Interstitial Lung Disease for the Rheumatologist: Pearls and Insights
Interstitial lung disease (ILD) is a potentially life-threatening complication of systemic autoimmune rheumatic diseases (SARDs). Its prevalence varies according to the underlying SARD, being highest in anti-synthetase and anti‑melanoma-differentiation-associated protein 5 (MDA5) syndromes, but affecting the greatest number of individuals in rheumatoid arthritis due to its higher overall frequency. Because ILD onset may precede, coincide with, or follow SARD diagnosis, rheumatologists may uncover an undiagnosed SARD during ILD evaluation or, conversely, detect ILD through screening of patients with established SARD. The spectrum of SARD-ILD is broad: some patients have mild, stable disease, others experience slowly progressive disease, and some deteriorate rapidly despite treatment, leading to oxygen dependence, lung transplantation, or death. Drug therapies, including immunosuppressive and anti‑fibrotic agents, can slow the progression of SARD-ILD. This article addresses three key clinical questions pertinent to rheumatologists. First, we explore clinical, serological, and morphological features that can aid in diagnosing SARD in patients with ILD, offering practical pearls. Second, we examine screening—covering who to screen, when, how, and at what frequency. Finally, we outline our approach to SARD-ILD management.
© Canadian Rheumatology Today 2025 https://creativecommons.org/licenses/by-nc-nd/4.0
Latest Developments in Imaging for Axial Disease in Psoriatic Arthritis
Axial disease in psoriatic arthritis (axPsA), affecting the sacroiliac joints (SIJ) and spine, is recognized as one of the domains in the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) treatment recommendations for psoriatic arthritis (PsA). Accurate recognition of this manifestation is crucial for comprehensive management of this disease. It is defined according to both clinical and imaging features. Clinically, inflammatory back pain (IBP) is a key feature; however, findings from a recent Canadian inception cohort study—Screening for Axial Spondyloarthritis in Psoriasis, Iritis, or Colitis Cohorts 1 and 2 (SASPIC1 and 2)—which included patients with psoriasis and undiagnosed back pain, showed no differences in the frequency of IBP or non-steroidal anti-inflammatory drug (NSAID) responsiveness between those diagnosed with axPsA and individuals with other causes of chronic back pain. Similarly, data from the global Axial Involvement in Psoriatic Arthritis (AXIS) cohort revealed only minor numerical differences in NSAID responsiveness or frequency of IBP, according to the ASAS criteria, between participants with and without axial involvement when evaluated by central reviewers. Recent post-hoc studies of clinical trials in PsA have attempted to identify axPsA according to a Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) threshold of ≥4. However, MRI-based assessment of axPsA in a large European cohort of 581 PsA patients, recruited across 17 European registries within the EuroSpA network, indicated that a BASDAI ≥4 did not discriminate PsA patients with axial disease from those without. Moreover, only 25–45% of patients with radiographic features of axPsA have been reported to have IBP, with some patients being clinically perceived as asymptomatic. Additionally, axSpA-based IBP criteria have demonstrated limited specificity for axPsA. Studies using MRI have reported poor correlation between sacroiliitis on imaging and both the presence and type of back pain.
Management of Adult Patients with Lupus Nephritis: Therapeutic Algorithm Based on the Current Treatment Guidelines
Lupus nephritis (LN) is one of the most significant manifestations of systemic lupus erythematosus (SLE) affecting approximately 35–40% of patients in large cohort studies. It is usually diagnosed in the early phases of the disease; among those with LN, approximately 80% are diagnosed at or shortly after disease onset. LN is characterized by histological and clinical heterogeneity and substantially affects survival. A meta-analysis of 18,309 LN patients reported a 10-year risk for the development of end-stage kidney disease (ESKD) of nearly 17% overall and 33% among those with LN class IV (diffuse proliferative form). Early detection and timely management are essential for optimizing outcomes. Given that LN patients are often asymptomatic, it is recommended that all lupus patients, particularly early in the disease course, undergo routine screening every 3–6 months. This includes assessment of proteinuria with urinary protein‑ or albumin‑to‑creatinine ratio (and 24 hour urine protein if indicated), urinary sediment and serum creatinine, regardless of disease activity. If abnormal findings that cannot be explained by alternative causes are detected (proteinuria ≥500 mg/day, active urinary sediment with acanthocytes ≥5% or red blood cell casts or white blood cell casts, increased serum creatinine) a renal biopsy should be performed, as it remains the gold standard for confirming the diagnosis, management planning, and informing the prognosis. Herein, we present a step-by step approach to the current management of adult LN as recommended by the 2024 American College of Rheumatology (ACR), the 2025 updated European Alliance of Associations for Rheumatology (EULAR), as well as the 2024 KDIGO (Kidney Disease: Improving Global Outcomes) guidelines. New treatment options that will be available in the near future are also discussed briefly. Should emphasize that the focus is on adult LN approach. The ACR guidelines also discuss children, so I think it should be acknowledged that the focus here is for adults. If the author is not going to talk about the KDIGO guidelines (which are more recent than the EULAR guidelines), they should be at least acknowledged early on and perhaps just mention some of the differences between ACR/KDIGO as readers it’s been a point of debate and discussion at multiple lupus meetings.
IL-17 Inhibition vs IL-23 Inhibition for Psoriatic Arthritis: An Ongoing Debate
The interleukin-17 (IL-17) and interleukin-23 (IL-23) pathways play a central role in the pathogenesis of psoriatic disease (PsD). This review outlines the immunobiology of these cytokine pathways and summarizes the current evidence on the efficacy and safety of IL-17 and IL-23 inhibitors across PsD domains, including peripheral arthritis, axial arthritis, enthesitis, dactylitis, psoriasis, and inflammatory bowel disease (IBD). IL-17 inhibitors, which target the effector cytokines IL-17A, IL-17F, or their receptors, have demonstrated robust efficacy in psoriasis, peripheral arthritis, and axial disease. IL-23 inhibitors act upstream by targeting the p19 subunit of IL-23 and show comparable efficacy in peripheral arthritis and psoriasis, though evidence for efficacy in axial disease remains limited. While IL-17 inhibitors carry a risk of IBD exacerbation, IL-23 inhibitors are considered therapeutic options for patients with coexisting IBD. In addition, radiographic progression appears better suppressed by IL-17 inhibitors, although emerging data suggest that IL-23 blockade may offer delayed benefits. Both IL-17 and IL-23 drug classes exhibit favourable safety profiles, with clinical trials suggesting slightly better tolerability for IL-23 inhibitors. Future directions include head-to-head comparisons, biomarker-guided treatment selection, and trials assessing long-term structural outcomes. Understanding the tissue- and cell-specific effects of inhibiting these cytokine pathways is key to optimizing therapy in PsD.
Psoriatic arthritis (PsA) is a chronic, inflammatory musculoskeletal disease that often develops in individuals with psoriasis (PsO), typically following an average latency period of 7 years. Without treatment, PsA can lead to irreversible joint damage, functional impairment, and a range of comorbidities. Despite therapeutic advances, only a minority of patients achieve sustained remission, highlighting the need for new approaches, including disease prevention and early interception. This review explores the emerging concept of PsA prevention in individuals with psoriasis, by addressing modifiable risk factors—such as severe skin disease, nail involvement, and obesity—and predictors such as arthralgias and asymptomatic abnormalities on musculoskeletal ultrasound. Notably, PsO patients represent a unique preventive opportunity in rheumatology, as many treatments address both PsO and PsA, potentially minimizing additional therapeutic risks. A recently proposed framework by the European Alliance of Associations for Rheumatology (EULAR) outlines three stages of progression from PsO to PsA, ranging from individuals ‘at higher risk’, to those with ‘subclinical PsA’, and finally to those with ‘clinical PsA’. Findings from observational studies suggest that treatment of modifiable risk factors may reduce PsA incidence, though prospective data remain limited. Subclinical inflammation detected on imaging and the presence of arthralgia may identify individuals at imminent risk who could benefit from escalation of therapy. Nonetheless, further refinement of this population is necessary to avoid overtreatment. Ongoing clinical trials are expected to help clarify whether early intervention can truly intercept PsA and alter its natural history. Ultimately, success in PsA prevention will require multidisciplinary collaboration, refinement of risk stratification, and thoughtful integration of these screening strategies into clinical practice.
Idiopathic Inflammatory Myopathy-Associated Cancer: A Review of Risk Factors and Screening Recommendations
Idiopathic inflammatory myopathies (IIMs) are a group of rare autoimmune diseases that are characterized by autoimmune myositis. However, systemic extramuscular manifestations are frequently observed. IIMs have been associated with cancer, and given the increased frequency of co-incident cancers in IIM, malignancy screening in newly diagnosed IIM patients is an important consideration. That being said, cancer risk varies across IIM subtypes, antibody specificities, and with clinicodemographic factors. As such, cancer screening should be tailored using a risk stratification approach. This review discusses the evidence regarding cancer risk in IIM, as well as recently-published guidelines for cancer screening in IIM.
What Can We Tell Our Patients About Rheumatoid Arthritis Risk?
You are seeing a 45-year-old female with a chief complaint of joint pain in the hands and feet. The symptoms have been apparent for 6 months. There was no preceding illness. She reports morning stiffness of the affected joints. The patient denies any joint swelling. Her medical history is notable for a strong family history of Rheumatoid Arthritis, and she currently smokes one pack of cigarettes daily. On physical examination, the joints appear normal, with full range of motion and no obvious tenderness to palpation. There is no evidence of synovitis or rashes. Laboratory investigations show elevated anti-citrullinated protein antibody level of 135, and her rheumatoid factor level is 45. C-reactive protein is within normal limits. Radiographs of the hands and feet are normal. Questions: 1. What is her likelihood of developing rheumatoid arthritis within the next 3 years? 2. Are there any other tests you need to order? 3. Can rheumatoid arthritis be prevented in this individual? What advice can you provide her?
Capillaroscopy in Systemic Autoimmune Rheumatic Diseases: A Clinical Tool Linking Diagnosis and Pathogenesis
Systemic autoimmune rheumatic diseases (SARDs) including systemic lupus erythematosus (SLE), systemic sclerosis (SSc), and idiopathic inflammatory myopathies (IIMs) are multisystemic, potentially life-threatening autoimmune diseases. These diseases are associated with the highest frequency of disease-associated morbidity and mortality among rheumatic diseases, largely because their complex pathophysiology remains poorly and incompletely understood. Mortality in SARDs is associated with profound vascular dysfunction ranging from cardiovascular disease to more discreet localized vascular complications including Raynaud’s phenomenon (RP), digital ulcers, and pulmonary arterial hypertension (PAH). These vascular complications stem from damage to endothelial cells caused by immune complex deposition, platelet activation, autoantibodies that promote thrombosis (e.g., antiphospholipid antibodies), and immune dysregulation. The relationship between endothelial cell dysfunction and SARDs was first recognized by Maurice Raynaud in the 19th-century, particularly in the context of localized digital ischemia and gangrene. RP is a frequently-encountered problem in clinical practice, with a prevalence in the general population ranging from approximately 5–18%. While most cases of RP are not associated with SARDs, patients with SARDs commonly experience RP. This underscores the importance of vasculopathy related to endothelial dysfunction in the pathogenesis of SARDs. RP is often the earliest presenting feature in up to 20% of patients with SARDs. Indeed, greater than 95% of patients with SSc experience RP.11 Patients with SLE, IIMs including anti‑synthetase syndrome (ASyS), and Sjögren’s disease are also commonly affected. Hence, a closer evaluation for microvascular changes is paramount in the clinical assessment of patients with SARDs. This article will review how nailfold video capillaroscopy is emerging as a valuable point-of-care tool for diagnosis and risk stratification by providing a window into the underlying endothelial dysfunction observed in these conditions.
Glucagon-like-peptide 1 (GLP-1) Receptor Agonists in Rheumatologic Disease
Obesity is a complex chronic disease that increases the risk of long-term medical complications and reduces lifespan due to excess body fat or adiposopathy. As of 2016, obesity affects 8.3 million (26.4%) of the Canadian population. Severe obesity, defined as a body mass index (BMI) >35 kg/m2, affects an estimated 1.9 million Canadians. The financial burden of obesity, including both direct and indirect costs, was estimated to be $7.1 billion in 2010. The pathophysiology of obesity is complex and involves a combination of genetic, metabolic, behavioural, and environmental factors. The hypothalamus regulates appetite and energy expenditure, while the mesolimbic area controls the emotional, pleasurable, and rewarding aspects of eating. The cognitive lobe is responsible for overriding the hedonic drive of the mesolimbic system. Adipose tissue itself contributes to its regulation through the release of leptin in proportion to fat mass. Leptin binds to receptors in the hypothalamus to reduce appetite and increase energy expenditure. Similarly, insulin binds to receptors in the arcuate nucleus of the hypothalamus also reducing appetite and increasing energy expenditure.
The Past, Present and Future of Antinuclear Antibody (ANA) Testing
This article is in memory of Dr. Eng M. Tan (Emeritus: The Scripps Research Institute) and acknowledges the remarkable mentorship and tremendous contributions to our understanding of anti-nuclear antibodies (ANA). Dr. Tan passed away in 2024 at the age of 97. More than 70 years have passed since the discovery of the lupus erythematosus (LE) cell and the development of the LE cell test, which led to the ‘tipping point’ for the discovery of antinuclear antibody (ANA), or what should more correctly be referred to as anti-cellular antibodies (ACA). Paralleling the evolution of ANA testing based on the indirect immunofluorescence assay (IFA) on cryopreserved organ sections in the 1960s and through the early 1970s was an ‘explosion’ in the spectrum of ANA and a remarkable transition in technologies used to detect ANA. This included the transition to IFA on HEp-2 cell substrates beginning in the late 1970s. While some of the ‘octogenarian’ immunoassays such as double immunodiffusion, hemagglutination, complement fixation, radioimmunoassay, and counterimmunoelectrophoresis are fading into oblivion, the ANA IFA has prevailed because of its world-wide use as a screening test for systemic autoimmune rheumatic diseases (SARD), diagnostic criteria for autoimmune hepatitis, a risk factor for the development of uveitis in juvenile idiopathic arthritis, and the entry criterion for classification of systemic lupus erythematosus (SLE). ANA testing, once regarded the domain of rheumatologists and clinical immunologists, has witnessed a widening spectrum of clinicians using these tests because of its links to a growing spectrum of autoimmune and autoinflammatory conditions. All of this is set against the background of remarkable advances in autoantibody detection, especially the emergence of newer high-throughput (i.e., faster turn-around‑time for results), multi-analyte array technologies (MAAT). These technologies use comparatively small serum or plasma volumes and provide higher specificity while detecting a broad range of SARD autoantibodies.
The Impact of Chimeric Antigen Receptor (CAR) T Cell Therapy: Its Potential to Reshape Rheumatology Practice
In recent years, genetically modified T cell therapy, using chimeric antigen receptor (CAR)‑engineered T cells, has revolutionized the field of rheumatology. While CAR T cell therapy is approved by government agencies, including Health Canada, as a standard treatment for B cell lymphoproliferative malignancies, it has also shown remarkable efficacy in refractory cases of rheumatic diseases, including systemic lupus erythematosus, systemic sclerosis, idiopathic inflammatory myopathies, ANCA-associated vasculitis, and rheumatoid arthritis. A single infusion of CAR T cells has demonstrated the potential to induce long-term drug-free remission in most cases. This therapy achieves profound B cell depletion in both blood and tissues—an effect not typically observed with conventional antibody-based B cell-target therapies. Despite its transformative potential, several challenges remain, including questions around long-term safety, high costs, limited accessibility, and the absence of standardized guidelines, which complicate its broader application. Rheumatologists face practical uncertainties, such as determining the optimal timing for treatment, selecting suitable patients, and identifying which diseases might benefit the most from this therapy. This editorial explores the fundamental principles of CAR T cell therapy, highlights the unresolved challenges, and provides insights into how rheumatologists can optimize its use for managing rheumatic diseases. (Please note that this manuscript was written in April 2025. Given the rapid advancements and emerging evidence in this field, there may be updates by the time this article is published.)
Imaging for Diagnosis and Differential Diagnosis of Axial Spondyloarthritis
Spondyloarthritis refers to a group of inflammatory rheumatic diseases characterized by shared clinical features, such as inflammatory involvement of the axial skeleton, a specific pattern of peripheral joint involvement (usually asymmetric mono- or oligoarthritis, predominantly involving the lower extremities), enthesitis, and dactylitis. Common extra-musculoskeletal manifestations include acute anterior uveitis, psoriasis, and inflammatory bowel disease (Crohn’s disease and ulcerative colitis). Axial spondyloarthritis (axSpA) denotes the subset of spondyloarthritis with predominant involvement of the spine and sacroiliac joints. The term axSpA encompasses both non-radiographic disease (no definite structural damage on X-rays of the sacroiliac joints) and radiographic disease, which has historically been referred to as ankylosing spondylitis. In clinical practice, these entities represent a spectrum. axSpA may initially present without X-ray changes and in some patients, may later progress to classic ankylosing spondylitis. In this article, we will review the approach to diagnosing (versus classifying) axSpA and examine the role of imaging modalities in diagnosing axSpA and distinguishing it from common mimics.
Echoes of Change: How Ultrasound Has Transformed Giant Cell Arteritis Detection
Giant cell arteritis (GCA) is the most common form of vasculitis affecting adults. The diagnosis of GCA is suspected in patients older than 50 years of age with a new headache and elevated inflammatory markers. Once the diagnosis of GCA is suspected, patients require urgent treatment with glucocorticoids to prevent ischemic complications such as blindness and stroke. As there are many causes for headache, diagnosing GCA can be a ‘headache’ for many rheumatologists. For years, rheumatologists have relied on the temporal artery biopsy (TAB) as the gold standard for diagnosing GCA, despite the 33–92% sensitivity. As patients with suspected GCA remain on high doses of glucocorticoids, which have multiple side-effects and potential adverse events, rapid access to tests that have a greater impact on clinical decision‑making is essential. Vascular imaging is a non‑invasive tool that can help diagnose, monitor, and predict the course of GCA. This article will focus on how ultrasound has transformed the detection of GCA and its potential to reduce some of the ‘headaches’ faced by both rheumatologists and patients.
© Canadian Rheumatology Today 2024 https://creativecommons.org/licenses/by-nc-nd/4.0
Contemporary Management of Raynaud’s Phenomenon
Raynaud’s phenomenon (RP) is defined as reversible pallor, and also rubor or cyanosis especially digits and it is very common on the general population. It can be an early sign of a connective tissue disease, especially scleroderma and may negatively impact patients’ quality of life. Lifestyle modifications including smoking cessation, cold-avoidance, and avoidance of medications that could worsen RP should be considered as first-line therapies. For those who are resistant to conservative measures, dihydropyridine calcium channel blockers (CCBs) are the preferred first-line treatment. The majority of treatment trials in RP study nifedipine, but other drugs such as amlodipine and felodipine. Otherwise, there is evidence supporting the use of topical nitrates and oral phosphodiesterase type 5 (PDE5) inhibitors. Intravenous prostaglandins (prostacyclins, PGI2 such as iloprost and PGE1 which is alprostadil) can be used for refractory cases. There remains a paucity of data for the benefit of botulism toxin, fluoxetine, or bosentan for treating RP in these patients.
The 2023 ACR/EULAR Classification Criteria for Antiphospholipid Syndrome: Implications for the Inclusion of Participants in Research vs Diagnosis in Clinical Practice
Antiphospholipid syndrome (APS) was first described in patients with systemic lupus erythematosus in 1983, and the primary version in 1989. Multiple clinical manifestations have been associated with antiphospholipid antibodies (aPL) including venous and arterial thromboses, transient ischemic attack (TIA), obstetric complications, thrombocytopenia, hemolytic anemia, livedo reticularis, transverse myelitis, cognitive dysfunction, cutaneous ulcers, Libman-Sacks endocarditis, and a peculiar type of nephropathy. Antiphospholipid antibodies include lupus anticoagulant (LAC), anticardiolipin antibodies (aCL) IgG and IgM, and anti‑beta‑2‑glycoprotein antibodies (aβ2GPI) IgG and IgM. Other antibodies such as anti-prothrombin and anti-prothrombin/phosphatidylserine have been proposed as biomarkers of APS, particularly in cases where the standard antibodies are negative, but they are not officially accepted. Since 1999, the original Sapporo Criteria and its revised 2006 version have been used for the classification of patients in research studies and for the diagnosis of patients with APS. Despite the broad spectrum of clinical manifestations and serological markers considered by physicians as part of the APS, the original and revised versions of Sapporo Criteria include only venous, arterial and microvascular thrombotic events and specific obstetric events among the clinical manifestations, and aCL IgG and IgM antibodies, aβ2GPI-I antibodies IgG and IgM or lupus anticoagulant as the serological markers. Consequently, APS was diagnosed as obstetric and/or thrombotic syndrome, not considering other non-criteria manifestations associated to aPL antibodies. The major limitation of these criteria is that they do not reflect the systemic nature of APS. Due to the importance of classification criteria in research, the ACR and EULAR assumed the responsibility of encouraging the development and validation of new and improved classification criteria for various rheumatic diseases, including APS, based on the current standards of measurement.
An Update on the Benefits and Safety Profile of Hydroxychloroquine
Hydroxychloroquine, an antimalarial drug developed in 1950, has been used for decades in the management of various systemic autoimmune rheumatic diseases. By targeting both the innate and adaptive immune systems, it exerts widespread immunomodulatory effects to attenuate the inflammatory response and exert antirheumatic effects. Its favourable safety profile, coupled with proven benefits in improving disease activity and decreasing morbidity and mortality, especially in patients with systemic lupus erythematosus and rheumatoid arthritis, has solidified its place in the long-term management of patients with rheumatic diseases. Recently, therapeutic drug level monitoring has been used to predict the risks of disease flares and prevent treatment-related toxicity. This review article briefly reviews the benefits of using hydroxychloroquine in the management of systemic autoimmune rheumatic diseases, its common and serious adverse effect profile, and the role of drug blood level monitoring in improving patient-related health outcomes.
Lupus Nephritis (LN) is a common and severe manifestation of systemic lupus erythematosus (SLE), impacting up to 40% of SLE patients. Despite advancements in understanding the pathogenesis of LN, outcomes have not significantly improved since the early 2000s. LN patients face higher mortality, emphasizing the importance of achieving disease remission. Screening for nephritis involves regular monitoring, especially within the first 5 years of SLE diagnosis. Monitoring includes urinalysis, serum creatinine, and immune serology. Kidney biopsy remains the gold standard for LN diagnosis and classification, providing crucial information for treatment decisions. The standard of care involves hydroxychloroquine for all LN patients, with immunosuppressive treatments tailored to the histologic class. The recently approved medications, belimumab and voclosporin, offer additional therapeutic alternatives. Approximately 20% of LN patients exhibit features of thrombotic microangiopathy, warranting anticoagulation. Optimizing glucocorticoid dosing is recommended, favouring lower doses to minimize adverse effects. Lifelong monitoring is essential, as flares can occur at any point, emphasizing the need for continued immunosuppression. Given the lack of renal response in 30–60% of patients, the addition of combination therapies, such as calcineurin inhibitors or belimumab, should be considered. Duration of treatment is crucial, considering the progressive loss of podocytes and nephron function, which may lead to chronic kidney disease. Regular monitoring, maintenance immunosuppression, and lifestyle modifications contribute to preventing flares and improving long-term outcomes for LN patients.
Sjogren’s Syndrome: Strategies for Treatment
Sjogren’s syndrome, characterized by dry eyes, dry mouth, and immunological hyperactivity, has been one of the most difficult rheumatic diseases to differentiate and define. After many hours of consensus group development, studies on large cohorts/registries of over 1500 patients in totality and following national, European, American, and finally consensus iterations, criteria have been agreed upon for the classification of this disease. In the final analysis, these criteria are objective and accessible for measurement, and a number of them can be documented in clinical practice. To treat Sjogren’s syndrome effectively, it is important to rely upon objective evidence with respect to the diagnosis of this disease, as well as the specific component of the condition that one is attempting to manage.
Updates in Treatment of Refractory Inflammatory Myositis
Idiopathic immune myopathies (IIM), also known as myositis, are a heterogeneous group of autoimmune diseases with varying phenotypes, prognoses, and treatment responses. They are primarily characterized by muscle inflammation, however, many patients have extramuscular involvement including skin rash, arthritis, interstitial lung disease (ILD), cardiomyopathy, and gastrointestinal dysmotility. The discovery of myositis-specific autoantibodies (MSAs) has been a major advancement in the field of IIMs, shaping the new landscape of the clinical, phenotypical, histological, and serological correlations. Based on this discovery, IIM can be more specifically classified into dermatomyositis (DM) (including amyopathic DM), antisynthetase syndrome (ASyS), immune-mediated necrotizing myopathy (IMNM), inclusion body myositis (IBM), polymyositis (PM), and overlap myositis (OM). An increasing number of histological studies have revealed a misdiagnosis of PM because many patients who were previously diagnosed with PM were later reclassified to other forms of IIM, including IBM, IMNM, ASyS, or DM without a rash.
What the Rheumatologist Needs to Know about IBD Treatment
Inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), affect almost 1% of the Canadian population and are characterized by debilitating gastrointestinal (GI) symptoms including chronic diarrhea, rectal bleeding and abdominal pain. Beyond involvement of the GI tract, up to half of patients with IBD will also experience extraintestinal manifestations (EIMs) or be diagnosed with comorbid immune-mediated inflammatory diseases (IMIDs), which are associated with substantial morbidity and impaired quality of life. The most common of these are inflammatory joint diseases, including peripheral and axial spondyloarthritis or concomitant rheumatoid (RA) or psoriatic arthritis (PsA), affecting up to 1 in 5 patients with IBD.
Management of Rheumatologic Immune-Related Adverse Events (Rh-irAEs) – An Overview of Immunosuppressive Therapies
Cancer treatment has entered a new era with the expanding role of immunotherapy, in particular immune checkpoint inhibitors (ICIs). ICIs, including those that target cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), programmed death protein-1 (PD-1), and programmed death ligand-1 (PD-L1), work by blocking the intrinsic down-regulators of the immune system, leading to sustained activation of effector T-cells to enhance endogenous anti-tumour immune responses.
Shifting Paradigms in the Treatment of Systemic Lupus Erythematosus
For many years, therapeutic options for patients with systemic lupus erythematosus (SLE) have been extremely limited. However, over the past decade, with the approval of new drugs and several promising phase II trials, treatment paradigms are gradually shifting toward multi‑targeted therapies for lupus nephritis (LN) and earlier usage of biologics in extra-renal lupus. Below, we will present three patient cases that illustrate how, through a multidisciplinary clinic environment, we have incorporated these shifting treatment paradigms into our delivery of care. Finally, we will conclude with a discussion of emerging therapies, which have the potential to further shift, and ultimately transform, treatment paradigms.
Exploring Newer Topical Therapies for Inflammatory Skin Diseases: A Guide for Rheumatologists
Understanding the pathogenesis of many inflammatory skin diseases and their associated signalling pathways has revealed multiple promising therapeutic targets. Given the chronic nature of many of these conditions, products with long-term safety and efficacy are desired. While topical corticosteroids have been the mainstay of topical therapies for years, they are burdened by concerns over long-term safety (i.e., atrophy, striae, telangiectasias), risk of absorption with systemic glucocorticoid side effects, and patient apprehension regarding steroid use. Similarly, topical calcipotriol and retinoids may be ineffective and can cause irritation. Although topical calcineurin inhibitors (i.e., pimecrolimus, tacrolimus) have been approved for atopic dermatitis, their off-label use for many inflammatory conditions may be limited by tolerability issues such as stinging and burning, and lack of effectiveness. The emergence of newer targeted small molecules for topical application, including topical phosphodiesterase-4 inhibitors (PDE4i), topical Janus kinase inhibitors (JAKi), and a therapeutic aryl hydrocarbon modulating agent (TAMA), offer promising new options and will be reviewed here and summarized in Table 1.
Osteoporosis in 2024: Frequency, Monitoring and Treatment
Osteoporosis is a chronic condition characterized by decreased bone mineral density (BMD) and deterioration of bone architecture, leading to an increased risk of fractures. It is the most common metabolic bone disease globally. It is estimated that more than two million Canadians aged 40 years and older have osteoporosis. Approximately 80% of Canadians who have sustained a fracture due to osteoporosis do not receive appropriate care, leaving them at an elevated risk for subsequent fractures, deconditioning, and premature death.1 Many clinical practice guidelines exist on the management of osteoporosis and fracture prevention. Several of them have separate definitions for patients deemed very high and high risk for fracture and, as such, have specific criteria for the use of anabolic and antiresorptive treatments.
Screening and Management of Atherosclerotic Cardiovascular Disease in Inflammatory Arthritis: A Comprehensive Approach for the Rheumatologist
Inflammatory arthritis (IA) is associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD) and contributes to significant morbidity and mortality. Early identification and treatment of conventional cardiovascular disease (CVD) risk factors are pivotal in mitigating ASCVD risk among the IA population. Equally crucial is the proactive management of inflammatory disease, necessitating a thorough discussion of the risks and benefits, particularly regarding the use of some advanced therapeutic agents indicated for IA, which may carry an increased risk of CVD in high‑risk subgroups. This article reviews the current evidence for optimal CVD screening in IA. We underscore the importance of a holistic approach that incorporates conventional risk assessment tools, biomarkers, imaging techniques, and interdisciplinary cooperation.
Axial Spondyloarthritis Treatment Recommendations in 2024: Where Are We Now?
As 2024 continues to evolve, so do treatment recommendations for the management of spondyloarthritis (SpA), including ankylosing spondylitis (AS) and non-radiographic axial spondyloarthritis (nr-axSpA). From a Canadian perspective, we eagerly await the publication of the Canadian Rheumatology Association (CRA)/Spondyloarthritis Research Consortium of Canada (SPARCC) Living Treatment Recommendations for the Management of Axial Spondyloarthritis (axSpA), currently in press. Until these recommendations for axSpA treatment with a Canadian perspective arrive – where are we now?