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تعداد آیتم قابل مشاهده باقیمانده : 3 مورد

Psoriatic juvenile idiopathic arthritis: Management and prognosis

Psoriatic juvenile idiopathic arthritis: Management and prognosis
Author:
Peter A Nigrovic, MD
Section Editor:
Marisa Klein-Gitelman, MD, MPH
Deputy Editor:
Siobhan M Case, MD, MHS
Literature review current through: Apr 2025. | This topic last updated: Jul 18, 2024.

INTRODUCTION — 

Psoriatic juvenile idiopathic arthritis (psJIA), or alternately juvenile psoriatic arthritis (JPsA), is a condition that can range widely in presentation and severity. Frank cutaneous psoriasis is not always evident, and the extent of articular involvement may vary from mild enthesitis (inflammation of sites at which ligaments, tendons, and other fibrous structures insert into bone) to polyarticular involvement of multiple axial (spine, sacroiliac joints) and peripheral joints.

The treatment and prognosis of psJIA are discussed here. The epidemiology, pathogenesis, clinical manifestations, and diagnosis of psJIA are discussed separately, as is psoriatic arthritis (PsA) in adults.

●(See "Psoriatic juvenile idiopathic arthritis: Epidemiology, clinical manifestations, and diagnosis".)

●(See "Clinical manifestations and diagnosis of psoriatic arthritis".)

●(See "Treatment of psoriatic arthritis".)

●(See "Pathogenesis of psoriatic arthritis".)

TREATMENT — 

The treatment of psoriatic juvenile idiopathic arthritis (psJIA) primarily depends on the type and degree of disease manifestations, including the presence of axial arthritis, uveitis, and psoriasis.

Goals of therapy — The primary goal in treating psJIA is to extinguish synovitis and avoid irreversible damage to cartilage and bone. This is particularly critical for the growing skeleton, where injury to growth plates and growth centers can cause permanent derangement of bone shape and length [1,2]. Other goals of therapy include controlling symptoms, addressing functional limitations from joint damage, and improving quality of life. However, it is important to note that the absence of reported pain and functional impairment are imperfect guides to successful therapy, since children may adapt remarkably well to ongoing arthritis [3].

General approach to treatment — Treatment of psJIA is highly dependent on the extent and degree of joint involvement (eg, axial versus peripheral arthritis, mild versus severe disease) and specific disease manifestations (eg, uveitis). Given the potential for irreversible joint damage and chronic nature of this condition, providers should follow patients closely and escalate therapy as needed. Management should be conducted in consultation with a pediatric rheumatologist, dermatologist, and pediatric ophthalmologist whenever possible.

The basic treatment algorithm of psJIA is similar to that employed in other subtypes of JIA (algorithm 1 and algorithm 2) and includes various types of therapies such as nonsteroidal antiinflammatory drugs (NSAIDs), intraarticular (IA) glucocorticoids, conventional synthetic disease-modifying antirheumatic drugs (csDMARDs), and various biologic DMARDs (bDMARDs) (table 1) [4].

Our approach to treatment is consistent with that outlined in the American College of Rheumatology (ACR)/Arthritis Foundation (AF) 2019 treatment guidelines [4].

Pretreatment testing — Patients with psJIA frequently require systemic immunosuppressive therapy and may need screening for chronic infections (eg, tuberculosis and hepatitis B) prior to starting treatment.

Initial therapy — The general approach to initial therapy is outlined in the algorithm (algorithm 1), with drug dosing in the table (table 1). Treatment of psJIA often begins with NSAIDs, which may be used temporarily as monotherapy for mild disease. More often, NSAIDs are used as adjunctive therapy together with IA glucocorticoids in patients with arthritis in ≤2 medium- to large-sized joints, with csDMARDs for patients with moderate to severe peripheral arthritis, or, more rarely, with bDMARDs in patients with certain features (eg, joint damage, involvement of certain joints) that place them at higher risk for severe complications.

NSAIDs for most patients — In patients with psJIA who do not have a contraindication to NSAIDs, we use NSAIDs as a temporary adjunctive therapy to help reduce pain and swelling while awaiting the full efficacy of other treatments. As examples, patients who receive IA glucocorticoid injections may benefit from taking concomitant NSAIDs for one or two weeks, and those taking csDMARDs may use NSAIDs for several months. Less commonly, NSAIDs may be used initially as the sole therapy for patients with mild axial and/or peripheral arthritis that has lasted for less than two months; however, NSAIDs typically do not lead to remission and thus should not be used as monotherapy for moderate to severe arthritis [4]. (See 'csDMARDs for most patients with moderate to severe peripheral arthritis' below.)

When NSAIDs are used for patients with psJIA, the dosing, contraindications, and evidence are the same as those for other types of JIA. Dosing is specified in the table (table 1), and efficacy is discussed elsewhere. (See "Spondyloarthritis in children", section on 'NSAIDs for most patients'.)

If NSAIDs are being used without other immunosuppressive therapy and patients have persistent symptoms despite four to six weeks of treatment, we start additional therapy depending on their clinical disease manifestations. (See 'Treatment of refractory disease' below.)

Evidence to support the use of NSAIDs in patients with psJIA is very limited. Based on probability estimates for patients with oligoarticular JIA, there is a low probability (less than 20 percent) that NSAIDs alone will induce remission within two months of therapy [5].

Intraarticular glucocorticoids — In patients with psJIA who have arthritis in large- to medium-sized joints that are amenable to injection, IA injection of glucocorticoids may be used as part of the initial therapy. While this procedure may require sedation, especially in younger children, it can offer more targeted and rapid control of synovitis than NSAIDs or csDMARDs. Dosing of injectable glucocorticoids is summarized in the table (table 1). It is unusual to inject more than three to four joints, although multiple joints can be injected as an adjunct to systemic disease-modifying therapy. More information about performing IA glucocorticoid injections in children is provided separately. (See "Joint aspiration or injection in children: Indications, technique, and complications" and "Intraarticular and soft tissue injections: What agent(s) to inject and how frequently?".)

The use of IA glucocorticoid injections in psJIA has not been specifically studied, but decision analysis in oligoarticular JIA suggests that a strategy of upfront IA glucocorticoid injection is preferable to a trial of NSAIDs followed by IA for refractory disease due to the low likelihood of remission on NSAIDs alone [5].

csDMARDs for most patients with moderate to severe peripheral arthritis — In most patients with psJIA who have moderate to severe peripheral arthritis (eg, arthritis that affects multiple joints, causes debilitating symptoms, and/or persists for >2 months), we start a csDMARD in addition to an NSAID and/or IA glucocorticoids. However, patients who also have high-risk features (eg, joint damage, involvement of certain joints) may need more aggressive therapy. (See 'Tumor necrosis factor inhibitors for high-risk features' below.)

Initiation of a csDMARD at diagnosis is preferable to delaying therapy while awaiting the result of an NSAID trial in patients presenting with moderate or severe arthritis or arthritis of multiple joints [4]. Data to support the use of csDMARDs in the initial treatment of psJIA are very limited; however, in a trial of patients with early polyarticular JIA, methotrexate was an effective treatment option and the likelihood of achieving clinically inactive disease was higher in patients who started therapy sooner after symptom onset [6]. In addition, there is a low likelihood of remission on NSAID monotherapy [5].

csDMARDs generally are not effective for axial arthritis in adults and by extension are not used as the primary therapy to treat axial arthritis in patients with psJIA [4,7]. However, in psJIA patients with both axial and peripheral arthritis, methotrexate or sulfasalazine may sometimes be used together with a bDMARD that treats axial arthritis. (See 'Axial arthritis' below.)

Methotrexate — The most commonly used csDMARD is methotrexate, which is recommended as first-line therapy in the ACR/AF 2019 treatment guidelines [8]. More than 80 percent of psJIA patients are treated with methotrexate over the course of their illness [9]. Methotrexate is typically well tolerated in children with psJIA. By contrast, adults with psoriatic arthritis (PsA) have higher risk of hepatotoxicity than adults with rheumatoid arthritis, possibly because of the higher prevalence of obesity and associated steatohepatitis in adult psoriasis [10].

When methotrexate is used for patients with psJIA, the dosing is outlined in the table (table 1); the contraindications, adverse effects, and additional supportive evidence for treating patients with JIA are detailed elsewhere. (See "Polyarticular juvenile idiopathic arthritis: Treatment and prognosis", section on 'Methotrexate'.)

Sulfasalazine — Sulfasalazine is an alternative, especially for arthritis affecting large joints in the lower extremities, although it is not effective for comorbid uveitis, and trial data in adult PsA provide conflicting evidence of efficacy [11-14].

When sulfasalazine is used for patients with psJIA, the dosing is outlined in the table (table 1); the contraindications, adverse effects, and additional supportive evidence for treating patients with JIA are detailed elsewhere. (See "Polyarticular juvenile idiopathic arthritis: Treatment and prognosis", section on 'Sulfasalazine'.)

Tumor necrosis factor inhibitors for high-risk features — In most patients with psJIA who have moderate to severe peripheral arthritis with high-risk features (eg, joint damage, involvement of the cervical spine, temporomandibular joint [TMJ], and/or hip), we start a tumor necrosis factor (TNF) inhibitor in addition to an NSAID and/or IA glucocorticoids. When evaluating for joint damage in patients with JIA, it is important to recognize that plain radiographs typically disclose erosions in children later than in adults because of the ossification status of immature joints and the relatively greater thickness of cartilage in children. A lack of erosions should therefore not be considered reassuring; patients with a severely affected joint who do not have detectable erosions on radiographs should be monitored closely for the potential need to escalate therapy.

When TNF inhibitors are used for patients with psJIA, the dosing is outlined in the table (table 1); contraindications, adverse effects, and supportive evidence for treating patients with JIA are detailed elsewhere. (See "Polyarticular juvenile idiopathic arthritis: Treatment and prognosis", section on 'Tumor necrosis factor inhibitors'.)

Data to support the use of TNF inhibitors as part of the initial management of patients with psJIA who have high-risk features are very limited. However, arthritis in certain joints can cause significant functional limitations, especially in growing children, and must be rapidly controlled. TNF inhibitors achieve full efficacy more quickly than csDMARDs and have fewer adverse effects than systemic glucocorticoids, which is the other fast-acting option. The use of a bDMARD for initial therapy in patients with polyarticular JIA who have high-risk features is included in the ACR/AF 2019 JIA treatment guidelines [8].

Given the difficulty of assessing the activity of arthritis of the TMJ by clinical examination and the long-term consequences of active disease on mandibular growth, we regard the TMJ to be high risk and consider using a TNF inhibitor as initial therapy in affected children. This differs slightly from the ACR 2021 guidelines for TMJ arthritis in the setting of JIA, which recommend a bDMARD and/or a csDMARD such as methotrexate for patients who do not respond to initial therapy with an NSAID and/or IA glucocorticoids [15]. More information on the diagnosis and treatment of TMJ arthritis as a complication of JIA is provided separately. (See "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Temporomandibular joint arthritis'.)

Medications to avoid — Systemic glucocorticoids are typically avoided because they can provoke a flare of cutaneous psoriasis when tapered [16]. In addition, some rheumatologists believe that PsA is less responsive to systemic glucocorticoids than other types of arthritis, although this observation has yet to be rigorously tested. Based on these issues, we avoid oral glucocorticoids in most patients. An exception is the use of low- to moderate-dose oral glucocorticoids as short-term "bridge" therapy while awaiting the effect of slower-acting csDMARDs in highly symptomatic patients. Similarly, we typically avoid hydroxychloroquine as there is some evidence that it may worsen psoriasis [17].

Assessing response to treatment — Clinical remission, typically on medication, is achieved in the majority of patients in both older and younger subgroups [18,19]. As an example, in a large cohort of children diagnosed with JIA between 2005 to 2010, 91 percent of patients with psJIA attained inactive disease within two years and 47 percent achieved remission (defined as inactive disease >12 months after discontinuing treatment) within five years [20].

The frequency of monitoring after starting therapy depends somewhat on the type of therapy used, but patients are generally reevaluated after four to eight weeks. The best way to monitor for disease activity and response to therapy in patients with psJIA is regular clinical monitoring of symptoms and physical examination findings. Laboratory tests and imaging studies are of limited value in the management of psJIA. More information on each component of assessment is provided below:

●Symptoms – When taking a history, we include questions about pain as well as limitations in activities and in meeting developmental milestones. However, active disease can be missed on history as children may adapt remarkably well to ongoing arthritis and may not vocalize pain or have obvious functional limitations [3].

●Examination findings – We perform a comprehensive musculoskeletal examination with particular attention to the following components:

•Range of motion in affected joints should be tracked over time (eg, noting the limits of joint hyperextension and flexion).

•The interincisor distance should be monitored to assess possible TMJ involvement. (See "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Temporomandibular joint arthritis'.)

•The modified Schober test should be used for those with lumbar spine involvement.

•Tracking growth and potential limb length discrepancies is also important. Falling off of expected growth curves may be a sign of uncontrolled disease or other complications (eg, evolving inflammatory bowel disease). (See "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Leg-length discrepancy'.)

●Laboratory tests – As in other subtypes of JIA, laboratory studies may be normal despite ongoing destructive arthritis. The frequency and type of laboratory testing is therefore based on the treatments the patient is receiving. We also periodically check erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) in patients who historically have had elevated inflammatory markers with disease flares. When ESR and/or CRP elevations are related to arthritis, they should normalize during remission; however, they are nonspecific and may remain modestly elevated in patients with severe persistent psoriasis [21]. (See "Psoriatic juvenile idiopathic arthritis: Epidemiology, clinical manifestations, and diagnosis", section on 'Laboratory findings'.)

●Imaging – Imaging is not uniformly necessary for diagnosis or management. We perform ultrasonography and/or magnetic resonance imaging (MRI) if there is concern for a possible disease flare based on patient symptoms that is not clinically apparent on examination. Radiographs have a relatively low sensitivity in children, as it may take months or years for there to be visual evidence of synovitis and its consequences for bone. We typically do not follow serial imaging in patients who are in remission. The use of imaging in the diagnosis of psJIA is discussed elsewhere. (See "Psoriatic juvenile idiopathic arthritis: Epidemiology, clinical manifestations, and diagnosis", section on 'Radiologic studies'.)

Treatment of refractory disease — We consider patients to have refractory disease if they do not respond to NSAIDs or IA glucocorticoids within four to six weeks or to csDMARDs within eight weeks. In patients who do not respond to initial therapy, we rapidly proceed to other csDMARDs or bDMARD depending on the disease manifestations and previous treatments. The choice of immunosuppressive therapy depends on the types of clinical manifestations that are present, as agents have varying efficacy for treating specific aspects of psJIA (eg, axial arthritis) and related complications (eg, uveitis). We start with one type of immunosuppressive therapy that can treat all of the patient's clinical manifestations. As an example, patients with axial arthritis and psoriasis would typically start a TNF inhibitor or an interleukin 17 (IL-17) inhibitor, as these agents can treat both manifestations. The general approach to treatment of refractory disease is outlined in the algorithm (algorithm 2), with drug dosing in the table (table 1).

Axial arthritis — In most patients with psJIA who have active axial arthritis despite NSAIDs, we add a TNF inhibitor. IL-17 inhibitors (eg, secukinumab) are an alternative therapy in patients with severe skin psoriasis who do not have comorbid uveitis, since IL-17 inhibitors have limited evidence for efficacy in uveitis. csDMARDs and IL-12/23 inhibitors are typically ineffective for axial disease [4,22].

When bDMARDs are used for patients with psJIA, the dosing, contraindications, and adverse effects are the same as those for other types of JIA and are detailed elsewhere (table 1). (See "Polyarticular juvenile idiopathic arthritis: Treatment and prognosis", section on 'Tumor necrosis factor inhibitors' and "Spondyloarthritis in children", section on 'bDMARD for most patients'.)

Treatment should be initiated in patients with psJIA who experience axial symptoms or show limitation of spinal mobility, even if changes have not yet developed on plain radiograph [8]. Of note, spinal radiographs are much less sensitive in detecting early sacroiliitis than MRI. Therefore, we typically avoid plain radiographs, and the attendant gonadal radiation, and instead proceed directly to noncontrast MRI as the preferred mode of imaging in children with symptoms suggestive of sacroiliitis [23]. (See "Psoriatic juvenile idiopathic arthritis: Epidemiology, clinical manifestations, and diagnosis", section on 'Radiologic studies'.)

Treatment of axial arthritis in children with psJIA is based primarily upon experience with adult ankylosing spondylitis and pediatric enthesitis-related arthritis (ERA) [8,24,25], which is discussed in more detail elsewhere and briefly summarized below (see "Spondyloarthritis in children", section on 'bDMARD for most patients'):

●TNF inhibitors – TNF inhibitors specifically approved by the US Food and Drug Administration (FDA) for psJIA (in children age two years and older) include etanercept and golimumab, based on extrapolation for adult efficacy data and pediatric safety and pharmacokinetic data [26]. However, all of the available TNF inhibitors are believed to work comparably, with the exception of etanercept, which is less effective for uveitis (table 2). More than one-half of psJIA patients receive TNF antagonists at some point during the course of their illness [9].

Anti-TNF therapy is highly effective for axial disease in ERA [27]. Early initiation may be particularly important in young people, since childhood-onset axial arthritis may be more severe than adult-onset disease [28].

Data support the possibility that early initiation of therapy may result in a more favorable outcome, although studies in adults with longstanding disease have not consistently shown reduced radiographic progression [29-33].

●IL-17 inhibitors – Secukinumab (a human IL-17A antagonist) is FDA approved for psJIA in children ≥2 years of age. A randomized withdrawal trial of secukinumab in children with psJIA and ERA showed efficacy, with similar safety to that reported in adult disease [34]. Additional supportive data come from adults with PsA, where the efficacy of secukinumab is comparable with TNF inhibitors and is superior in improvement of associated skin psoriasis, with similar safety [35]. Moreover, IL-17 inhibitors can benefit axial disease, including in patients whose disease has not responded to TNF inhibitors [36-41]. No data are available to support its use in patients with comorbid uveitis. The IL-17A antagonist ixekizumab is approved for adult PsA and also for moderate to severe plaque psoriasis in children at least six years of age, and so it represents a potential alternative to secukinumab.

Peripheral arthritis — In patients without axial arthritis who have active peripheral arthritis despite NSAIDs and/or IA glucocorticoids, we start a csDMARD, specifically methotrexate or sulfasalazine. This process is the same as when csDMARDs are started as part of the initial therapy for patients with moderate to severe peripheral arthritis. (See 'csDMARDs for most patients with moderate to severe peripheral arthritis' above.)

●csDMARDs versus TNF inhibitors – There are no trials comparing treatment approaches for refractory peripheral arthritis in psJIA, but several trials in patients with early polyarticular JIA have compared methotrexate with TNF inhibitors as initial therapy:

•In one trial of 60 patients with polyarticular JIA, the rates of inactive or minimally active disease were higher in the group randomly assigned to infliximab and methotrexate compared with the group assigned to methotrexate alone [42].

•In another trial of 85 children with polyarticular JIA who were randomly assigned to methotrexate alone versus a combination of methotrexate, etanercept, and a prednisone taper, the rate of inactive disease after six months was not significantly different between the groups [6].

In the absence of more definitive differences and in light of other issues with bDMARDs including cost, regulatory issues, and parental concerns about potential adverse effects, a csDMARD is often used for peripheral arthritis related to non-systemic JIA before proceeding to a bDMARD [8].

In patients without axial arthritis who have moderate to severe peripheral arthritis despite csDMARDs, we add a TNF inhibitor or, less commonly, switch to an alternative csDMARD such as leflunomide [4]. IL-17 inhibitors (eg, secukinumab) and IL-12/23 inhibitors (eg, ustekinumab) are alternatives to TNF inhibitors in patients with severe skin psoriasis who do not have comorbid uveitis. Anti-TNF agents are also effective for dactylitis and enthesitis [4].

The use of TNF and IL-17 inhibitors is described above (see 'Axial arthritis' above). Ustekinumab (a human antagonist of the receptors for IL-12 and IL-23, which share a common protein component termed the P40 subunit) is approved for psJIA in children ≥6 years of age, based on extrapolation from adult efficacy data and pediatric safety and pharmacokinetic data (table 1) [26,43-45]. It is generally not effective for patients with axial arthritis or uveitis [22,46].

Dactylitis — Dactylitis in PsA reflects a composite of arthritis, tenosynovitis, and especially prominent enthesitis of the many attachments of ligaments, tendons, and joint capsules in the fingers and/or toes [47]. Scintigraphic studies confirm the presence of TNF localized to the dactylitic digit [48].

In most patients with psJIA who have persistent dactylitis despite NSAID therapy, we suggest adding a TNF inhibitor rather than a csDMARD. An alternative option in patients who do not have axial arthritis is adding methotrexate, which may be preferred when the dactylitis is isolated and mild.

In children with psJIA and dactylitis, csDMARDs such as methotrexate generally have limited utility, although improvement of dactylitis with treatment has been reported [49]. While evidence to support one type of bDMARD over another for patients with dactylitis related to psJIA is extremely limited, TNF inhibitors are typically the first bDMARD selected for those with dactylitis and have been shown to be an effective treatment in adults with PsA [50,51]. Other biologic therapies with proven benefit in adults with PsA include IL-12/23 inhibitors (eg, ustekinumab), IL-17 inhibitors (eg, secukinumab), phosphodiesterase-4 (PDE4) inhibitors (eg, apremilast), and Janus kinase (JAK) inhibitors [52-56]. There are also reports of effective treatment using local glucocorticoid injection into the digital flexor tendon sheath, with a response rate of 87 percent in one adult observational series [57].

Psoriasis — Cutaneous manifestations of pediatric psoriasis are phenotypically similar to skin involvement in adults, although findings can be subtle and there is a higher prevalence of nail changes in psJIA than in pediatric psoriasis without arthritis [58]. Conventional psoriasis treatment is appropriate for skin disease associated with psJIA, although articular manifestations favor use of systemic agents that are also effective for skin disease, including methotrexate, TNF blockers, IL-17 inhibitors (eg, secukinumab, ixekizumab), and IL-12/23 inhibitors (eg, ustekinumab). Of note, ixekizumab is a type of human IL-17A antagonist that is FDA approved for moderate to severe psoriasis, but not specifically psJIA, in children ≥6 years of age.

Data from adult psoriasis and PsA suggest that therapy directed against IL-17 is likely to provide the best relief for resistant cutaneous psoriasis; IL-17 inhibitors are effective for axial disease but not known to be effective for comorbid uveitis. IL-12/23 inhibitors (eg, ustekinumab) may also be more effective for patients with prominent cutaneous disease, although this treatment is not effective for axial arthritis. (See "Treatment of psoriatic arthritis" and "Chronic plaque psoriasis in adults: Overview of management".)

More information on the presentation and treatment of psoriasis in children is discussed separately. (See "Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis" and "Psoriasis in children: Management of chronic plaque psoriasis".)

Uveitis — Treatment for uveitis in psJIA is similar to that in other subtypes of JIA, which is discussed in detail separately. (See "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Chronic anterior uveitis' and "Uveitis: Treatment".)

Chronic anterior uveitis is treated initially with topical corticosteroids, usually together with oral or subcutaneous methotrexate. Resistant disease often responds to an anti-TNF antibody such as infliximab or adalimumab (the anti-TNF receptor fusion protein etanercept is less effective for uveitis). Third-line agents include mycophenolate mofetil, tocilizumab, and cyclosporine. Uveitis has a very strong tendency to recur if DMARD therapy is discontinued [59].

Acute anterior uveitis may also occur, typically in children with axial disease; this form of uveitis is less frequently sight-threatening than chronic anterior uveitis and typically responds to topical corticosteroids or oral glucocorticoids. (See "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Acute anterior uveitis'.)

Third-line therapies — When patients with psJIA have symptoms that are refractory despite the above options, they may benefit from combination therapy and/or alternative biologics. The choice of immunosuppressive therapy depends on the types of clinical manifestations that are present and results of prior therapies. As an example, if a patient's axial arthritis is well controlled on a TNF inhibitor but they have refractory peripheral arthritis, a csDMARD such as methotrexate may be added. By contrast, a patient with axial arthritis that does not respond to TNF or IL-17 inhibitors may benefit from substituting a JAK inhibitor.

Alternative biologic therapies that may be used to treat refractory psJIA include the following:

●Abatacept – Abatacept (a T-cell costimulatory blocker) is approved for psJIA in children ≥2 years of age, based on extrapolation from adult efficacy data and pediatric safety and pharmacokinetic data. Of note, abatacept is only modestly effective for PsA and is not effective for axial spondyloarthritis in adults [60], but it is effective and well tolerated for peripheral arthritis in polyarticular JIA [61-63]. (See "Polyarticular juvenile idiopathic arthritis: Treatment and prognosis", section on 'Abatacept'.)

●JAK inhibitors – The JAK inhibitors tofacitinib, baricitinib, and upadacitinib have been found to be effective in JIA, including in studies that had a limited number of children with psoriatic JIA [64,65], and have clinical efficacy in adults with active PsA or ankylosing spondylitis [66]. We generally reserve JAK inhibitors for patients who do not respond to or tolerate other therapeutic options due to potential safety concerns. One patient in the baricitinib trial experienced a pulmonary embolism that was considered related to the study drug. The impact of JAK inhibitors on growth in children is undefined yet potentially of concern, since growth hormone signals via JAK2. The impact of JAK inhibitors on cancer risk remains controversial, and no data are available in children. (See "Overview of the Janus kinase inhibitors for rheumatologic and other inflammatory disorders", section on 'Malignancy' and "Polyarticular juvenile idiopathic arthritis: Treatment and prognosis", section on 'Small molecule inhibitors'.)

●Apremilast – Clinical similarities between adult and pediatric PsA suggest that they form a spectrum of disease, a possibility supported by genetic evidence [67-69]. Based upon this similarity, agents useful in adult PsA are likely to be effective in psJIA, including apremilast (a PDE4 inhibitor). Apremilast has been effective for peripheral arthritis and enthesitis in adult PsA [70,71] but does not appear to treat axial disease in ankylosing spondylitis [72]. The tolerance of apremilast is often limited by adverse effects such as diarrhea and, less commonly, mood changes including depression and suicidal ideation [61-63]. (See "Treatment of psoriatic arthritis".)

Physical therapy — We refer patients with psJIA for adjunctive physical therapy if they are at risk of developing functional limitations, especially when there is axial arthritis or arthritis of large peripheral joints that impact mobility (eg, hips, knees). While supportive evidence is very limited, physical therapy is recommended by pediatric treatment guidelines [73].

Tapering therapy — After patients have been in a period of sustained remission on therapy, it is usually appropriate to attempt to taper therapy. The approach to assessing the response to treatment is described above. (See 'Assessing response to treatment' above.)

For patients who have achieved remission, the approach to tapering therapy depends on the agent being used and may need to be modified for patients with aggressive, widespread, or refractory disease. In general, we take the following approaches:

●NSAIDs – For patients who achieve remission on NSAIDs alone, we continue therapy for at least two months before considering a taper. For patients who are in remission on NSAIDs with another therapy (eg, IA glucocorticoid, csDMARD, biologic), we generally use NSAIDs only as needed once patients are in remission. In one adult trial, standing-dose versus as-needed NSAIDs resulted in measurable radiographic improvement, but the effect was small, and the finding was not replicated in a second comparably sized randomized controlled trial [74,75]. Potential adverse effects of NSAIDs may outweigh the benefits; in one observational study, standing-dose NSAIDs were associated with a 12 percent increase in incident hypertension [76].

●Disease-modifying therapy – In general, the author’s approach is to continue treatment of psJIA that is well tolerated until skeletal growth is largely complete, especially for patients with uveitis or sacroiliitis and/or whose disease was highly polyarticular or difficult to control. Due to the risks outlined below, the decision to discontinue DMARD therapy in patients with psJIA requires careful shared decision-making between provider and patient/family. For patients who elect to trial a discontinuation of therapy, the author's preference is to taper therapy over six months rather than to discontinue treatment abruptly. Dose reduction is an option for many patients receiving TNF inhibitor therapy, where extrapolation from adult data suggests that many patients in remission can tolerate either a reduced frequency or a reduced dose [77]. By contrast, while small decreases in csDMARD dosing may be necessary to improve tolerability, in general csDMARD dosing should be maintained at the level found originally to be effective. This is because dose reduction of csDMARDs (eg, methotrexate) appears to be associated with a risk of disease flare [78].

In general, children who require csDMARD or bDMARD therapy to achieve remission in JIA exhibit a high likelihood of disease flare if medications are fully discontinued [79,80]. Chronic anterior uveitis is particularly problematic, flaring within two years in >80 percent of patients discontinuing DMARD therapy [59]. Further, children who flare their JIA after drug discontinuation often experience prolonged periods of active arthritis and in some cases may have involvement of new joints and/or require a more intensive treatment regimen to maintain remission [79,81,82]. As an example, one study of 24 patients with psJIA or ERA who flared off of treatment found that seven patients (nearly 30 percent) still had active disease 12 months later [81]. Adult data indicate that axial arthritis, including sacroiliitis, is particularly unlikely to remain in remission of treatment is stopped [77]. Nevertheless, one long-term outcomes study found that 10 of 21 psJIA patients evaluated 30 years after disease onset were in remission off medication [83].

IMMUNIZATIONS — 

Many patients with psoriatic juvenile idiopathic arthritis (psJIA) require immunosuppressive therapy, which makes patients more vulnerable to infection and can also dampen the protective response formed through vaccination. The decrease in vaccine immunogenicity seen in children taking various types of immunosuppression is presumably similar to that observed in adults (table 3). In certain scenarios, standard vaccine schedules may be modified and/or immunosuppressive therapies may be held to improve the vaccine response. Patients on immunosuppression may also qualify for additional boosters of certain vaccines (eg, coronavirus disease 2019 [COVID-19] vaccines); the recommendations may vary based on age and the timing and type of previous vaccines (eg, pneumococcal vaccines).

Ideally, patients with psJIA should receive all of the recommended vaccinations prior to starting systemic immunosuppressive therapy; however, exceptions may be made when patients have moderate to severe arthritis. More detail on the optimal management of standard childhood and adult vaccination in JIA, including the administration of live-virus vaccines, is discussed in detail separately. (See "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Immunizations' and "Immunizations in autoimmune inflammatory rheumatic disease in adults".)

COMPLICATIONS AND ASSOCIATED CONDITIONS — 

In addition to monitoring disease activity, patients with psoriatic juvenile idiopathic arthritis (psJIA) should be monitored for signs and symptoms of other conditions related to spondyloarthritis:

●Psoriasis – Some patients who are categorized as having psJIA do not have psoriasis at disease onset but may develop it later [84]. Manifestations of psoriasis in children can be different, including subtle findings in the scalp, ears, and diaper area (figure 1). The diagnosis of psoriasis in children is discussed separately. (See "Psoriasis in children: Epidemiology, clinical manifestations, and diagnosis".)

●Inflammatory bowel disease – Inflammatory bowel disease is more common in patients with forms of spondyloarthritis, including psJIA. It should be suspected in the setting of altered stooling habits, weight loss or decreased vertical growth, and/or iron deficiency anemia. The workup for inflammatory bowel disease is detailed separately. (See "Clinical presentation and diagnosis of inflammatory bowel disease in children".)

●Uveitis – Patients with psJIA are at risk of developing associated uveitis, which is most often asymptomatic until it affects vision [68]. Monitoring for uveitis related to all types of JIA is discussed separately. (See "Oligoarticular juvenile idiopathic arthritis" and "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Chronic anterior uveitis'.)

Other potential complications of JIA are discussed in detail separately. (See "Juvenile idiopathic arthritis: Immunizations and complications", section on 'Complications'.)

PROGNOSIS — 

The long-term outcome of children with psoriatic juvenile idiopathic arthritis (psJIA) has improved with the expanding repertoire of available therapies [85]. Nevertheless, compared with other patients with JIA, observational data suggest that those with psoriatic arthritis (PsA) accumulate more inflamed joints and are less likely to enter sustained remission [86]. In one cohort study of 31 patients with psJIA, poor outcomes and long-term disability were seen principally in patients who experienced a long delay in diagnosis or in whom effective therapy was not instituted, often through clinician or caregiver reluctance to take the steps necessary to induce remission. In addition, patients who were diagnosed in the "prebiologic era" (before approximately 2000 in pediatric rheumatology) tended to have worse outcomes. A longitudinal cohort study from this era found persistently active disease in 70 percent of patients with psJIA and physical activity limitations in one-third [87]. In another series, one-third of patients with psJIA still required disease-modifying antirheumatic drug (DMARD) therapy during a follow-up period of at least 15 years [88].

Data on the outcomes of patients with psJIA who have axial arthritis are limited. Axial disease in adults with PsA tends to run a milder course than in those with ankylosing spondylitis [89]. However, this may be overshadowed in children by the early onset of disease, as children with ankylosing spondylitis do accumulate more joint damage compared with adults [28].

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Juvenile idiopathic arthritis" and "Society guideline links: Uveitis".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Psoriatic arthritis in children (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Psoriatic juvenile idiopathic arthritis – Psoriatic juvenile idiopathic arthritis (psJIA), or alternately juvenile psoriatic arthritis (JPsA), is a relatively common subtype of JIA. Its clinical presentation can be highly variable: frank cutaneous psoriasis is not always evident, and the extent of articular involvement may vary from mild enthesitis to polyarticular involvement of multiple axial and peripheral joints. (See "Psoriatic juvenile idiopathic arthritis: Epidemiology, clinical manifestations, and diagnosis" and "Classification of juvenile idiopathic arthritis".)

●Treatment – Treatment of psJIA is highly dependent on the extent and degree of joint involvement (eg, axial versus peripheral arthritis, mild versus severe disease) and specific disease manifestations (eg, uveitis). The basic treatment algorithm of psJIA is similar to that employed in other subtypes of JIA, with a few exceptions. (See 'General approach to treatment' above.)

•Initial therapy – Initial therapy for most patients involves a nonsteroidal antiinflammatory drug (NSAID) and, for patients with arthritis in ≤2 large- to medium-sized joints, intraarticular (IA) glucocorticoid injections (algorithm 1 and table 1) (see 'NSAIDs for most patients' above and 'Intraarticular glucocorticoids' above). Other therapies are added for certain patient groups:

-csDMARDs for patients with moderate to severe peripheral arthritis – In most patients with psJIA who have moderate to severe peripheral arthritis, we suggest starting a conventional synthetic disease-modifying antirheumatic drugs (csDMARD) in addition to an NSAID and/or IA glucocorticoids, rather than using an NSAID and/or IA glucocorticoids alone (Grade 2C). We use methotrexate for most patients. (See 'csDMARDs for most patients with moderate to severe peripheral arthritis' above.)

-TNF inhibitors for patients with high-risk features – In most patients with psJIA who have moderate to severe peripheral arthritis with high-risk features (eg, joint damage, involvement of the cervical spine, temporomandibular joint [TMJ], and/or hip), we start a tumor necrosis factor (TNF) inhibitor in addition to an NSAID and/or IA glucocorticoids, rather than using an NSAID and/or IA glucocorticoids alone or adding a csDMARD (Grade 2C).

•Assessing response to treatment – Clinical remission, typically on medication, is achieved in the majority of patients with psJIA. Patients with psJIA require close clinical monitoring of symptoms and examination findings because laboratory studies may be normal despite ongoing destructive arthritis. (See 'Assessing response to treatment' above and 'Complications and associated conditions' above.)

●Treatment of refractory disease – Patients are considered to have refractory disease if they do not respond to NSAIDs or IA glucocorticoids within four to six weeks or to csDMARDs within eight weeks. Subsequent treatment depends on the specific clinical manifestations (algorithm 2 and table 1). (See 'Treatment of refractory disease' above.)

•Axial arthritis – In most patients with psJIA who have active axial arthritis despite NSAIDs, we suggest adding a TNF inhibitor rather than starting a csDMARD (Grade 1B). Interleukin 17 (IL-17) inhibitors (eg, secukinumab) are an alternative therapy in patients with severe skin psoriasis who do not have comorbid uveitis. (See 'Axial arthritis' above.)

•Peripheral arthritis – In patients without axial arthritis who have active peripheral arthritis despite NSAIDs and/or IA glucocorticoids, we suggest adding a csDMARD rather than starting a biologic (Grade 2C). In patients without axial arthritis who have moderate to severe peripheral arthritis despite csDMARDs, we add a TNF inhibitor or, less commonly, switch to an alternative csDMARD. IL-17 inhibitors (eg, secukinumab) and IL-12/23 inhibitors (eg, ustekinumab) are alternatives to TNF inhibitors in patients with severe skin psoriasis who do not have comorbid uveitis. (See 'Peripheral arthritis' above.)

•Dactylitis – In most patients with psJIA who have persistent dactylitis despite NSAID therapy, we suggest adding a TNF inhibitor rather than a csDMARD (Grade 2C). An alternative option in patients who do not have axial arthritis is adding methotrexate, which may be preferred when the dactylitis is isolated and mild.

●Prognosis – Most patients respond to therapy. Poor outcomes and long-term disability are seen principally in patients who had a long delay in diagnosis and/or in whom effective therapy was not instituted, often through clinician or caregiver reluctance to take the steps necessary to induce remission. (See 'Prognosis' above.)

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Topic 16366 Version 25.0

References

1 : Leg-length discrepancies in monoarticular and pauciarticular juvenile rheumatoid arthritis.

2 : Growth in Still's disease.

3 : Identifying children with chronic arthritis based on chief complaints: absence of predictive value for musculoskeletal pain as an indicator of rheumatic disease in children.

4 : 2019 American College of Rheumatology/Arthritis Foundation Guideline for the Treatment of Juvenile Idiopathic Arthritis: Therapeutic Approaches for Non-Systemic Polyarthritis, Sacroiliitis, and Enthesitis.

5 : Optimal treatment of knee monarthritis in juvenile idiopathic arthritis: a decision analysis.

6 : Trial of early aggressive therapy in polyarticular juvenile idiopathic arthritis.

7 : Methotrexate for ankylosing spondylitis.

8 : 2019 American College of Rheumatology/Arthritis Foundation Guideline for the Treatment of Juvenile Idiopathic Arthritis: Therapeutic Approaches for Non-Systemic Polyarthritis, Sacroiliitis, and Enthesitis.

9 : Disease-modifying antirheumatic drug use in the treatment of juvenile idiopathic arthritis: a cross-sectional analysis of the CARRA Registry.

10 : Therapies for peripheral joint disease in psoriatic arthritis. A systematic review.

11 : Sulfasalazine in the treatment of juvenile chronic arthritis: a randomized, double-blind, placebo-controlled, multicenter study. Dutch Juvenile Chronic Arthritis Study Group.

12 : Sulfasalazine for the management of juvenile rheumatoid arthritis.

13 : Sulfasalazine therapy for psoriatic arthritis: a double blind, placebo controlled trial.

14 : Sulphasalazine in psoriatic arthritis: a randomized, multicentre, placebo-controlled study.

15 : 2021 American College of Rheumatology Guideline for the Treatment of Juvenile Idiopathic Arthritis: Therapeutic Approaches for Oligoarthritis, Temporomandibular Joint Arthritis, and Systemic Juvenile Idiopathic Arthritis.

16 : Therapies for axial disease in psoriatic arthritis. A systematic review.

17 : Chloroquine therapy in psoriatic arthritis.

18 : Patients with juvenile psoriatic arthritis comprise two distinct populations.

19 : 2019 American College of Rheumatology/Arthritis Foundation Guideline for the Screening, Monitoring, and Treatment of Juvenile Idiopathic Arthritis-Associated Uveitis.

20 : The outcomes of juvenile idiopathic arthritis in children managed with contemporary treatments: results from the ReACCh-Out cohort.

21 : C-reactive protein in psoriasis: a review of the literature.

22 : Three Multicenter, Randomized, Double-Blind, Placebo-Controlled Studies Evaluating the Efficacy and Safety of Ustekinumab in Axial Spondyloarthritis.

23 : Detection of inflammatory sacroiliitis in children with magnetic resonance imaging: is gadolinium contrast enhancement necessary?

24 : 2019 Update of the American College of Rheumatology/Spondylitis Association of America/Spondyloarthritis Research and Treatment Network Recommendations for the Treatment of Ankylosing Spondylitis and Nonradiographic Axial Spondyloarthritis.

25 : Children With Enthesitis-Related Arthritis and Possible Benefits From Treatments for Adults With Spondyloarthritis.

26 : Intravenous Golimumab in Patients with Polyarticular Juvenile Idiopathic Arthritis and Juvenile Psoriatic Arthritis and Subcutaneous Ustekinumab in Patients with Juvenile Psoriatic Arthritis: Extrapolation of Data from Studies in Adults and Adjacent Pediatric Populations.

27 : A Randomized, Double-Blind, Placebo-Controlled Multicenter Study of Adalimumab in Pediatric Patients With Enthesitis-Related Arthritis.

28 : Clinical outcomes and progression to orthopedic surgery in juvenile- versus adult-onset ankylosing spondylitis.

29 : Critical appraisal of assessment of structural damage in ankylosing spondylitis: implications for treatment outcomes.

30 : Radiographic findings following two years of infliximab therapy in patients with ankylosing spondylitis.

31 : Efficacy of adalimumab in the treatment of axial spondylarthritis without radiographically defined sacroiliitis: results of a twelve-week randomized, double-blind, placebo-controlled trial followed by an open-label extension up to week fifty-two.

32 : The impact of tumor necrosis factorαinhibitors on radiographic progression in ankylosing spondylitis.

33 : Effect of Therapy on Radiographic Progression in Axial Spondyloarthritis: A Systematic Review and Meta-Analysis.

34 : Secukinumab in enthesitis-related arthritis and juvenile psoriatic arthritis: a randomised, double-blind, placebo-controlled, treatment withdrawal, phase 3 trial.

35 : Secukinumab versus adalimumab for treatment of active psoriatic arthritis (EXCEED): a double-blind, parallel-group, randomised, active-controlled, phase 3b trial.

36 : Secukinumab in patients with psoriatic arthritis and axial manifestations: results from the double-blind, randomised, phase 3 MAXIMISE trial.

37 : Secukinumab, an Interleukin-17A Inhibitor, in Ankylosing Spondylitis.

38 : Secukinumab efficacy in anti-TNF-naive and anti-TNF-experienced subjects with active ankylosing spondylitis: results from the MEASURE 2 Study.

39 : Efficacy, safety, and tolerability of secukinumab in patients with active ankylosing spondylitis: a randomized, double-blind phase 3 study, MEASURE 3.

40 : Ixekizumab, an interleukin-17A antagonist in the treatment of ankylosing spondylitis or radiographic axial spondyloarthritis in patients previously untreated with biological disease-modifying anti-rheumatic drugs (COAST-V): 16 week results of a phase 3 randomised, double-blind, active-controlled and placebo-controlled trial.

41 : Ixekizumab for patients with non-radiographic axial spondyloarthritis (COAST-X): a randomised, placebo-controlled trial.

42 : Aggressive combination drug therapy in very early polyarticular juvenile idiopathic arthritis (ACUTE-JIA): a multicentre randomised open-label clinical trial.

43 : Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial.

44 : Efficacy of ustekinumab in biologic-naïve patients with psoriatic arthritis by prior treatment exposure and disease duration: data from PSUMMIT 1 and PSUMMIT 2.

45 : Efficacy of ustekinumab in biologic-naïve patients with psoriatic arthritis by prior treatment exposure and disease duration: data from PSUMMIT 1 and PSUMMIT 2.

46 : Risankizumab, an IL-23 inhibitor, for ankylosing spondylitis: results of a randomised, double-blind, placebo-controlled, proof-of-concept, dose-finding phase 2 study.

47 : Enthesitis as a component of dactylitis in psoriatic juvenile idiopathic arthritis: histology of an established clinical entity.

48 : Scintigraphic detection of TNF-driven inflammation by radiolabelled certolizumab pegol in patients with rheumatoid arthritis and spondyloarthritis.

49 : Methotrexate Efficacy in the Tight Control in Psoriatic Arthritis Study.

50 : GO-DACT: a phase 3b randomised, double-blind, placebo-controlled trial of GOlimumab plus methotrexate (MTX) versus placebo plus MTX in improving DACTylitis in MTX-naive patients with psoriatic arthritis.

51 : Etanercept and Methotrexate as Monotherapy or in Combination for Psoriatic Arthritis: Primary Results From a Randomized, Controlled Phase III Trial.

52 : Effect of certolizumab pegol on signs and symptoms in patients with psoriatic arthritis: 24-week results of a Phase 3 double-blind randomised placebo-controlled study (RAPID-PsA).

53 : Efficacy and safety of ustekinumab in psoriatic arthritis patients with peripheral arthritis and physician-reported spondylitis: post-hoc analyses from two phase III, multicentre, double-blind, placebo-controlled studies (PSUMMIT-1/PSUMMIT-2).

54 : Secukinumab improves active psoriatic arthritis symptoms and inhibits radiographic progression: primary results from the randomised, double-blind, phase III FUTURE 5 study.

55 : Apremilast monotherapy in DMARD-naive psoriatic arthritis patients: results of the randomized, placebo-controlled PALACE 4 trial.

56 : Tofacitinib or Adalimumab versus Placebo for Psoriatic Arthritis.

57 : Effectiveness of steroid injection for hand psoriatic dactylitis: results from a multicentre prospective observational study.

58 : Childhood psoriasis: a clinical review of 1262 cases.

59 : Predictors of Relapse after Discontinuing Systemic Treatment in Childhood Autoimmune Chronic Uveitis.

60 : Treatment of active ankylosing spondylitis with abatacept: an open-label, 24-week pilot study.

61 : Abatacept in children with juvenile idiopathic arthritis: a randomised, double-blind, placebo-controlled withdrawal trial.

62 : Abatacept in the treatment of patients with psoriatic arthritis: results of a six-month, multicenter, randomized, double-blind, placebo-controlled, phase II trial.

63 : Efficacy and safety of abatacept, a T-cell modulator, in a randomised, double-blind, placebo-controlled, phase III study in psoriatic arthritis.

64 : Tofacitinib in juvenile idiopathic arthritis: a double-blind, placebo-controlled, withdrawal phase 3 randomised trial.

65 : Baricitinib in juvenile idiopathic arthritis: an international, phase 3, randomised, double-blind, placebo-controlled, withdrawal, efficacy, and safety trial.

66 : Efficacy and safety of upadacitinib in patients with active ankylosing spondylitis (SELECT-AXIS 1): a multicentre, randomised, double-blind, placebo-controlled, phase 2/3 trial.

67 : Fine-mapping the MHC locus in juvenile idiopathic arthritis (JIA) reveals genetic heterogeneity corresponding to distinct adult inflammatory arthritic diseases.

68 : The Juvenile Psoriatic Arthritis Cohort in the CARRA Registry: Clinical Characteristics, Classification, and Outcomes.

69 : Biological classification of childhood arthritis: roadmap to a molecular nomenclature.

70 : Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor.

71 : Therapeutic benefit of apremilast on enthesitis and dactylitis in patients with psoriatic arthritis: a pooled analysis of the PALACE 1-3 studies.

72 : A Phase III Randomized Study of Apremilast, an Oral Phosphodiesterase 4 Inhibitor, for Active Ankylosing Spondylitis.

73 : 2021 American College of Rheumatology Guideline for the Treatment of Juvenile Idiopathic Arthritis: Recommendations for Nonpharmacologic Therapies, Medication Monitoring, Immunizations, and Imaging.

74 : Nonsteroidal antiinflammatory drugs reduce radiographic progression in patients with ankylosing spondylitis: a randomized clinical trial.

75 : Effect of continuous versus on-demand treatment of ankylosing spondylitis with diclofenac over 2 years on radiographic progression of the spine: results from a randomised multicentre trial (ENRADAS).

76 : Nonsteroidal Antiinflammatory Drug Use and Association With Incident Hypertension in Ankylosing Spondylitis.

77 : Dose Tapering and Discontinuation of Biologic DMARDs in Axial Spondyloarthritis: A Narrative Review (2023 SPARTAN Annual Meeting Proceedings).

78 : Effect of Half-Dose vs Stable-Dose Conventional Synthetic Disease-Modifying Antirheumatic Drugs on Disease Flares in Patients With Rheumatoid Arthritis in Remission: The ARCTIC REWIND Randomized Clinical Trial.

79 : Impact of medication withdrawal method on flare-free survival in patients with juvenile idiopathic arthritis on combination therapy.

80 : Prevention of disease flares by risk-adapted stratification of therapy withdrawal in juvenile idiopathic arthritis: results from the PREVENT-JIA trial.

81 : Disease Recapture Rates After Medication Discontinuation and Flare in Juvenile Idiopathic Arthritis: An Observational Study Within the Childhood Arthritis and Rheumatology Research Alliance Registry.

82 : Joint-Specific Memory and Sustained Risk for New Joint Accumulation in Autoimmune Arthritis.

83 : Disease progression into adulthood and predictors of long-term active disease in juvenile idiopathic arthritis.

84 : Subpopulations within juvenile psoriatic arthritis: a review of the literature.

85 : A decade of progress in juvenile idiopathic arthritis treatments and outcomes in Canada: results from ReACCh-Out and the CAPRI registry.

86 : Psoriasis and associated variables in classification and outcome of juvenile idiopathic arthritis - an eight-year follow-up study.

87 : Juvenile psoriatic arthritis: followup and evaluation of diagnostic criteria.

88 : Juvenile psoriatic arthritis: longterm outcome and differentiation from other subtypes of juvenile idiopathic arthritis.

89 : Axial Disease in Psoriatic Arthritis study: defining the clinical and radiographic phenotype of psoriatic spondyloarthritis.