and-tear form of arthritis that happens as a result of damage to or overuse of a joint, usually over a long period of time. About 30 million Americans have osteoarthritis. You can also have osteoarthritis at the same time as other kinds of arthritis that are inflammation- or immune-related, such as rheumatoid arthritis, gout, psoriatic arthritis, or ankylosing spondylitis.
In osteoarthritis, the cartilage — the smooth, rubbery connective tissue on the end of bones that cushions the joint, helping bones move smoothly and easily — wears down until the bones are painfully rubbing against each other. This cartilage breakdown also causes the bones in the joint to undergo changes, including the appearance of bone spurs. Bone spurs are bony projections that develop alone the edges of bones in the joints, also knowns as osteophytes. Tendons, ligaments, and muscles are also affected and there can be inflammation in the joint.
“OA isn’t just about the cartilage,” says Lisa A. Mandl, MD, MPH, a rheumatologist at Hospital for Special Surgery in New York City, who specializes in the treatment of rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and osteoarthritis. “It is a disease of the whole joint. The ligaments are weak, the tendons are frayed, the muscles are weak.” This generally happens slowly and worsens over time. Weight-bearing joints like the hips, knees, and spine are most vulnerable to osteoarthritis. Other common spots are the hands, wrists, and shoulders.
Osteoarthritis is often thought to be “less serious” than autoimmune forms of arthritis like rheumatoid arthritis. While that may be the case to a certain extent (the systemic inflammation an autoimmune illness like RA can impact organs and systems throughout your body), OA can take a significant toll on how you feel and function. In fact, according to a new study, published in the journal Arthritis & Rheumatology, the “disease burden” is similar among OA and RA patients at the time of diagnosis; but six months into treatment, RA patients often tend fare better. This may be because RA has many disease-modifying drug options, while OA’s treatments tend to focus more on symptom management.
Many experts believe that anyone who lives long enough will eventually develop some degree of osteoarthritis in some joints. Still, osteoarthritis isn’t caused by any one specific risk factor. Rather, certain risk factors, as outlined below, make you more susceptible to developing osteoarthritis in one or several joints.
Age is the strongest non-modifiable risk factor for OA, says Dr. Mandl. Approximately 14 percent of adults aged 25 and older have symptomatic OA of at least one joint while at least 34 percent of adults aged 65 and older have OA. Worldwide estimates are that 10 percent of men and 18 percent of women aged 60 years old and over have symptomatic OA.
The reason behind this risk for OA increasing with age aren’t fully known. Possible causes could be loss of normal bone structure, overuse of joints over time, and increased stiffness of ligaments and tendons. “It’s just general life experience over time,” says Christopher Collins, MD, an attending rheumatologist and associate program director of the rheumatology division at MedStar Washington Hospital Center and an associate professor of medicine at Georgetown University Medical Center in Washington, D.C. “It’s like a car. After a while, some of the parts start to wear down.”
Sex plays a role in osteoarthritis risk. Yes, both women and men get OA. But it’s more common in men until age 45. After that age, osteoarthritis is more common in women, according to the National Institute on Aging.
The risk of OA by sex also depends on the joints. Knee and hand osteoarthritis are more common in women than men; the frequency of hip OA is the same in women and men, says Dr. Mandl. She says that it’s unknown for sure why this happens. It may be that force hits the knee and body differently in women compared to men. Previously, researchers had thought that it was because men and women experienced stress on the joints at different ages.
Newer research has found a connection between estrogen and joint health. A report in the Journal of Mid-Life Health found that menopause is associated with the onset and progression of OA in women, which may explain why OA affects older women more commonly than older men. Still, Dr. Mandl stresses that this link is unclear and hard to prove.
An injury related to playing sports, a fall, a vehicle accident, or other physical trauma can cause OA in adults of any age. Sports-related knee trauma, such as a strain or tear of the ACL (anterior cruciate ligament), has been linked to an increased risk of developing knee OA, research shows. In fact, Dr. Mandl says that half of people who have ruptured their ACL will have severe OA within a decade. In fact, any kind of surgery to the knee increases the risk of OA down the road, she says. Even joint-related injuries that happened years ago and seemingly healed can increase your risk of developing osteoarthritis. Common injuries that can lead to OA include torn cartilage, dislocated joints, and ligament injuries.
The onset of osteoarthritis can also be linked to a repetitive activity that damages the joints like operating a jackhammer with your hands or sitting on your knees while laying bricks, says Mark C. Genovese, MD, the James W. Raitt professor of medicine and director of the rheumatology clinic in the division of immunology and rheumatology at Stanford University Medical Center in Palo Alto, California.
Your weight is the biggest modifiable risk factor for developing osteoarthritis, says Dr. Mandl. Excess weight places additional stress on weight-bearing joints, especially your knees and hips, she says. A report in Obesity Reviews found that losing 10 pounds can help manage OA and lead to improvement in symptoms, pain, function, and quality of life.
“Even losing five pounds can make a difference,” says Dr. Mandl. “The heavier you are, the more likely you are to develop knee OA and for it to progress and become more severe. It’s never too late to lose weight.” Fat tissue also produces proteins that can cause harmful inflammation in and around your joints. Being overweight also can speed the progression of the disease on weight-bearing joints like knees, feet, and lower back, says Dr. Genovese.
People who do certain activities for hours may be more likely to develop stiffness and joint pain. Activities include repetitive bending, kneeling, and squatting. Joints commonly affected by this include the hands, knees, and hips. The mechanism for the association remains unclear, though joint loading (force on a wearing-bearing joint during activity) and repetitive damage may be a factor. A paper in the journal Best Practice & Research in Clinical Rheumatology found — not surprisingly — that doing heavy manual work is a risk factor of osteoarthritis. Researchers from the United Kingdom found that those with the highest risk have worked in agriculture and farming for 10 or more years.
OA tends to run in families, especially if you have genetic joint defects. You’re more likely to have osteoarthritis symptoms if your parents, grandparents, or siblings have the condition. Researchers don’t know why OA runs in families. While genetics are a risk factor, no one gene has been identified as causing the condition. “We believe that there is a large genetic component with the development of OA,” says Dr. Genovese. “But there is not a single gene association the way you might see with other diseases.”
Though they’re not common, medical conditions that involve bleeding near a joint can cause osteoarthritis to worsen or new symptoms to develop. If you have hemophilia (where blood doesn’t clot normally) or avascular necrosis (the death of bone tissue due to a lack of blood supply), you may have symptoms associated with OA. “Blood is irritating and really destructive to the joint,” says Dr. Mandl.
If you have other forms of arthritis, such as gout or rheumatoid arthritis, you’re more at risk for developing osteoarthritis too. RA is an autoimmune disease in which your immune system mistakenly attacks the joints. This triggers inflammation that thickens the synovial tissue lining the inside of the joint, causing swelling and pain in around the joints. Gout is a painful and acute onset of arthritis caused by the buildup of uric acid (a normal waste product in your body) in the blood. When uric acid is elevated in the blood, it can accumulate in your joints and trigger an inflammatory response that causes severe pain and swelling.
People born with certain diseases or health problems are more likely to develop OA. Examples include increased joint laxity (being double-jointed), some dysplasias (abnormal growths of bone and cartilage), and Paget’s disease (a type of bone inflammation).
Other conditions that can lead to OA include peripheralneuropathies (nervous system disease) and neuromuscular disorders that put abnormal stress on the joint. Certain metabolic diseases like diabetes and hemochromatosis (where your body has too much iron) make you prone to OA as well as bone deformities like those born with malformed joints or defective cartilage.
If you suspect your joint pain or other symptoms could be OA, and you have some osteoarthritis risk factors (or even if you don’t), see your primary health care provider. You may need a referral to a specialist such as a rheumatologist or orthopedist for further testing and treatment.
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.
Knowing there could be a lag between objective measures of improvement and patient–reported outcomes could help prevent over-treatment.
When a rheumatologist measures disease activity in a patient with rheumatoid arthritis (RA), objective clinical measures like C-reactive protein levels in the blood and swollen joint count are essential to factor in, but so are patient-reported measures including pain and fatigue. While both are certainly important, there may be some benefit to evaluating clinical factors and patient-reported measures independently rather than combining both into a composite disease activity score.
(You can use our ArthritisPower app to track your symptoms and disease activity and share your results with your doctor.)
According to a new study, presented at the 2019 American College of Rheumatology/Association of Rheumatology Health Professionals Annual Meeting in Atlanta, there may be some lag time between when objective tests show that patients are getting better and when patients actually start to feel better.
The researchers, led by Janet Pope, MD, MPH, at Western University in Ontario, analyzed data on 986 patients. They found that the time it took for to reach remission or low disease activity varied widely depending on whether or not patient-reported factors were used as the goalpost.
When the Clinical Disease Activity Index (CDAI), which relies on solely clinical measures, was used, it took patients an average of 12.4 months to reach low disease activity. Yet it took the same group of patients getting the same exact treatment nearly 19 months to reach low disease activity when it was defined by patient global assessment of disease activity (PtGA).
Knowing that this lag time of several months exists is important, because it suggests that health care providers shouldn’t necessarily rush to change up a patient’s treatment regimen if clinical scores are good; waiting it out a few months to see if pain and inflammation improve might be a better option.
“Careful interpretation of [patient-reported outcomes] and composite scores could impact management, including prevention of overtreatment and unnecessary switching of DMARDs,” the authors concluded.
Although biologics cross the placenta, research shows they lead to few infections in babies after they’re born.
The prospect of pregnancy can be daunting for women with inflammatory arthritis. Not only can disease flares occur, but a host of medications — including the commonly prescribed methotrexate — are off-limits because of concerns about birth defects and complications. There’s also a worrisome information gap on the effects of many medications during pregnancy, since pregnant women are usually excluded from clinical trials.
One type of medication, tumor necrosis factor inhibitors (TNF inhibitors), is increasingly used during pregnancy after animal studies did not show a risk to the developing fetus. But that left open the question of whether the drugs, as they suppress the immune system in expectant moms in order to manage their disease, might also lessen immune response in their newborns, leaving babies more vulnerable to infection after they’re born.
Last year, researchers at McGill University in Canada used a large health database in the United States to address that question for women with rheumatoid arthritis (RA). They found that that there was no excess risk for babies exposed to anti-TNF biologics compared to offspring of women with RA who didn’t take these drugs and to women without RA.
This year, the group is back with a similar analysis of serious infections in babies exposed to non-TNFi biologics, such as abatacept (Orencia), rituximab (Rituxan), tocilizumab (Actemra), ustekinumab (Stelara), and vedolizumab (ENTYVIO). Like TNFis, non-TNFi biologics can cross the placenta, leading to medication exposure than can equal or surpass that of the expectant woman. They also evaluated tofacitinib (Xeljanz), a small-molecule drug that may also cross the placenta (although that has not been confirmed).
“Our project innovates by using the largest cohort of pregnant women with chronic inflammatory diseases ever assembled to address drug safety in pregnant women, who are regularly excluded from clinical trials,” lead author Evelyne Vinet, MD, PhD, told the American College of Rheumatology in a press release.
The investigators tallied infections that occurred in 16,490 babies before their first birthdays that were serious enough to require hospitalization. All of their mothers had been diagnosed with an inflammatory disease, such as rheumatoid arthritis, ankylosing spondylitis, psoriasis, psoriatic arthritis, or inflammatory bowel disease. During pregnancy, 105 of the mothers took tofacitinib or non-TNFi biologics and 1,611 took TNFis. Infections in those children were compared to those in 164,553 babies born to unaffected mothers matched for age, year of delivery, and state of residence.
The researchers found just two cases of serious infections in exposed children, one whose mother received tofacitinib and one whose mother received abatacept. Overall, the proportion of serious infections in offspring of mothers with inflammatory disease was: 1.9% in those exposed to tofacitinib or non-TNFi biologics; 2.3% in those exposed to TNFis; and 2.1% of those exposed to neither type of drug. In comparison, the percent of serious infections in children born to unaffected mothers was 1.6%.
“Our data will help guide counseling and management of pregnant women with inflammatory arthritis that require non-TNFi biologics and tofacitinib during pregnancy,” says Dr. Vinet. Still, she considers this analysis to be just the first step in understanding the effect of these drugs during pregnancy.
“We need more data to confirm safety, particularly regarding other pregnancy outcomes. It is imperative that we further study this issue to provide firm evidence to guide treatment decisions prior to conception and throughout pregnancy,” she says.
Surprisingly, stronger opioids were the worst at relieving pain in a new multi-study analysis.
Despite concerns about safety and addiction, lots of people with osteoarthritis (OA) take opioids to address their chronic pain. A recent study in Sweden, for example, revealed that one in four patients with OA had been prescribed an opioid in the previous year — despite the fact that the drugs aren’t on the list of recommended treatments except in extreme circumstances or after surgery.
Opioid medications work by attaching to opioid receptors in the brain and spinal cord and reducing the pain messages that are sent to the brain.
With lots of people with many different kinds of chronic pain, including various forms of arthritis, taking the powerful drugs, researchers at Tufts Medical Center in Boston stepped back to ask whether opioids actually work to relieve pain and improve life for people with OA.
Their results, based on an analysis of 11,402 participants across 23 randomized controlled trials, were presented at the 2019 American College of Rheumatology/Association of Rheumatology Health Professionals Annual Meeting in Atlanta.
In all of the studies included in the analysis, opioids were compared against a placebo. Here’s what the authors found:
“’Strong opioids’ underperformance was the study’s most interesting finding, and likely due to the relationship between pain relief and tolerability of opioids based on dose,” study lead author Raveendhara R. Bannuru, MD, PhD, told the American College of Rheumatology in a press release.
In the studies, twice as many people taking strong opioids (such as morphine, oxycodone, fentanyl, and high doses of tramadol) dropped out because of side effects than those who took weak opioids (such as codeine, dihydrocodeine, and lower doses of tramadol).
“In light of this evidence, clinicians and policymakers should reconsider the utility of strong opioids in the management of OA,” says Dr. Bannuru.
The less-than-impressive results are consistent with the latest guidelines from the Osteoarthritis Research Society International (OSRI), which strongly recommends against using opioids in OA involving the knees, hips, or multiple joints.
Female patients were much more likely to have a dual diagnosis.
Small studies have suggested an overlap between spondyloarthritis (SpA) and fibromyalgia, but now a larger meta-analysis confirms it: About 17 percent of SpA patients also have fibromyalgia, compared to 2 to 8 percent of the general population that has fibromyalgia.
These findings, which were based on an analysis of 15 earlier observational trials, were presented at the 2019 American College of Rheumatology/Association of Rheumatology Professionals (ACR/ARP) Annual Meeting in Atlanta.
The researchers determined that females with SpA were significantly more likely than men to have the dual diagnosis of fibromyalgia. They also found that people who live with both conditions are more apt to have higher levels of SpA disease activity. Whether that’s a coincidence or related to the underlying pathology of these conditions is unclear.
SpA is an umbrella term for a few types of inflammatory arthritis. Axial spondyloarthritis is the most common kind of SpA. It includes two general subgroups: ankylosing spondylitis, which is when there is damage to the spine or sacroiliac joints that is visible on X-rays, and non-radiographic axial spondyloarthritis, which is when there is inflammation but no damage you can see on X-rays. Peripheral spondyloarthritis, reactive arthritis, psoriatic arthritis, and enteropathic arthritis (associated with inflammatory bowel disease) are also types of SpA.
People with SpA often need to take disease-modifying antirheumatic drugs (DMARDs) and/or biologic drugs to slow or stop the progression of the disease.
According to the American College of Rheumatology, fibromyalgia is not a form of arthritis but rather a neurological condition that causes widespread pain and fatigue. Fibromyalgia is often treated with over-the-counter pain relievers as well as certain antidepressants and anti-seizure drugs that have been shown to reduce fibromyalgia symptoms.
In addition to occurring in patients at the same time, it’s also possible that spondyloarthritis can be mistaken for fibromyalgia and therefore not properly diagnosed.
And a few factors seemed to be responsible, including being obese and also having fibromyalgia.
When most people think about rheumatoid arthritis (RA), they focus on joint pain, swelling, and stiffness. While those issues are certainly common, they tend to co-exist with another symptom — overwhelming fatigue — that can be harder for friends and family to understand.
Fatigue is more than being a little tired. Earlier this year, a Chronicwoman/Chronicillness poll found that 89 percent of people with arthritis (including but not limited to RA) said that fatigue interfered with their ability to go about their everyday activities. An important question for treating RA, then, is this: Does severe fatigue resolve when patients receive proper RA treatment?
Fortunately, a new study says yes: 70 percent of newly diagnosed patients who initially presented with high levels of fatigue “reported significant improvements in fatigue” within a year.
These findings, which were presented at the 2019 American College of Rheumatology/Association of Rheumatology Health Professionals Annual Meeting in Atlanta, focused on more than 1,000 Canadian patients who had been recently diagnosed with RA and started on a disease-modifying antirheumatic drug (DMARD), such as methotrexate or sulfasalazine. They suggest that treating RA with these drugs also leads to less fatigue, though whether the medication is directly responsible is unclear. It’s equally likely that patients become more energized as a result of their joint pain and stiffness improving.
Although this is mostly good news, the researchers, led by Susan J. Barlett, PhD, from McGill University in Montreal, found that a substantial portion of participants — 30 percent — did not experience a major improvement in their level of fatigue. Those in this camp were typically more likely to be obese or have fibromyalgia in addition to RA. Some had simply reported less fatigue to begin with, so there was less room for improvement.
“Debilitating fatigue is common around the time of RA diagnosis and is associated with more active disease, worse pain and disability, and [osteoarthritis]/back pain, obesity, depression, poor sleep, and major stressors in the previous year,” the authors wrote. “Early [methotrexate] use and optimizing weight, sleep, and mood may help address persistent fatigue when RA inflammation is well controlled.”
