INTRODUCTION — Peripheral spondyloarthritis (SpA) is the term for patients with features of SpA whose symptoms and findings are predominantly or entirely peripheral rather than axial; these features include arthritis, which is predominantly of the lower limbs and/or asymmetric; enthesitis; and dactylitis. Some patients with peripheral SpA also have a current or past history of back pain, but the back pain is not the predominant feature.
Patient groups with peripheral SpA include those with psoriatic arthritis (PsA), reactive arthritis, SpA related to inflammatory bowel disease (IBD; Crohn disease and ulcerative colitis), and a subset of patients with these manifestations who do not meet established definitions for one of these three forms of SpA. Patients with predominantly axial SpA, such as ankylosing spondylitis and nonradiographic axial SpA, are not included within the peripheral SpA category, regardless of whether peripheral manifestations of musculoskeletal involvement, which may be seen in some patients with axial SpA, are also present [1,2].
A clear distinction between the clinically defined subsets of patients with peripheral SpA is often lacking. As examples, in a number of patients, skin manifestations of psoriasis do not occur until after the manifestation of rheumatic symptoms; preceding infections in patients with a reactive arthritis may be clinically asymptomatic (as an example, with chlamydia); and IBD can also be asymptomatic when patients present with musculoskeletal symptoms [3,4].
An overview of the treatment of peripheral SpA in adults will be presented here. The clinical manifestations and diagnosis of peripheral SpA; the classification of SpA; and the clinical manifestations, diagnosis, and treatment of ankylosing spondylitis, nonradiographic axial SpA, PsA, reactive arthritis, arthritis associated with IBD, and SpA in children are discussed in more detail separately. (See "Clinical manifestations and diagnosis of peripheral spondyloarthritis in adults" and "Overview of the clinical manifestations and classification of spondyloarthritis" and "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults" and "Diagnosis and differential diagnosis of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults" and "Clinical manifestations and diagnosis of psoriatic arthritis" and "Spondyloarthritis in children" and "Reactive arthritis" and "Treatment of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults" and "Clinical manifestations and diagnosis of arthritis associated with inflammatory bowel disease and other gastrointestinal diseases".)
GENERAL PRINCIPLES — The ultimate treatment goal in all patients with peripheral spondyloarthritis (SpA) is to optimize short- and long-term health-related quality of life, which is accomplished through use of a combination of nonpharmacologic and pharmacologic treatments to control inflammation, prevent structural damage to the joints, and preserve function and social participation. Collaborative ("shared") decision-making by the patient and clinician is especially important in establishing specific treatment goals and making choices between therapeutic options [5]. (See 'Nonpharmacologic and preventive therapies' below and 'Pharmacotherapy' below and 'Monitoring' below.)
Most patients benefit from care by an expert in rheumatologic disease, such as a rheumatologist, and care should be coordinated with appropriate specialists depending upon the clinical features, such as a dermatologist for psoriasis, gastroenterologist for inflammatory bowel disease (IBD; Crohn disease and ulcerative colitis), or an ophthalmologist with expertise in uveitis.
There are relatively limited data that directly address the treatment of peripheral SpA; treatment of peripheral SpA that is not associated specifically with psoriasis, IBD, or an infection has been the subject of only a few randomized trials, all involving tumor necrosis factor (TNF) inhibitors [6-9]. Further but indirect evidence regarding treatment of patients with peripheral SpA has been provided by trials of a range of agents directed against a variety of targets in patients with axial SpA and psoriatic arthritis (PsA) [5,10]. (See 'Pharmacotherapy' below.)
An overview of our approach to the management of peripheral SpA is provided here. The respective treatment approaches for patients with peripheral SpA specifically within the context of PsA, IBD (Crohn disease and ulcerative colitis), and reactive arthritis are described in more detail separately. (See "Treatment of psoriatic arthritis" and "Treatment of arthritis associated with inflammatory bowel disease", section on 'Treatment approach' and "Reactive arthritis", section on 'Treatment'.)
NONPHARMACOLOGIC AND PREVENTIVE THERAPIES — The following issues are of importance in the treatment of peripheral spondyloarthritis (SpA) in addition to drug therapy [10]:
●Exercise, physical therapy, and occupational therapy – Patients should be referred for physical and occupational therapy, encouraged to exercise, referred as needed for orthotics, and educated about joint protection.
●General health and lifestyle issues – Attention to general health issues and comorbidities that are common in SpA, especially obesity and metabolic syndrome, is important for patients with peripheral SpA [11,12]. Patients with obesity (class I or greater, with body mass index [BMI] ≥30 kg/m2) and psoriatic arthritis (PsA) had higher disease activity and showed a diminished response and adherence to tumor necrosis factor (TNF) inhibitors compared with patients who were not obese [13]. Patients should be counseled about proper eating habits and referred to nutritionists for further counseling if appropriate. (See "Obesity in adults: Overview of management".)
●Patient education – Patients should be educated as to the nature of their condition and the importance of follow-up for appropriate management of comorbidities. Smoking cessation should be advised because cigarette smoking is generally believed to have an adverse effect on SpA, in addition to its adverse effects upon cardiovascular risk and other aspects of health [14]. Patients may also benefit from screening for depression, participation in patient support groups, and arthritis self-help programs. (See "Overview of smoking cessation management in adults" and "Screening for depression in adults".)
Patients should be instructed about their medications and the proper use of topical and oral medications, as well as the need for regular drug administration and monitoring of disease activity and for side effects of therapies. Preventive measures (eg, screening for latent tuberculosis, administration of immunizations) that are appropriate for the individual medications being used are important components of treatment for all patients.
PHARMACOTHERAPY — Choice of therapy is based upon the selection of agents that will be effective alone or in combination for the clinical manifestations that are present in a given patient. Most patients with peripheral spondyloarthritis (SpA) have peripheral arthritis [1], and most of the treatments for the different clinical manifestations overlap, but some are more effective for one or another feature. Treatment options for the manifestations of arthritis, enthesitis, and dactylitis can differ [15,16]; therefore, these manifestations are discussed separately. (See 'Arthritis' below and 'Enthesitis' below and 'Dactylitis' below and 'Back pain' below.)
Treatment choices, particularly the use of biologic therapies such as a tumor necrosis factor (TNF) inhibitor, may also be influenced by the presence of findings of another disease associated with peripheral SpA that may require one of these agents, such as psoriasis, inflammatory bowel disease (IBD; Crohn disease and ulcerative colitis), and uveitis. (See 'Extraarticular manifestations' below.)
Use of TNF inhibitors, interleukin (IL) 17 inhibitors, and Janus kinase (JAK) inhibitors in peripheral SpA would be considered as "off-label" by regulatory bodies in the United States and the European Union, unless patients also have active axial SpA, psoriasis, or active IBD, which are among the US Food and Drug Administration (FDA)- and European Medicines Agency (EMA)-approved indications for these agents. Similarly, some TNF inhibitors have received regulatory approval for uveitis by the FDA and the EMA as well, but not for the SpA-typical anterior uveitis. These regulatory factors may limit the availability of certain agents, depending upon the patient's particular diagnosis [16].
Arthritis
Initial therapy — In patients with mild arthritis, we suggest treatment with nonsteroidal antiinflammatory drugs (NSAIDs), for example, naproxen 500 mg twice daily or celecoxib 200 mg twice daily. Patients with a limited number of swollen joints (up to three) amenable to arthrocentesis and joint injection may benefit from intraarticular glucocorticoid injections [17-21]. (See "Joint aspiration or injection in adults: Technique and indications" and "Intraarticular and soft tissue injections: What agent(s) to inject and how frequently?" and "Joint aspiration or injection in adults: Complications".)
In patients with arthritis of greater severity that does not respond adequately to trials of at least two different NSAIDs alone lasting two to four weeks each, and if appropriate to local glucocorticoid injections, we suggest a low to moderate dose of a daily oral glucocorticoid (eg, prednisone begun at 10 to 20 mg once daily, depending upon severity, tapered to 5 to 7.5 mg daily after a significant reduction in signs and symptoms, then tapered off after several weeks). However, there are no clinical trials to guide the dose or the duration, which should be individualized to employ the lowest dose for the shortest time necessary to alleviate signs and symptoms of inflammation [17-22]. We prefer to use glucocorticoids, whenever possible, only as a temporary "bridge therapy" until disease control is achieved with a disease-modifying antirheumatic drug (DMARD) or until spontaneous remission. (See 'Resistant to initial therapy' below.)
Resistant to initial therapy — In patients without an adequate response to initial therapy (ie, those who have active arthritis despite a two-week trial of each of two different NSAIDs), we suggest a nonbiologic conventional DMARD, such as sulfasalazine (SSZ; 2 to 3 g daily), methotrexate (MTX; up to 25 mg once weekly), or leflunomide (LEF; 20 mg daily) [18-21]. The choice of agent depends upon comorbidities and clinician and patient preference. These agents are also appropriate for those with recurrent disease activity following intraarticular administration of glucocorticoids, despite ongoing NSAIDs, and patients who require sustained systemic therapy with moderate- or higher-dose glucocorticoids (prednisone at greater than 5 to 7.5 mg daily), as well as patients with NSAID intolerance.
Although these nonbiologic DMARDs are similar with respect to their effectiveness for treating peripheral arthritis, in patients with concomitant psoriasis, we prefer MTX and, to a lesser extent, LEF or SSZ; MTX and LEF [15,16,23] may be of some benefit for the skin disease. SSZ is not effective for psoriatic skin involvement. However, we prefer SSZ in patients with features of IBD.
A trial with any one of these drugs usually lasts at least two to three months. The precautions, dosing, and adverse effects of these agents when used for the treatment of inflammatory arthritis are described in detail separately. (See "Sulfasalazine: Pharmacology, administration, and adverse effects in the treatment of rheumatoid arthritis" and "Use of methotrexate in the treatment of rheumatoid arthritis" and "Major side effects of low-dose methotrexate" and "Pharmacology, dosing, and adverse effects of leflunomide in the treatment of rheumatoid arthritis".)
Evidence supporting the use of nonbiologic DMARDs in patients with SpA is described separately. The use of SSZ in peripheral SpA is supported by evidence of benefit in patients with reactive arthritis, psoriatic arthritis (PsA), and peripheral arthritis in ankylosing spondylitis (see "Treatment of psoriatic arthritis"). Support for the use of MTX and LEF is provided by evidence of benefit in PsA. (See "Treatment of psoriatic arthritis".)
Resistant to nonbiologic DMARD
TNF inhibitor therapy — In patients with peripheral arthritis resistant to nonbiologic DMARD therapy (after trials of either one or two agents, depending upon regulatory and payor requirements), we suggest a biologic DMARD, usually one of the TNF inhibitors (eg, adalimumab 40 mg every two weeks, golimumab 50 mg every four weeks, or etanercept 50 mg every week) [6-9,16]. Alternative agents include infliximab and certolizumab, although no randomized controlled trials have been done with these agents in peripheral SpA. The dosing, precautions, and adverse effects of these agents are described in detail separately. (See "Treatment of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'TNF inhibitors' and "Treatment of psoriatic arthritis".)
The TNF inhibitors are also used instead of conventional nonbiologic DMARDs in patients who require them for control of extraarticular manifestations of their condition, such as moderate to severe psoriasis or IBD, and TNF inhibitors are also effective for the reduction of concomitant flares of anterior uveitis. Among TNF inhibitors, the effectiveness against anterior uveitis is lowest with the soluble TNF receptor etanercept; thus, in patients with uveitis, we prefer agents that are monoclonal antibodies, such as infliximab and adalimumab [17,24,25]. Biologic agents are usually not required in patients with reactive arthritis because the condition is self-limited in most patients. (See "Reactive arthritis", section on 'Treatment'.)
TNF inhibitors and other biologic DMARDs have proven beneficial in multiple randomized trials for peripheral arthritis in PsA, as described in detail separately (see "Treatment of psoriatic arthritis"). In addition, three randomized trials have shown significant benefit with the TNF inhibitor adalimumab in patients with non-psoriatic peripheral SpA [6-8]. In one trial involving 165 patients with active non-psoriatic peripheral SpA (by Assessment of SpondyloArthritis International Society [ASAS] criteria) and an inadequate response to or intolerance of NSAIDs, adalimumab (40 mg every two weeks) was significantly more likely compared with placebo to result in at least 40 percent improvement in a composite clinical endpoint at 12 weeks (39 versus 20 percent of patients) [6]. Similarly, in a randomized trial involving a total of only 40 patients, significant benefit with adalimumab, compared with placebo, was also demonstrated by several indices after 12 weeks [7]; the discontinuation of the TNF inhibitor after 12 or 24 weeks resulted in a relapse in 73 percent of patients within 16 weeks (mean of 10 weeks) [26]. The mean duration of disease in the above two studies was approximately seven years.
A third study evaluated the usefulness of the TNF inhibitor golimumab, compared with placebo, in a randomized trial of 60 patients with very early peripheral SpA [8]. Unlike the previous two studies with TNF inhibitors, the pretrial symptom duration of these patients was <12 weeks. Remission, defined as complete absence of peripheral arthritis, enthesitis, and dactylitis, was achieved more frequently at weeks 12 and 24 with golimumab (70 to 75 percent) than with placebo (15 to 20 percent). Fifty percent of patients who entered remission remained symptom-free after 2.4 to 5.8 years [27]. The use of MTX after discontinuation of golimumab did not prevent relapses [28]. Unlike the two previous adalimumab trials in patients with peripheral SpA, this golimumab trial also included patients with PsA.
Alternatives to TNF inhibitors — The choice of other biologic agents or targeted synthetic DMARDs, such as IL-17 inhibitors or JAK inhibitors, depends upon the presence or absence of clinical features other than peripheral SpA and limitations due to regulatory requirements and cost.
In patients with peripheral SpA with an inadequate response to NSAIDs and conventional nonbiologic DMARDs, in whom axial symptoms are present, the anti-IL-17A monoclonal antibodies secukinumab and ixekizumab are additional treatment alternatives. In the United States and the European Union, secukinumab and ixekizumab are available for the treatment of ankylosing spondylitis and PsA and seem to be beneficial for peripheral SpA manifestations as well [29,30]. The use and efficacy of secukinumab and ixekizumab in such patients are described in detail separately. The JAK inhibitors tofacitinib and upadacitinib are alternatives to TNF and IL-17A inhibitors. (See "Treatment of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults".)
In patients with peripheral SpA in the presence of psoriasis and after failure of at least one conventional nonbiologic DMARD, alternative agents we use, if needed, are any of the several medications available for the treatment of PsA. These include the phosphodiesterase-4 inhibitor apremilast; the JAK inhibitors tofacitinib and upadacitinib; and the IL-12/23 inhibitor ustekinumab. These agents have not been formally evaluated in patients with non-psoriatic peripheral SpA, but may be beneficial, as indicated by the evidence in patients with PsA and, in our experience, in other patients with these clinical manifestations of peripheral SpA. The use and efficacy of these agents is described in detail separately. (See "Treatment of psoriatic arthritis".)
Enthesitis — In patients with enthesitis, such as Achilles tendinopathy or plantar fasciitis, we use an NSAID as the initial therapeutic agent. Conventional nonbiologic DMARDs are generally ineffective for enthesitis [18-21]. As an alternative or in addition to NSAIDs, local peritendinous glucocorticoid injections may benefit patients with enthesitis (eg, at the greater trochanter or plantar fascia), although injection of the Achilles tendon should be avoided due to greater risk of tendon rupture, and many experts also avoid injection in the regions of the patellar and quadriceps tendons because of risk of tendon rupture in these locations as well [17]. For the same reason (risk of tendon rupture with glucocorticoid injection), retrocalcaneal bursitis should be injected under ultrasound guidance [31]. (See "Intraarticular and soft tissue injections: What agent(s) to inject and how frequently?".)
In patients in whom treatment with NSAIDs and/or local glucocorticoid injections are inadequate, we use a biologic agent, usually a TNF inhibitor, based upon the available but limited randomized trial data, clinical experience, and expert opinion in patients with non-psoriatic forms of peripheral SpA [6,8,9].
One randomized trial of adalimumab in patients with non-psoriatic peripheral SpA found that adalimumab was superior to placebo in decreasing the enthesitis count, a clinical measure based upon the number of tender entheses [6]. Another randomized trial investigated the effect of etanercept, compared with placebo, on heel enthesitis (confirmed by inflammation seen on magnetic resonance imaging [MRI]) over 12 weeks of treatment in patients with peripheral SpA, including patients with psoriasis, and showed superiority of etanercept over placebo [9]. Two-thirds of the patients treated with etanercept showed more than 50 percent improvement compared with 8.3 percent in the placebo group.
More evidence in support of these agents is provided by subgroup analyses of clinical trials involving patients with PsA [19-21] or axial SpA [32]. In PsA, pooled analysis showed that TNF inhibitors have the same efficacy against enthesitis as anti-IL-17 inhibitors and the anti-IL-12/23 antibody ustekinumab [33].
We do not use SSZ or MTX for treatment of enthesitis alone in patients with peripheral SpA. In a 2014 systematic review of treatments for enthesitis in patients with PsA, SSZ was noted not to be effective, and neither MTX nor local injections of glucocorticoids were found to have been studied adequately [34]. Benefit was reported in trials of several TNF inhibitors, including infliximab, golimumab, and certolizumab. Enthesitis in patients with PsA can also be treated with apremilast, secukinumab, ixekizumab, ustekinumab, tofacitinib, and upadacitinib. (See "Treatment of psoriatic arthritis".)
Dactylitis — Other than when associated with PsA, dactylitis is uncommon in patients with peripheral SpA. We use NSAIDs as initial therapy. Dactylitis usually becomes less painful with time, and we would generally not use a biologic agent for dactylitis alone. In those patients with dactylitis who require additional treatment because of pain, we use a biologic agent such as a TNF inhibitor rather than a conventional nonbiologic DMARD. The Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) 2015 recommendations also stated that local glucocorticoid injections could be considered for this manifestation [18,35].
We do not use SSZ, MTX, and LEF for treatment of dactylitis alone in patients with peripheral SpA. The best evidence regarding treatment of dactylitis comes from PsA. Dactylitis is a hallmark of PsA. In a systematic review of dactylitis associated with PsA, SSZ and LEF were noted to be ineffective, while several biologic agents, including the TNF inhibitors infliximab and certolizumab and the IL-12/23 inhibitor ustekinumab were found likely to be effective [33,36]. Also, secukinumab and ixekizumab and the JAK inhibitors tofacitinib and upadacitinib have been proven beneficial for dactylitis in patients with PsA [29,30,37,38]. (See "Treatment of psoriatic arthritis".)
Back pain — In patients with accompanying axial symptoms, NSAIDs should be used as first-line treatment as in patients with axial SpA. If NSAIDs are inadequate for treatment of axial involvement alone, we do not use conventional synthetic DMARDs such as SSZ, MTX, and LEF. We prefer a TNF inhibitor for such patients. In patients in whom one or two TNF inhibitors are inadequate or not tolerated, we prefer an anti-IL-17 antibody or a JAK inhibitor. The treatment of axial SpA is described in detail separately. (See "Treatment of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults" and "Treatment of psoriatic arthritis" and "Treatment of arthritis associated with inflammatory bowel disease", section on 'Management of spondylitis and sacroiliitis'.)
Extraarticular manifestations — Extraarticular manifestations, such as psoriasis, uveitis, and IBD, should be managed in collaboration with the appropriate respective specialists and may influence the choice of therapies. (See "Treatment of psoriasis in adults" and "Uveitis: Treatment" and "Overview of the medical management of mild (low risk) Crohn disease in adults" and "Overview of medical management of high-risk, adult patients with moderate to severe Crohn disease" and "Medical management of low-risk adult patients with mild to moderate ulcerative colitis" and "Management of the hospitalized adult patient with severe ulcerative colitis".)
MONITORING — Patients should be followed regularly for monitoring of disease activity and medication safety. The frequency of visits and laboratory assessment depend upon disease activity, the response to therapy, and the risks of the medications being used. We follow patients with higher levels of disease activity at least monthly and patients with well-controlled disease on medical therapy every three to six months.
Our assessment includes:
●Clinical assessment – Clinical assessment should include a focused history and examination directed at the patient's known manifestations and screening for other features associated with peripheral spondyloarthritis (SpA). Because of the paucity of information regarding long-term outcomes in patients with peripheral SpA (see 'Prognosis' below), patients should be monitored carefully for signs of the development of psoriasis, Crohn disease/ulcerative colitis, axial SpA, and the diseases included in the differential diagnosis of peripheral SpA. (See "Clinical manifestations and diagnosis of peripheral spondyloarthritis in adults", section on 'Clinical manifestations' and "Clinical manifestations and diagnosis of peripheral spondyloarthritis in adults", section on 'Peripheral SpA subgroups' and "Clinical manifestations and diagnosis of peripheral spondyloarthritis in adults", section on 'Differential diagnosis'.)
●Global assessment measures and composite indices – Unlike axial SpA, there are no preferred indices for monitoring disease activity in peripheral SpA. Frequently, the non-disease-specific parameters of the patient's global assessment of well-being and global assessment of pain over the past week, as well as the clinician's global assessment of current disease activity, are used in practice. Disease-specific measures such as the Disease Activity Index for Psoriatic Arthritis (DAPSA) score and Psoriatic Arthritis Disease Activity Score (PASDAS) developed for psoriatic arthritis and the Ankylosing Spondylitis Disease Activity Score (ASDAS) calculated using the C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR) developed for axial SpA [39] also perform well [40]. Among the three, the ASDAS calculator is accessible at the Assessment of SpondyloArthritis International Society (ASAS) website and can be downloaded as an app, together with information regarding its use and interpretation.
●Musculoskeletal examination – In all patients, we also monitor joint, heel, and digital swelling, including the number and severity of the affected areas. Patients with involvement of lower extremities will have difficulties ambulating. This can serve as another index of disease severity.
●Laboratory measures – In those patients with elevated CRP or ESR, these measures can serve as laboratory parameters for disease activity. Other laboratory measures may be required for monitoring of drug safety.
PROGNOSIS — The disease outcomes in peripheral spondyloarthritis (SpA) associated with psoriasis, inflammatory bowel disease (IBD; Crohn disease and ulcerative colitis), and reactive arthritis are discussed in detail separately (see "Clinical manifestations and diagnosis of arthritis associated with inflammatory bowel disease and other gastrointestinal diseases" and "Reactive arthritis", section on 'Prognosis' and "Treatment of psoriatic arthritis"). There is a paucity of information regarding the prognosis of patients with peripheral SpA that is not associated with one of these three conditions.
Peripheral SpA is often a chronic disease, although there are probably more spontaneous remissions in patients with peripheral SpA with reactive arthritis than with other forms of SpA, including psoriatic arthritis (PsA) [41]. Among 165 patients with active peripheral SpA enrolled in a clinical trial of a tumor necrosis factor (TNF) inhibitor and who had not responded adequately to either nonsteroidal antiinflammatory drugs (NSAIDs) or nonbiologic disease-modifying antirheumatic drugs (DMARDs), the mean duration of symptoms at the time of entry of the trial was six to eight years. This would suggest that peripheral SpA is a chronic disease [6]; however, patients with a shorter and more benign course of their disease might not have been included in this trial. More long-term data are needed. For patients whose disease activity was suppressed by the TNF inhibitor adalimumab, discontinuation of adalimumab after 12 or 24 weeks of therapy usually led to a relapse within two to three months [26].
Some evidence also suggests that patients with SpA, including peripheral SpA, may be at increased risk of cardiovascular disease, particularly in association with chronic disease that is poorly controlled. (See "Clinical manifestations and diagnosis of psoriatic arthritis", section on 'Comorbidities' and "Clinical manifestations of axial spondyloarthritis (ankylosing spondylitis and nonradiographic axial spondyloarthritis) in adults", section on 'Cardiovascular disease'.)
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: Spondyloarthritis".)
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.)
●Beyond the Basics topics (see "Patient education: Reactive arthritis (Beyond the Basics)" and "Patient education: Axial spondyloarthritis, including ankylosing spondylitis (Beyond the Basics)" and "Patient education: Psoriatic arthritis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●The ultimate treatment goal in patients with peripheral spondyloarthritis (SpA) is to optimize health-related quality of life through the use of a combination of nonpharmacologic and pharmacologic treatments to control inflammation, prevent structural damage to the joints, and preserve function, social participation, and other quality-of-life outcomes. Patients benefit from care by an expert in rheumatologic disease, such as a rheumatologist, and care should be coordinated with appropriate specialists (eg, dermatologists in patients with psoriatic arthritis [PsA]), depending upon the other clinical features that are present. (See 'General principles' above.)
●Choice and target of therapy should be individualized, based upon disease manifestations, comorbidities, and patient and clinician preferences. Usually, choice of therapy is based upon the selection of agents that will be effective alone or in combination for the clinical manifestations that are present in a given patient. The specific management strategies for peripheral SpA in the context of PsA, inflammatory bowel disease (IBD; Crohn disease and ulcerative colitis), and reactive arthritis are described in more detail separately. (See 'Pharmacotherapy' above and 'General principles' above and "Treatment of psoriatic arthritis" and "Treatment of arthritis associated with inflammatory bowel disease", section on 'Treatment approach' and "Reactive arthritis", section on 'Treatment'.)
●In patients with mild arthritis, we initiate treatment with nonsteroidal antiinflammatory drugs (NSAIDs). Patients with a limited number of swollen joints amenable to arthrocentesis and joint injection may benefit from intraarticular glucocorticoid injections. In patients in whom these measures are inadequate to control the arthritis, we use a low to moderate dose of daily oral glucocorticoids (eg, prednisone started at a dose of 10 to 20 mg daily, depending upon disease severity). (See 'Initial therapy' above.)
●In patients with peripheral arthritis that responds inadequately to NSAIDs, intraarticular glucocorticoids, and low-dose oral glucocorticoids, we suggest a nonbiologic disease-modifying antirheumatic drug (DMARD), such as sulfasalazine (SSZ; 2 to 3 g daily), methotrexate (MTX; up to 25 mg once weekly), or leflunomide (LEF; 20 mg daily), rather than a biologic DMARD (Grade 2C). The choice of agent depends upon comorbidities and clinician and patient preference. (See 'Resistant to initial therapy' above.)
●In patients with peripheral arthritis resistant to nonbiologic DMARD therapy (after trials of either one or two agents, depending upon regulatory and payer requirements), we switch to a biologic DMARD. We generally prefer one of the tumor necrosis factor (TNF) inhibitors (ie, adalimumab, golimumab, certolizumab, etanercept, or infliximab, used in the same doses as in other forms of SpA) as the initial biologic agent in this setting. Alternative choices include the interleukin (IL) 17 inhibitors (secukinumab and ixekizumab) and the Janus kinase (JAK) inhibitors (tofacitinib and upadacitinib). (See 'Resistant to nonbiologic DMARD' above and 'TNF inhibitor therapy' above and 'Alternatives to TNF inhibitors' above.)
●In patients with enthesitis, such as Achilles tendinopathy or plantar fasciitis, we suggest an NSAID as the initial therapeutic agent (Grade 2C). Peritendinous glucocorticoid injection may be of benefit in some regions, but should be avoided in others, particularly the Achilles tendon. In patients in whom treatment with NSAIDs and/or local glucocorticoid injections are inadequate, we use a biologic agent such as a TNF inhibitor (as in patients with arthritis), an IL-17 inhibitor, or a JAK inhibitor rather than a conventional DMARD such as SSZ, MTX, or LEF. (See 'Enthesitis' above.)
●In patients with dactylitis, we use NSAIDs as initial therapy. In patients who require treatment for persistent dactylitis resistant to NSAIDs and who need a DMARD for the management of other disease manifestations, we treat with a biologic DMARD, such as a TNF inhibitor (as in patients with arthritis) or an IL-17 inhibitor rather than a conventional nonbiologic DMARD such as SSZ, MTX, or LEF. (See 'Dactylitis' above.)
●Disease activity can be monitored by general measures such as the patient's global assessment of well-being or intensity of pain in the past week and the clinician's global assessment of disease activity or by disease-specific measures developed for PsA and axial SpA. (See 'Monitoring' above.)
