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Expert Perspective on the Management of Psoriatic Arthritis

Rheumatoid Arthritis Quiz

Learn more about the latest developments in rheumatoid arthritis

Focus on Rheumatoid Arthritis

Lana Dykes is the Editor of Rheumatology Network. She is an experienced editor and technical writer with a demonstrated history of working in the banking and publishing industries. She enjoys cooking, yoga, and drawing. 

Rheumatology Network interviewed Janet Pope, MD, MPH, to delve into her recent Congress of Clinical Rheumatology (CCR) East presentations, “Treatment Strategies for the Unresponsive Patient with Rheumatoid Arthritis” and “2021 Year in Review: Clinical Pearls.” Pope is Professor of Medicine and Division Head of Rheumatology at Western University in London, Canada.

What are some of the treatment strategies that you suggest for patients with rheumatoid arthritis (RA) who are unresponsive to their current medication?

In rheumatoid arthritis, roughly 1/6 to 1/3 of patients are considered difficult to treat. This could mean that the drugs stopped working, never worked, the patient does not tolerate them, or there's contraindications to them. So, in this pool of patients, which isn't too uncommon, we go through an algorithm based on guidelines. The American College of Rheumatology (ACR), for instance, has guidelines. And basically, we try to continue to treat the patient to get them into remission or low disease activity, because that gives better quality of life and less joint damage down the road. The algorithms we tend to use are our conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) like methotrexate, and in Canada, we use other csDMARDs and combine them. In the US, it would often be adding a different drug, such as a biologic disease-modifying antirheumatic drug (bDMARD) like a tumor necrosis factor (TNF) inhibitor, or possibly an oral JAK inhibitor.

After that, we really don't know what to do next. We usually go out of class to something else, but we don't know, in any one patient, what will be their home run drug. And even if we find a home run drug, it might not last forever. So that's sort of the dilemma in these difficult-to-treat patients. It is evidence based, but we also fly by the seat of our pants.

I asked rheumatologists at the CCR what they would do next. The options were split and there was no consensus, and they were all right answers potentially. We need research that will help us to define what will be the next best treatment. In rheumatology, for RA treatment, we have lots of options. But as I say, we don't know what one will be the best for benefit and tolerability and for the longest amount of time. By the data, it’s probably better to go out of the TNF class to something else to get a deeper and longer response on the average patient.

The other thing is to not give up trying work with your patient and trying to see what's driving the difficulty. Are they not taking it because they don't tolerate it? Can they afford it? Are they afraid because their friend told them there might be issues with the drug? We also must look at the reasons why someone might be difficult-to-treat that isn't necessarily related to the drug but related to taking the drug and the fear or the access tissues.

Your second presentation focuses on the clinical pearls from the last year. What are some of your favorite developments that you discussed?

One thing that's really interesting is there are a lot of trials that have gone on with gout involving treating to a target and what we know about gout. For example, common risk factors of crystal arthritis are age, poor kidneys, alcohol, and diuretics. It's very common that people living with gout, if we target the uric acids to try to lower it, you don't have to target it too low. You get no added benefit coupled with more potential drug changes and side effects. So, targeting to a normal level is good enough.

We also know that uric acid itself is a risk factor for heart attack. It’s independent risk factor for coronary artery disease. They've looked at studies on treating asymptomatic uric acid, which have yielded mixed results; some indicate it decreases cardiovascular risk, but some don’t.

There were also a lot of trials last year in osteoarthritis where drugs or injections weren't successful. Some drugs that might be disease-modifying have, in the long run, not proven to be of any greater benefit than our standard of care and have potential neuropathy or nerve toxicity side effects. So, they're not going to be developed further, as far as I can tell, unfortunately.

There's also a lot of news about injecting platelet-rich plasma, stem cells, and other expensive products into joints. And, in general, the benefit is not there when you compare it to a standard of care in randomized controlled trials. I'm not saying that in all cases it's non-beneficial, but in general, platelet-rich plasma is not going to help your knee osteoarthritis. It might help elbow tendonitis, but that's not as common as knee osteoarthritis.

Some of it has to do with trial design, but when new results come out, we're enthusiastic and then over time, we have to ask ourselves if these products are actually going to be effective for our patients or not.

Articles

Janet Pope, MD, MPH, explains her treatment strategies for unresponsive patients with rheumatoid arthritis as well as clinical pearls of 2021. 

Janet Pope, MD, MPH: Treating Unresponsive Rheumatoid Arthritis

Rheumatology Network interviewed Julie J Paik, MD, MHS, to discuss her Congress of Clinical Rheumatology (CCR) East presentations “Clinicoserological Spectrum of Inflammatory Myopathy in the Context of Systemic Rheumatic Diseases” and “Can Autoantibody Profiles Predict Myositis Phenotype and Disease Course?” Paik is Assistant Professor of Medicine and Director of Clinical Trials at Johns Hopkins Myositis Center, Division of Rheumatology.

Can you give me some of the key takeaways of your spectrum of inflammatory myopathy in rheumatology presentation?

I highlighted key pearls about how to classify different subgroups of myositis, which then enables clinical providers to better subset these diseases. Sometimes, when someone comes in with weakness, you're thinking about a lot of differential diagnoses. But when you divide up the different types of myositis into distinct subgroups, it's better to have a plan of attack in terms of treatment and diagnosis So, I went over the key subgroups: dermatomyositis, polymyositis, immune-mediated necrotizing myopathy, and inclusion body myositis.

Then within each subgroup, I embedded in cases and went through how to approach the diagnosis. What are some of the key clinical features we should be aware of? What is the treatment algorithm for each subgroup? How do I treat this patient? And then I added in a layer of the emerging treatments and promising clinical trials in each subgroup. I also mentioned a clinical trial in immune-mediated necrotizing myopathy. There are, unfortunately, no clinical trials in inclusion body myositis where there's any data that can be read as positive results. Inclusion body myositis is difficult because there's no like treatment for it. I talk largely about dermatomyositis because there are a lot of a lot of pipelined clinical trials and drugs that are in development right now.

Can you speak a little bit more about some of those pipeline trials that you discussed?

It’s an exciting time for dermatomyositis because we have the first FDA-approved drug for dermatomyositis ever that is efficacious, which is intravenous immunoglobulin, as of July 2021. It should be easier for rheumatologists to prescribe it now because there's an FDA indication.

Another promising pipeline drug and promising treatment that I discussed was a phase 2/3 clinical trial of ravulizumab. It's a C5 inhibitor, a complement inhibitor, and the trial is about to start very soon. It's a multicenter, international trial of a complement inhibitor in adult dermatomyositis patients.

I was the principal investigator on a proof-of-concept study of a JAK inhibitor in refractory dermatomyositis or tofacitinib. There are ongoing phase 2 studies internationally looking at a JAK inhibitor in dermatomyositis based on some of the work that we've done that showed a very good response of JAK inhibitors in dermatomyositis.

How can autoantibody profiles predict myositis phenotype and its disease course?

It’s easier to look at these autoantibody associations by looking at those subgroups that I highlighted in my first talk. I went into the classic autoantibody associations we see in dermatomyositis and some of those updates regarding those phenotypic associations. First and foremost, one of the key pearls is that autoantibodies are helpful in diagnosis and prognosis. There are studies to show that these autoantibodies may even better predict someone's phenotype than a muscle biopsy. And so that's the reason why we order them. But specifically, in looking at dermatomyositis, I talked about some of the phenotypes. For example, anti-melanoma differentiation-associated gene 5 (MDA5) is associated with these “kissing papules” on the hands. The beauty of dermatomyositis is that I can tell the patient exactly what they have just by looking for these kissing papules or ulcers on the hands. And they also tend to have more rapidly progressive interstitial lung disease.

There’s also so much data and literature showing that link of cancer and transcription intermediary factor 1-gamma (TIF1-γ), which is a specific autoantibody associated with the dermatomyositis in the US cohorts, as well as in Asia and Europe. I made it a point that TIF1-γ is one of the most common autoantibodies. Not everyone who has TIF1-γ is going to have a cancer. But as a provider, you’re thinking about it in the context of someone not responding, like in refractory dermatomyositis. You really want to take a step back and analyze if they are not responding because they don’t have enough treatment or if there is a proven cancer, a cell malignancy, that's driving the disease process.

Is there anything else that you'd like our audience know before we wrap up?

One thing I did a highlight a lot throughout is that it's important that rheumatologists, or any providers treating myositis, aggressively treat patients early on so that they do not accumulate damage in their muscles because it's irreversible.

Julie J Paik, MD, MHS, discusses the clinicoserological spectrum of inflammatory myopathy in the context of rheumatic diseases and how autoantibody profiles can help predict myositis phenotype and disease course. 

Julie J Paik, MD, MHS: Inflammatory Myopathy in Systemic Rheumatic Diseases

Ingrid Torjesen is a UK-based freelance health journalist with more than 30 years of experience in health and medical communications. She works for numerous publications including Rheumatology Network, the BMJ and the Economist’s Intelligence Unit. Before her freelance career, her staff jobs included news editor of both Pulse and GP (the two leading UK weekly titles for primary care doctors), and opinion and features editor of the Health Service Journal (the UK’s leading health policy title). She also spent a few years working in Australia, including on Australian Doctor.

Usual interstitial pneumonia (UIP) pattern

Low rheumatoid factor immunoglobulin A (RF-IgA)

High-resolution computed tomography (HRCT) scores showing pulmonary impairment at baseline

Many rheumatoid arthritis (RA) patients experience lung manifestations such as interstitial lung disease, but what are the implications and who is most at risk?  Test your knowledge with this quiz.

Rheumatoid Arthritis Quiz: Interstitial Lung Disease

Rheumatology Network interviewed Leonard Calabrese, DO, to discuss his Congress of Clinical Rheumatology (CCR) East Conference presentations “Interferon History Immunology and Beyond,” “Immunology for the Rheumatology Provider Adjourns,” and “COVID Immunology and the Rheumatologist COVID-19: Autoimmune & Inflammatory Manifestations.” Calabrese is Professor of Medicine at the Cleveland Clinic.

Why is it important for rheumatologists to take immunology into account when treating their patients?

Rheumatologists, by definition, are clinical immunologists, which means that that is anyone who applies the principles of basic, translational, and clinical immunology to patient care. We do that every day in virtually almost all our patients. So, it's very important. And given how dynamic this field is, it's challenging to keep up, particularly if you're not doing work in research in this area or are associated with an academic center where it's constantly being discussed. So, we take this as an opportunity.

What is the history of utilizing interferons in rheumatology?

The history of interferon in rheumatology goes back a long way from their discovery in the mid 60s and the struggle to purify these compounds. It took almost 20 years to make these initial observations that interferon, particularly type 1 interferon, were present in excessive amounts in certain immune-mediated diseases, such as lupus, juvenile rheumatoid, and Sjogren’s. And over the ensuing 40 years, the field now has developed robustly to recognizing it's not only a biomarker but probably driving immunopathogenesis, in particular in lupus, and possibly in other diseases. It's been a long road.

What do you believe the future holds for interferons in this field?

I think that the centrality of interferon and driving a number of these diseases, in particular certain end organ manifestations, is very promising. We're also finding that this interferon signature is present in diseases outside of the centrality of rheumatology, and particularly the devastating syndrome of long COVID-19, where 8 months after recovery people who are persistently symptomatic develop regulations of multiple types of interferon, could be a treatable target.

Speaking of COVID, how does COVID-19 affect immunology in patients with rheumatic disease?

It's a complicated question. I think at first, patients with rheumatic diseases, by and large, respond somewhat similar to healthy patients when you control for comorbidities. So, if you're not on any therapy, and your diseases is inactive even though you have baseline rheumatoid arthritis, or mild lupus, or other conditions, and you don't have diabetes, obesity, or other traditional risk factors, patients do fairly comparably. But since our patients often have end organ damage, kidney damage, lung damage, etc, they are more frequently vulnerable to the sequelae of COVID-19. And finally, the biggest issue for our patients is therapy. The therapies that we use are immunosuppressive or immunomodulatory. We're now learning that not all these therapies are equal. As a matter of fact, they're not even close to being equal. Certain patients are highly immunocompromised, and others are not.

What are some of the inflammatory and autoimmune manifestations that you discussed in your presentation?

On one level, COVID-19 itself is an immunologically driven viral illness. So, the mere natural history of COVID-19 is immune-mediated. Most patients get over COVID with what we call phase 1 and phase 2. They acquire the virus and trigger an innate immune response. In the second week, you make some antibodies and cell-mediated immunity and you're better. However, a small population progressed to this hyper-inflammatory phase 3, which is characterized by elevated cytokines, acute phase reactants, clotting, and activation. That is a devastating sequela. For patients with rheumatic disease, there are also other questions. Can COVID activate their underlying rheumatic disease? We’re just starting to learn that it can occur. Most of the time, it does not, and usually it's modest. But can it manifest new autoimmune manifestations? Again, it’s a work in progress because there's compelling evidence that COVID-19 drives autoimmunity, even in healthy people. What that's doing to them right now is not totally clear.

In your opinion, what are some of the biggest challenges that are facing rheumatologists and immunologists today?

Rheumatologists, in particular, are challenged to keep pace with both their declarative knowledge about immunology. The field is like tsunami in terms of developments. What you learned in medical school and training is out of date if you've been out of school for more than a couple of years. And if you are keeping pace with declarative knowledge, you need to know the procedural knowledge of how to use it. What is the state-of-the-art in terms of diagnostics and biomarkers? How should we be using our targeted therapies? The landscape changes constantly and diseases, like COVID 19, have challenged all of us. This is a disease that 2 years ago didn't exist and now affects our patients. We need to master yet another disorder that is immunologically driven.

Is there anything else that you would like our audience to know before we wrap up?

The last thing I'd like to remind rheumatologists is that we are part of the next phase of the epidemic, which will be the continued exposure and vulnerability of our patients to endemic SARS-CoV-2 infection, and we need to be forthrightly involved in managing COVID-19 in the immunocompromised. That means educating our patients, educating ourselves, knowing where the care pathways are, and how to access antivirals and monoclonal antibodies in keeping our patients from severe sequelae of COVID-19. That's going to be an ongoing challenge and I hope everyone is buying into that.

Videos

Leonard Calabrese, DO, explains the history of interferon history in rheumatology, immunology for the rheumatologist, and COVID-19 immunology regarding autoimmune and inflammatory manifestations. 

Leonard Calabrese, DO: Immunology for the Rheumatologist 

Rheumatology Network interviewed Arthur Kavanaugh, MD, to discuss his recent Congress of Clinical Rheumatology (CCR) East presentations “The Immunopathogenesis of Psoriatic Arthritis and Immunologically Targeted Therapy” and “Hot Topics in Rheumatoid Arthritis.” Kavanaugh is Professor of Medicine and Director of the Center for Innovative Therapy at UC San Diego.

What are some of the hot topics in rheumatoid arthritis that you discussed at the CCR conference?

There are so many hot topics, but I really focused on the early disease and treatment of early diseases, even including pre-diagnosis of rheumatoid arthritis, and reviewed some of the data for that. I talked a little bit about the newer therapies and newer information on some of the older therapies, including discussing corticosteroids and touching on the optimization for non-steroidal anti-inflammatory drugs. I talked a little bit about the treatment paradigms and need for personalized medicine, which we don't have because we didn't really know which medicine to use and in which order for any individual patient, which is a little bit disappointing, but something that there's been a lot of research looking at. And finally, a lot of discussion about the safety and recent data with the ORAL surveillance study and putting the information from that in clinical context for the practicing rheumatologist.

What are some of the newer therapies in rheumatoid arthritis treatment that you discussed?

 The newer ones are the JAK inhibitors. They're the latest to enter the file of therapies that we have available to us for rheumatoid arthritis. We now have tofacitinib, which we've had for a while, and baricitinib, which we’ve have for some years, and upadacitinib is the most recent edition.

What are some of the key takeaways for rheumatologists?

It’s still interesting treating early rheumatoid arthritis or even pre-rheumatoid arthritis, but it's challenging because not all the patients meet the suspicion. They have clinically suspected arthralgia, but not all will develop rheumatoid arthritis. That raises issues about the how best to approach a treatment, including from an ethical standpoint, because we're trying not to over-treat patients.

Another take home point is that there is still an unmet need to figure out which therapy is going to be best for which patient both in terms of effectiveness and also in safety and tolerability. And finally, safety issues. Initially, they’re kind of scary and certainly safeties are important. But it's also important to be able to put it into context so that we can have discussions with our patients about the relative magnitude of the risk and the characteristics that may make people more or less likely to suffer some of the adverse events that we're talking about.

What are some of the challenges facing rheumatologists today?

There are not enough rheumatologists. We have a manpower issue. The prevalence of rheumatic diseases is increasing and we don't have enough fellows, which means we don't have enough young rheumatologists to even replace those who are going to leave the profession by retiring. While it's great to be busy, it's perhaps not so great to not have enough rheumatologists available.

What are the key takeaways from your immunopathogenesis of psoriatic arthritis presentation?

There is more understanding of the different components of the dysregulated immune system and the inflammatory response that seems very relevant in psoriatic arthritis. We've learned more from basic outcomes research in terms of imaging and biomarkers. We've also learned a lot from the results of studies of highly targeted therapies that have given us answers about which domains of psoriatic arthritis may respond as to what specific mechanisms of action. Domains such as skin psoriasis, nail psoriasis, enthesitis, dactylitis, as well as the affiliated conditions like anterior uveitis and also inflammatory bowel disease.

How can this targeted therapy treatment method help both patients and rheumatologists?

Patients want to feel better and they want to feel better across all aspects of their condition. The rheumatologist wants to help them get there and they want to find the therapy that works best for them and is the best for them.

Arthur Kavanaugh, MD, discusses his recent CCR East presentations “The Immunopathogenesis of Psoriatic Arthritis and Immunologically Targeted Therapy” and “Hot Topics in Rheumatoid Arthritis.” 

Arthur Kavanaugh, MD: Hot Topics in Rheumatoid Arthritis and Psoriatic Arthritis 

Healthy Lifestyle Modifications May Lower Risk of Genetically Induced Gout

While genetics are linked to gout diagnosis and lifestyle factors are related to risk, the association between healthy choices and risk mitigation remained unclear.

Rheumatoid Arthritis Quiz: RA and Cardiovascular Risk

Rheumatoid arthritis is known risk factor for cardiovascular disease, but how much do you know about the association? Test your knowledge with this quiz.

From Living BLISSfully to BEATing Lupus: Future Considerations for Biologic Therapy in SLE

After years of frustration and failure, trials of targeted biologic therapy in systemic lupus erythematosus are beginning to show success. New drugs, including anifrolumab (Saphnelo) and belimumab (Benlysta), are paving the way for an exciting new era. However, this raises new questions as to how these novel therapeutics will be incorporated into future clinical practice.

Long-term Data Suggests Deucravacitinib Safe, Effective for Treating Plaque Psoriasis

Data from the POETYK PSO long-term extension (LTE) trial showed deucravacitinib was clinically effective and safe for treating adult patients with moderate-to-severe plaque psoriasis.

Ustekinumab, TNFi Show Similar Persistence at 1 Year in Real-World PsA Study

One-year results from the PsABio study provide evidence on factors that may impact treatment selection and decisions in clinical practice.

Take 5 minutes to catch up on Rheumatology Network's highlights from the week ending May 14, 2022.

Rheumatology Network's Top 5: May 14, 2022

New safety data from the POETYK PSO long-term extension (LTE) trial showed deucravacitinib, an oral, selective allosteric tyrosine kinase 2 (TYK2) inhibitor, was clinically effective and safe for treating adult patients with moderate-to-severe plaque psoriasis, according to 

. Efficacy was maintained for up to 2 years, with 77.7% of patients achieving Psoriasis Area and Severity Index (PASI) 75 by week 60 and 58.7% achieving the static Physicians Global Assessment (sPGA) response rate of 0/1 (clear/almost clear skin).

Spanning 2482 patient years, results are consistent with previous phase 3, multicenter, randomized, double-blind POETYK PSO-1 (

) trials, which evaluated the safety and efficacy of deucravacitinib compared with apremilast and placebo for the treatment of moderate-to-severe plaque psoriasis. Common adverse events (AEs) reported, of which most were mild to moderate in severity, were headache, upper respiratory tract infection, and nasopharyngitis. Rates of serious AEs remained low during the 2-year LTE trial. The drug did not increase a patient’s risk of developing COVID-19 nor did it impact the severity of COVID-19 infection. No clinically meaningful changes from baseline were observed in laboratory values.

The drug represents a new class of small molecules and is the first and only TYK2 inhibitor being studied across multiple immune-mediated diseases, including psoriasis, psoriatic arthritis, lupus, and inflammatory bowel diseases. Deucravacitinib selectively inhibits TYK2, but does not interfere with JAK1, JAK2, or JAK3. It is currently under review with the US Food and Drug Administration (FDA), European Medical Association (EMA), and Japan’s Ministry of Health, Labor, and Welfare for the treatment of moderate-to-severe plaque psoriasis.

“Plaque psoriasis is a chronic, systemic immune-mediated disease associated with multiple serious comorbidities, and there remains a strong unmet need for new treatments, particularly oral medicines, as many patients are undertreated or are dissatisfied with current options,” stated Richard B Warren, Professor at The University of Manchester. “Long-term research showing durable efficacy, in addition to a well understood safety profile, is critical for clinicians and patients making treatment decisions, and these new two-year data underscore the potential of deucravacitinib to be an important new oral treatment option for people living with moderate to severe plaque psoriasis who require systemic therapy.”

Data from the POETYK PSO long-term extension (LTE) trial showed deucravacitinib was clinically effective and safe for treating adult patients with moderate-to-severe plaque psoriasis. 

Long-term Data Suggests Deucravacitinib Safe, Effective for Treating Plaque Psoriasis 

Rheumatology Network interviewed Anne Winkler, MD, to discuss her upcoming CCR East presentation, “Targeting Lupus Nephritis.” Winkler is an independent rheumatologist who does outreach work to help provide specialty rheumatology care to more underserved areas, including an affiliation with Mercy Hospital in Carthage, Missouri.

What sparked your interest in focusing on patients with lupus nephritis?

We finally have some agents that have been FDA-approved. Even though we have used agents which were not FDA approved, we're finally starting to get some that are effective, not just in lupus specifically, but in lupus nephritis. It’s essentially the number one killer of our lupus patients and certainly the thing we worry most about with our patients. Lupus nephritis is particularly prevalent in young women of color, a very underserved population, and access to health care for them can be difficult for a variety of reasons.

The other thing, not just in lupus nephritis, although what's nice about lupus nephritis is that we have very objective measures we can use to show efficacy, but I think we're also getting a better handle on how to treat lupus and using better measures in clinical trials.

The old measure was the systemic lupus erythematosus (SLE) responder index 4 (SRI-4), which was a very insensitive measure. Now they're using the British Isles Lupus Assessment Group-based Composite Lupus Assessment (BICLA), which puts more focus on the British Isles Lupus Assessment Group (BILAG), allowing us to finally see more agents that are going to be affected. We’re flying by the seat of our pants.

In terms of treatment, we seem to keep throwing options at people. For those of us who have had young patients die, particularly in lupus nephritis but in lupus as well, what's exciting about right now in the world of rheumatology is that we actually have things that show that our standard of care can be improved by some of these additional medicines that are now coming in. We’re on the forefront and we're going to see significantly more agents available for lupus in the next 5 years.

What are some of the unmet needs within this patient population?

Access to healthcare is the issue. A lot of these patients have trouble initially seeing a rheumatologist. They have trouble having their disease recognized. Not every rheumatologist is as attuned to doing the screens and learning guidelines. We’re supposed to screen every 3 months for the first 5 years for high-risk patients. I'm not sure every rheumatologist is as cognizant as they should be. Additionally, I also have patients who have trouble physically getting to the clinic. They're young, they may be trying to work, they may have little kids, it's hard for them to take off to even come to the clinic, etc. Plus, I’m sure you’re aware of the rheumatologist shortage.

One of the good things is that we're moving more and more toward more women in the field of rheumatology. Not that men haven’t done a great job, but I think sometimes women are a little more attuned to those socioeconomic factors that are so important to our young patients, and particularly for those with lupus or lupus nephritis.

There’s also a disconnect between patients showing up in the emergency room, probably having listened to providers, and actually getting them in the office to get started on treatment. The ER is not the place to start treatment. It’s not their area of expertise. However, if you look at some of the data, there's still many patients who aren't on immunosuppressive within 3 and 6 months of biopsy. They should be on treatment 2 days after their biopsy.

I recently spoke with a doctor who specialized in lupus, and he said that even if a patient is symptomatic, even if they have a rash and aches and pains, it can sometimes take his patients to up to 5 years to reach his clinic because it's like a puzzle to diagnosis. A puzzle that can be sometimes fatal.

Lupus is very hard to diagnose. It's one of those things that, if you're experienced, you can see it. When a patient shows up in clinic, we can kind of just walk in the room and have a sense that this person has lupus. Whereas primary caregivers, and it’s not their fault, have very little training in rheumatology. They don't really know the questions to ask. And that makes it difficult.

The other thing is that they will often do an antinuclear antibody (ANA) test, which is 1 very small part of making a lupus diagnosis. They don’t know how to interpret the results. I don't know how many times we see a patient with back pain where somebody did an ANA test on them. An ANA has nothing to do with back pain. These doctors are grappling with something they've had no experience with, no education, and that's not their fault. But it really would be nice if they had some because they might have a better clue about what questions to ask.

Anne Winkler, MD, discusses her upcoming CCR East presentation, “Targeting Lupus Nephritis.” 

Anne Winkler, MD: Targeting Lupus Nephritis

Patients with ankylosing spondylitis (AS) had a poor adherence to exercise therapy, with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) noted as a significantly associated factor, according to a study published in 

“Although the treatment of AS has been revolutionized with the advent of biological therapies, rehabilitation is still a promising nonpharmacological therapy in AS, which usually include aerobic exercise, respiratory kinesiotherapy, strengthening, stretching, and balance and gait training,” investigators stated. “In AS, the main goals of exercise focus on pain control, prevention and delay of stiffness, improvement of function and gait, and correction of deformity in combination with pharmacological therapy. However, reports on adherence to physical exercises in patients with AS are relatively rare, and the criteria for adherence to exercises have been inconsistent.”

In this cross-sectional study, data collected included the subject’s sociodemographic (age, sex, body mass index [BMI], education level, smoking habits, outpatient information, and family history), radiographic, disease-related, and laboratory information. Eligible patients were between 18 and 50 years of age, did not have a history of psychiatric disorders or cognitive disfunction, and completed the Exercise Attitude Questionnaire (EAQ) questionnaire.

Adherence to exercise therapy was analyzed using the 18-item EAQ with a 4-point Likert scale. Cases were grouped as either poor adherence or good adherence using the cutoff score of 60. A multivariate logistic regression model was used to identify possible factors related to poor adherence to exercise therapy.

Of 185 outpatients that completed the questionnaire, 146 patients (78.9%) were considered to have poor adherence (EAQ score ≤ 60) to exercise therapy (with only 39 patients [21.1%] exhibiting good adherence). The mean EAQ score among participants was 49.4 (IQR, 40.7–59.3).

Patients in the poor adherence group were more likely to use NSAIDs, conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), and tumor necrosis factor-α inhibitors (TNFi) (p=0.001, p=0.027, p=0.018, respectively). However, the multivariate logistic model only reported significant associations between current NSAID usage (OR=3.517; p=0.016; 95% CI, 1.259–9.827). Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were also significantly higher in patients with poor adherence (p=0.025 and p=0.014, respectively).

The single-center, cross-sectional nature of the study limited it and, as such, results were not generalizable. Further, exercise adherence tends to decline over time. The small sample size did not allow for investigators to draw correlations between other risk factors. Lastly, certain sociodemographic influences, such as marital status, dietary choices, disease-related factors, and income were not included in the assessment.

“Lack of adherence to exercise therapy is a major concern in the treatment of patients with AS,” investigators concluded. “Clinically, there is an urgent need to develop comprehensive strategies to improve adherence to exercise therapy in patients with AS, and future studies can aim to determine the reasons behind the lack of adherence to exercise therapy.”

Ma S, Zhang L, Man S, et al. Patient-reported adherence to physical exercises of patients with ankylosing spondylitis [published online ahead of print, 2022 May 3]. 

. 2022;10.1007/s10067-022-06189-w. doi:10.1007/s10067-022-06189-w

Of 185 outpatients that completed the questionnaire, 146 patients (78.9%) were considered to have poor adherence to exercise therapy.

Poor Exercise Adherence Reported in Patients with Ankylosing Spondylitis 

A healthy lifestyle was associated with a lower risk of gout, mitigating risk related to genetic factors by almost a third, according to a study published in 

“Risk genes linked to the development of gout have been identified, and lifestyle factors are related to gout risk. It remains unclear whether healthy lifestyle factors can mitigate the genetic risk of gout,” investigators stated. “We aimed to explore whether and to what extent a healthy lifestyle can mitigate the risk of gout related to genetic factors.”

A total of 416,481 healthy controls (ages 37-74) were identified at baseline within the UK Biobank database, which recruited more than 500,000 participants. Information including sex, education, body mass index (BMI), disease history, socioeconomic status, employment status, and age was collected. Polygenic risk for developing gout was analyzed and categorized as low, middle, and high. Healthy lifestyle factors were listed as no or moderate alcohol consumption, regular physical activity, no smoking, and a healthy diet. Participants were placed into 3 categories: unfavorable (0 or 1), intermediate (2), and favorable (3 or 4).

Over the following 12.1 years, 6206 participants developed gout. Those who ultimately received a gout diagnosis were more likely to older, male, physically inactive, smokers, excessive alcohol drinkers, had lower educational attainment and socioeconomic status, and had an unhealthy diet. The hazard ratios (HRs) and 95% confidence intervals (CIs) of gout was 1.44 (1.35-1.54) for the middle cohort and 1.77 (1.66-1.89) for the high genetic risk when compared with participants with low genetic risk.

HRs of gout were 0.63 (0.59-0.67) for participants with a favorable lifestyle and 0.79 (0.75-0.85) for those with an intermediate lifestyle, compared with unfavorable habits. Gout related to a favorable lifestyle was 0.64 for low those with low genetic risk, 0.65 for those with middle genetic risk, and 0.62 for those with high genetic risk. A significant additive interaction was reported between participants with an unfavorable lifestyle and a high genetic risk for developing gout.

In terms of joint analysis, when compared with participants with a low genetic predisposition and a favorable lifestyle, the HRs of gout were 2.39 (2.12-2.70)/3.12 (2.79-3.52) for those with middle or high genetic predispositions coupled with unfavorable lifestyle choices, and 1.53 (1.35-1.74)/1.98 (1.74-2.24) for patients with middle and high genetic predisposition and favorable lifestyle profiles, respectively.

The large sample study coupled with the long follow-up period strengthened the study, in addition to the standardized measures of data collection and comprehensive diagnoses. However, any changes in lifestyle factors after baseline were not evaluated. Further, gout diagnosis was determined using medical records, which opens up the possibility that well-controlled gout or patients with minor flares may not have been recorded in hospitalization records, resulting in underestimation. Generalizability may be hindered because most patients were of White British descent and those who volunteered for the UK Biobank tended to be more health-conscious than those who did not participate, adding to underestimation of gout. While sources of bias were accounted for, confounding factors and reverse causation may remain.

“We found that genetic predisposition and unhealthy lifestyle factors were associated with increased risk of gout. However, a healthy lifestyle may attenuate the risk of gout related to genetic factors,” investigators concluded. “Our findings highlight the importance of maintaining a healthy lifestyle for the prevention of gout in people with a genetic predisposition.”

Zhang Y, Yang R, Dove A, et al. Healthy lifestyle counteracts the risk effect of genetic factors on incident gout: a large population-based longitudinal study. BMC Med. 2022;20(1):138. Published 2022 Apr 29. doi:10.1186/s12916-022-02341-0

While genetics are linked to gout diagnosis and lifestyle factors are related to risk, the association between healthy choices and risk mitigation remained unclear. 

Healthy Lifestyle Modifications May Lower Risk of Genetically Induced Gout 

There is no significant difference in between the age group

Rheumatoid Arthritis Quiz: RA and Cardiovascular Risk 

Jack Arnold, MBBS, is a clinical research fellow working within Dr. Edward Vital's lupus team at the Leeds Centre of Rheumatic and Musculoskeletal Medicine. He graduated Distinction in Clinical Sciences from University College London in 2015 and has previously worked as a clinical tutor for Harris Manchester College Oxford. His work primarily focuses on systemic lupus erythematosus (SLE), antineutrophil cytoplasm antibodies (ANCA)-associated vasculitis and new approaches to the classification of autoimmune connective tissue diseases.

Emerging evidence for the role of anifrolumab in active lupus nephritis has been provided by the recent phase II study (TULIP-LN by Jayne et al published recently in Annals of Rheumatic Disease).

In this double blinded study, 147 patients were randomized 1:1:1 to receive either a base regimen of anifrolumab (300mg monthly), an intensified regimen of 3 x 900mg doses followed by 300mg monthly, or standard of care therapy with mycophenolate mofetil and oral glucocorticoids. In total, 45 patients received the base regimen of anifrolumab, 51 received the intensified regimen, and 49 received placebo plus standard of care treatment.

The primary endpoint utilized in this trial was a change in 24-hour urine protein creatinine ratio from baseline to week 52. Secondary endpoints included complete renal response (CRR) at week 52 and several additional endpoints assessing steroid tapering and stricter definitions of renal response were also included.

Unfortunately, in this case the primary endpoint was not met with no significant differences in 24-hour urinary protein/creatinine ratio (UPCR) at week 52. However, there were numeric but non-statistically significant improvements in CRR, CRR with UPCR ≤0.5 mg/mg, CRR with inactive urinary sediment and sustained glucocorticoid reductions in the intensified anifrolumab group relative to the standard of care group.

Pharmacokinetic analysis revealed that anifrolumab exposure in the baseline regimen lupus nephritis group was approximately 50% that observed in non-renal SLE comparators. This was felt possibly to be due to renal loss associated with proteinuria in active nephritis patients. Further analysis by the authors suggested that the intensified anifrolumab regimen was necessary to achieve the desired clinical and serological impact on disease.

It is disappointing that the primary endpoint in this trial was not met, however there is cause for optimism. Robust pharmacokinetic and pharmacodynamic analysis carried out by the authors has yielded good data on the implications of active lupus nephritis on anifrolumab dosing in future work. Furthermore, the numerical improvements in key outcome measures such as sustained glucocorticoid reduction and CRR are encouraging. CRR represents a robust renal endpoint and steroid reduction is an outcome measure that matters to patients with immediate and long-term impacts on morbidity. Utilizing the intensified regimen of anifrolumab may in part address the dosing implications of lupus nephritis and may drive more robust positive findings in future work. Initial signs remain positive, but further work will clarify matters.

From a safety perspective the incidence of serious adverse events was comparable between the anifrolumab and control groups. Herpes-zoster (HZV) incidence was noted to be higher in the combined anifrolumab treated groups (16.7% vs 8.2%) which is in keeping with previous literature on the subject.2In a previous anifrolumab study, most cases of herpes zoster had been manageable with antiviral medication and had not necessitated cessation of anifrolumab.

 Patients with SLE are noted to be at higher risk of HZV infection even in the absence of anifrolumab therapy, in part due to their immunosuppressive therapy and the presence of multiorgan disease.

 Current EULAR guidance already recommends the consideration of HZV vaccination in high risk patients.

With that in mind, clinicians should already be considering HZV vaccination in high-risk lupus nephritis patients, even in the absence of anifrolumab therapy. That said, it is encouraging to note that the onset of zoster infection in these patients did not generally necessitate cessation of anifrolumab therapy.

In summary, the role of anifrolumab is expanding and this work provides encouraging initial results and guidance for further research. Lupus nephritis care is expanding with new agents after a prolonged period of stagnation. However, the role anifrolumab must play in driving improved outcomes remains unclear. TULIP-LN was a relatively small study focused on illustrating proof of concept for this indication, however the outcomes from this work are likely to have significant implications in driving more definitive research in the future.

1. Jayne D, Rovin B, Mysler EF, Furie RA, Houssiau FA, Trasieva T, et al. Phase II randomised trial of type I interferon inhibitor anifrolumab in patients with active lupus nephritis. Ann Rheum Dis [Internet]. 2022 Apr 1 [cited 2022 Apr 27];81(4):496–506. Available from: https://ard.bmj.com/content/81/4/496

2. Tummala R, Abreu G, Pineda L, Michaels MA, Kalyani RN, Furie RA, et al. Safety profile of anifrolumab in patients with active SLE: an integrated analysis of phase II and III trials. Lupus Sci Med [Internet]. 2021 Feb 1 [cited 2022 Apr 27];8(1):e000464. Available from: https://lupus.bmj.com/content/8/1/e000464

3. Mok CC. Herpes zoster vaccination in systemic lupus erythematosus: the current status. https://doi.org/101080/2164551520181514228 [Internet]. 2018 Jan 2 [cited 2022 Apr 27];15(1):45–8. Available from: https://www.tandfonline.com/doi/abs/10.1080/21645515.2018.1514228

4. Furer V, Rondaan C, Heijstek MW, Agmon-Levin N, Van Assen S, Bijl M, et al. 2019 update of EULAR recommendations for vaccination in adult patients with autoimmune inflammatory rheumatic diseases. Ann Rheum Dis [Internet]. 2020 Jan 1 [cited 2022 Apr 27];79(1):39–52. Available from: https://ard.bmj.com/content/79/1/39

5. Merrill JT, Furie R, Werth VP, Khamashta M, Drappa J, Wang L, et al. Anifrolumab effects on rash and arthritis: impact of the type I interferon gene signature in the phase IIb MUSE study in patients with systemic lupus erythematosus. Lupus Sci Med [Internet]. 2018 Nov 1 [cited 2021 Jul 12];5(1):e000284. Available from: https://lupus.bmj.com/content/5/1/e000284

In the double blinded study, patients were randomized to receive anifrolumab (300mg monthly), an intensified regimen of 3 x 900mg doses followed by 300mg monthly, or standard of care therapy with mycophenolate mofetil and oral glucocorticoids. 

Lupus Nephritis: TULIP-LN Hints at a Blossoming Role for Anifrolumab

Chris Wincup, MBBS, BSc, is a consultant Rheumatologist specializing in lupus and vasculitis at King's College Hospital. 

Clinical trials aiming to evaluate the efficacy and safety of new agents in the management of lupus have long been a thorny subject. Despite initial promise, Rituximab (a chimeric monoclonal antibody directed against CD20) failed to reach primary endpoints in 2 large trials.

 However, the drug continues to show efficacy in many large “off label” studies, meaning that it remains an option for treating active and refractory disease. Prior to the positive results of the BLISS trial of belimumab,

 it had been decades since a new agent had been licensed for use in the treatment of the disease. The landmark trial initially excluded patients with acute, severe lupus nephritis, and so questions were raised about the suitability of the drug in one of the most severe forms of the disease. This led to the follow-up BLISS-LN trial assessing the efficacy of belimumab in the context of renal disease, which similarly achieved its primary endpoint at 104 weeks (in this case a renal response consisting of improvement in proteinuria, estimated glomerular filtration rate and no additional rescue therapy required).

More recently, a combination of rituximab and belimumab has been evaluated in the Phase II, randomised placebo-controlled BEAT-Lupus trial.

 In this UK-based study, patients with active SLE were recruited to the trial and treated with Rituximab (N = 52). Half of the participants went on to receive monthly belimumab infusions whilst the other half received placebo. Once again, this study reached its primary endpoint, a significant reduction in IgG double-stranded DNA antibody titres at 52 weeks. A reduction in risk of severe flare was also observed on the belimumab treatment group. Furthermore, there was no abnormal safety signal identified. This supports combination biologic therapy may be a safe and effective treatment for refectory SLE.

Aside from biologic therapies that directly target B cell cells in lupus, additional success has been observed in the use of monoclonal antibodies directed against Interferon (IFN). Anifrolumab (directed against subunit 1 of the type I IFN receptor) has also recently found success in a phase III trial.

 The drug was evaluated in the TULIP study and showed a higher proportion of patients achieving the British Isles Lupus Assessment Group-based Composite Lupus Assessment (BICLA) response when compared with placebo at 52 weeks. Interestingly, follow-up studies have noted a more significant response in patients with a higher IFN signature.

This suggests that a more bespoke treatment plan based on individual pathological biomarkers may be within reach in the near future. As with belimumab before it, anifrolumab is now also currently under investigation in the context of nephritis.

Finally, a number of other therapeutic targets are entering into clinical trials in SLE. Daratumumab, which targets anti-CD38 (expressed by plasma cells) is already licensed for use in multiple myeloma. This has been proposed as an ideal agent in SLE, where plasma cells are often poorly responsive to conventional treatment. In 2020, the drug was used in 2 patients with severe lupus in which disease activity improved (as measured by SLEDAI-2K) and titres of anti-double stranded DNA antibodies also declined.

 Another potential immune target in SLE are plasmacytoid dendritic cells (pDCs), a key producer of Type I IFN, which are seen as a key mediator in the pathogenesis of the disease. BIIB059 is a humanised monoclonal antibody that binds to and inhibits pDC receptors, which in turn inhibits the production of IFN. This is already under investigation in SLE and initial data shows early promise.

To conclude, the biologic era is now truly upon us in the field of SLE. It is an exciting time as newer drugs become available to patients with the hope of better disease control, with the hope of reduced damage and improved tolerability of treatment. However, these advances raise a number of new challenges, such as identifying which patients to treat with which biologic therapy and at what time point. Should these drugs be used early in the disease course or at times of flare? In addition, combination biologic therapy is also showing early promise and will likely undergo further study as more drugs come onto the market.

Perhaps most importantly, given the wide array of immunological dysfunction and plethora of inflammatory mediators observed in the pathogenesis of the disease, it is now more important than ever to have better tools to stratify patients more effective to the most appropriate treatment. This will likely be the key mission for researchers in the coming years. There is plenty to be optimistic about. Now, the challenge is move towards personalized medicine in SLE.

1.Rovin BH, Furie R, Latinis K, Looney RJ, Fervenza FC, Sanchez-Guerrero J, et al. Efficacy and safety of rituximab in patients with active proliferative lupus nephritis: the Lupus Nephritis Assessment with Rituximab study. Arthritis and rheumatism. 2012;64(4):1215-26.

2.Merrill JT, Neuwelt CM, Wallace DJ, Shanahan JC, Latinis KM, Oates JC, et al. Efficacy and safety of rituximab in moderately-to-severely active systemic lupus erythematosus: the randomized, double-blind, phase II/III systemic lupus erythematosus evaluation of rituximab trial. Arthritis and rheumatism. 2010;62(1):222-33.

3.Furie R, Petri M, Zamani O, Cervera R, Wallace DJ, Tegzová D, et al. A phase III, randomized, placebo-controlled study of belimumab, a monoclonal antibody that inhibits B lymphocyte stimulator, in patients with systemic lupus erythematosus. Arthritis and rheumatism. 2011;63(12):3918-30.

4.Furie R, Rovin BH, Houssiau F, Malvar A, Teng YKO, Contreras G, et al. Two-Year, Randomized, Controlled Trial of Belimumab in Lupus Nephritis. The New England journal of medicine. 2020;383(12):1117-28.

5.Shipa M, Embleton-Thirsk A, Parvaz M, Santos LR, Muller P, Chowdhury K, et al. Effectiveness of Belimumab After Rituximab in Systemic Lupus Erythematosus : A Randomized Controlled Trial. Annals of internal medicine. 2021;174(12):1647-57.

6.Morand EF, Furie R, Tanaka Y, Bruce IN, Askanase AD, Richez C, et al. Trial of Anifrolumab in Active Systemic Lupus Erythematosus. The New England journal of medicine. 2020;382(3):211-21.

7.Vital EM, Merrill JT, Morand EF, Furie RA, Bruce IN, Tanaka Y, et al. Anifrolumab efficacy and safety by type I interferon gene signature and clinical subgroups in patients with SLE: post hoc analysis of pooled data from two phase III trials. Annals of the rheumatic diseases. 2022.

8.Ostendorf L, Burns M, Durek P, Heinz GA, Heinrich F, Garantziotis P, et al. Targeting CD38 with Daratumumab in Refractory Systemic Lupus Erythematosus. The New England journal of medicine. 2020;383(12):1149-55.

9.Furie R, Werth VP, Merola JF, Stevenson L, Reynolds TL, Naik H, et al. Monoclonal antibody targeting BDCA2 ameliorates skin lesions in systemic lupus erythematosus. J Clin Invest. 2019;129(3):1359-71.

Katie Robinson is a medical writer. She covers various health and medical topics for a professional audience.

In patients with psoriatic arthritis (PsA), the IL-12/23 inhibitor ustekinumab (Stelara, Janssen) and tumor necrosis factor inhibitors (TNFi) showed similar persistence, efficiency, and safety after 1 year of treatment, according to data from a real-world observational study, published in 

“These 1-year results from the PsABio study provide real-world evidence on factors which may impact treatment selection and help inform treatment decisions in clinical practice,” Laure Gossec, MD, PhD, professor of rheumatology at Sorbonne Université in Paris, France, and colleagues, stated. Patients “were more likely to remain on ustekinumab than TNFi when extensive skin disease was present and when methotrexate was not used as concomitant treatment…Women had lower treatment persistence with both treatments versus men, indicating they may require more comprehensive multidimensional therapy.”

Many randomized controlled trials have demonstrated efficacy and safety of biologics in PsA, but real-world comparison trials, particularly over the long term, are lacking. The PsABio real-world observational study has provided comparative data on ustekinumab and TNFi in PsA treatment over 6 months and indicated similar efficacy. This 1-year analysis looked at persistence, the primary outcome, as well as clinical effectiveness, and safety.

The study followed 991 patients with PsA prescribed first-line to third-line ustekinumab or TNFi. Drug persistence, effectiveness and safety were assessed every 6 months. For the effectiveness and safety analyses, 893 and 927 patients were included. Effectiveness was measured by the achievement of clinical Disease Activity Index for Psoriatic Arthritis (cDAPSA) low disease activity (LDA)/remission and minimal disease activity/very low disease activity (MDA/VLDA). Propensity score (PS)-adjusted comparisons were also performed.

At 1-year, drug persistence was similar in the ustekinumab (72.4%) and TNFi (70.5%) groups. PS-adjusted HR (95% CI) for stopping/switching ustekinumab versus TNFi was 0.82 (0.60; 1.13). For efficiency, cDAPSA LDA (including remission)/remission was achieved in 55.9%/22.1% of patients treated with ustekinumab and 67.1%/31.7% of those treated with TNFi; PS-adjusted ORs (95% CI) were 0.80 (0.57; 1.10) for cDAPSA LDA and 0.73 (0.49; 1.07) for remission. MDA/VLDA was achieved in 34.2%/11.9% of patients treated with ustekinumab and 43.1%/12.6% of treated with TNFi; PS-adjusted ORs (95% CI) were 0.89 (0.63; 1.26) for MDA and 0.90 (0.54; 1.49) for VLDA. The safety profiles were similar in both groups.

“This study has confirmed the strong impact of treatment line, gender and baseline extent of skin disease on persistence and demonstrated the effectiveness of ustekinumab or TNFi-based treatments in PsA, not only on physician-derived but also patient-reported outcomes, such as disease impact,” investigators concluded.

The final 3-year data from the PsABio study may provide further insights.

Persistence and effectiveness of the IL-12/23 pathway inhibitor ustekinumab or tumour necrosis factor inhibitor treatment in patients with psoriatic arthritis: 1-year results from the real-world PsABio Study

 [published online ahead of print, 2022 Feb 24]. 

Ustekinumab, TNFi Show Similar Persistence at 1 Year in Real-World PsA Study 

Rheumatoid Arthritis Quiz: Maximizing the Benefits of at Treat-to-Target Strategy

The American College of Rheumatology recommends that a treat-to-target strategy is followed for rheumatoid arthritis. Test your knowledge of how to maximize the potential benefits of this approach with this quiz.

Q&A: Long-Term Safety of Ixekizumab Use in Patients With Psoriatic Arthritis

In this Q&A, Gerd R. Burmester, MD, discussed the findings of his study that evaluated the exposure to ixekizumab, outcomes and medical history of patients with active psoriatic arthritis (PsA) who experienced adverse events.

Increased Risk of Aortic Regurgitation, Atrial Fibrillation in Patients With Radiographic Axial Spondyloarthritis

The European Alliance of Associations for Rheumatology (EULAR) recommends screening and early management of cardiovascular disease in patients with radiographic axial spondyloarthritis.

Cognitive Performance Significantly Lower in Patients With SLE

The cross-sectional analysis determined cognitive performance of patients with systemic lupus erythematosus was significantly lower when compared with controls in both motor speed and psychomotor speed domains.

Guselkumab Decreases Levels of Collagen-Degrading Biomarkers in Patients With PsA

Take 5 minutes to catch up on Rheumatology Network's highlights from the week ending May 7, 2022.