Spondyloarthritis¶

Chapter 374 | Part 11 – Rheumatology & Immunology · Part 11 – Rheumatology & Immunology · Chapter 374

Key Clinical Points¶

Spondyloarthritis (SpA) is a family of immune-mediated inflammatory arthritis disorders characterized by inflammation-induced bone loss coexisting with pathologic new bone formation.
Axial SpA (axSpA) is divided into radiographic (r-axSpA, also known as ankylosing spondylitis [AS]) and nonradiographic (nr-axSpA) based on sacroiliitis grade on plain radiographs.
Peripheral SpA (pSpA) includes psoriatic arthritis, reactive arthritis, IBD-associated arthritis, and undifferentiated SpA.
HLA-B27 is the strongest genetic risk factor for SpA; it is present in 85–90% of r-axSpA and 50–90% of nr-axSpA patients (compared to ~5% in the healthy population).
Inflammatory back pain (IBP) is characterized by insidious onset, improvement with exercise, and worsening with rest, distinguishing it from mechanical back pain.
TNF-α and IL-17 are signature cytokines driving disease across all domains (gut, skin, joint, spine).
Imaging: MRI is sensitive for early active inflammation (osteitis), while X-ray/CT show structural damage (sacroiliitis, syndesmophytes).
Treatment hierarchy: NSAIDs first-line; Biologics (TNFi, IL-17i, IL-23i) or JAK inhibitors for refractory cases.
Red flags for malignancy or infection include fever, weight loss, night pain, history of cancer, or advanced age.

DEFINITION & OVERVIEW¶

• Definition: Spondyloarthritis (SpA) is a family of immune-mediated inflammatory arthritis disorders sharing clinical, genetic, and pathologic characteristics. Recognized by Moll and Wright in 1974 as distinct from rheumatoid arthritis (RA). • Pathologic Hallmark: Inflammation-induced bone loss coexists with pathologic new bone formation at specific sites (sacroiliac joints, anterior spinal ligaments, or entheses in the peripheral skeleton). • Clinical Manifestations: Sacroiliitis, inflammatory spinal lesions, peripheral inflammatory arthritis, enthesitis (inflammation at tendon/ligament attachment), tendonitis, tenosynovitis, and dactylitis ('sausage digits'). • Distinction from RA: SpA is characterized by the absence of rheumatoid factor (RF) and nodules. • Prevalence: The cumulative prevalence of all conditions under SpA is 2–3% of the population. • Classification Spectrum (Table 374-1): • Axial SpA (axSpA): • Radiographic (r-axSpA, also called ankylosing spondylitis [AS]): Sacroiliitis grade 2 (bilateral), or grade 3/4 (unilateral or bilateral). • Nonradiographic (nr-axSpA): Sacroiliitis grade 1 (unilateral or bilateral) or grade 2 (unilateral). • Peripheral SpA (pSpA): • Psoriatic arthritis: Skin/nail involvement usually preceding arthritis, enthesitis, dactylitis. • IBD-associated: Crohn's disease or ulcerative colitis with inflammatory arthritis. • Reactive arthritis: Urethritis, history of infection (Salmonella, Shigella, Yersinia, Campylobacter, Chlamydia), mucosal ulcers, conjunctivitis, keratoderma blennorrhagica. • Undifferentiated peripheral SpA: Enthesitis, dactylitis, family history of SpA, HLA-B27, acute anterior uveitis. • Other conditions: SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis), Acne-associated arthritis, Hidradenitis suppurativa–associated arthritis.

EPIDEMIOLOGY¶

• Gender Distribution: • r-axSpA: 2:1 (Male:Female). • nr-axSpA: 1:1 ratio. • Geographic Variation: Prevalence of axSpA correlates with regional HLA-B27 frequency. In Europe, prevalence increases from south to north (e.g., Spain 0.1% vs. Norway 0.56%). • Prevalence Data: • USA: HLA-B27 ≈ 6%; axSpA 0.9–1.4% (of which 0.5% are AS). • Global axSpA range: 0.02–1.5%. • Risk Factors: • HLA-B27 positive individuals: 5% risk of axSpA. • First-degree relatives of affected individuals (HLA-B27+): 20% risk.

ETIOLOGY & PATHOPHYISIOLOGY¶

• Core Mechanism: Chronic immune-mediated inflammation coupled with structural damage. • Clinical Progression: Early diagnosis leads to a shift from r-axSpA (structural damage) to nr-axSpA. • Ankylosis: Uncontrolled axSpA may lead to complete ankylosis of the sacroiliac joints and the spine, termed 'bamboo spine'. • Genetic Associations (Section 3.1): • HLA-B27: MHC class I allele; strongest risk factor for SpA/axSpA. • Prevalence: 85–90% in r-axSpA; 50–90% in nr-axSpA (vs. ~5% in healthy population). • Mechanism Theories: • Arthritogenic peptide: HLA-B27 presents pathological microbial peptides to CD8+ T cells → cross-reactive human peptides → inflammation/molecular mimicry. • Homodimerization: HLA-27 homodimers interact with KIR3DL2 receptors on T and NK cells → IL-17 production. • UPR/Autophagy: HLA-B27 linked to unfolded protein responses (UPR) and autophagy → release of IL-23. • Subtypes: HLA-B2704 and HLA-B2705 confer risk; HLA-B2706 and HLA-B2709 do not. • Mechanical Stress: • Enthesitis occurs more often in lower limbs due to higher mechanical strain. • Physical labor in AS patients correlates with increased structural damage. • Barrier Integrity & Microbiome: • Loss of gut barrier → translocation of bacteria/microbial peptides (Salmonella, Shigella, Yersinia, Campylobacter, Chlamydia) → immune response. • HLA-B27 individuals show intestinal dysbiosis prior to clinical symptoms. • Cytokine Pathways (Section 3.2): • TNF-α: Produced by macrophages, neutrophils, and T cells; drives inflammation across all domains. • IL-17A: Key driver in axSpA; IL-17A blockade is effective in axSpA but may be limited in certain contexts (e.g., active IBD). • IL-23: Involved in joint and bone remodeling; IL-23i useful for both axSpA and pSpA. • JAK Inhibitors: Block multiple cytokines; effective across all domains of SpA.

CLINICAL FEATURES¶

• Axial Involvement: • Axial skeleton always involved; peripheral joints in 30–40%. • Hips are the most common nonspinal joint affected. • Inflammatory Back Pain (IBP) (Section 4.1): • Definition: Characterized by insidious onset, chronicity (>3 months), and improvement with exercise/worsening with rest. • Comparison (Table 374-4): • Age: IBP (<40–45 years) vs Mechanical (20–65 years). • Morning Stiffness: IBP (>30 min) vs Mechanical (<30 min). • Night Pain: IBP (Yes, usually after midnight) vs Mechanical (No, late day). • Exercise/Activity: IBP (Improves) vs Mechanical (Worsens). • Duration: IBP (Chronic) vs Mechanical (Acute or chronic). • NSAID Response: IBP (>50% relief in 48h) vs Mechanical (Limited). • Extraarticular Manifestations (Section 4.2): • Uveitis: Acute anterior uveitis. • Psoriasis: Skin and nail involvement. • IBD: Crohn's disease or ulcerative colitis. • Renal: IgA nephropathy; AA amyloidosis (late complication). • Cardiac: Conduction abnormalities; aortic valve insufficiency. • Pulmonary: Fibrosis, restrictive lung disease (due to spinal fusion).

DIFFERENTIAL DIAGNOSIS¶

• Mechanical Back Pain: Most common cause of chronic back pain; axSpA is the etiology in only 4–5% of cases. • Red Flags (Rule out malignancy/infection): • Fever, weight loss, night pain, history of cancer, advanced age.

DIAGNOSTIC APPROACH¶

Initial Assessment: Identify Inflammatory Back Pain (IBP) vs Mechanical pain; rule out 'red flags'.
Imaging (X-ray): • Positive for definite sacroiliitis → r-axSpA (Ankylosing Spondylitis).
Clinical Evaluation (if X-ray negative): • Count SpA features (IBP, inflammatory arthritis, uveitis, dactylitis, enthesitis, psoriasis, IBD, family history, NSAID response, high CRP). • ≥ 4 features + compelling clinical picture → nr-axSpA.
Advanced Imaging (if X-ray negative and < 4 features): • MRI of SI joints positive for sacroiliitis → nr-axSpA. • If MRI positive, check for compelling clinical picture or HLA-B27 positivity → nr-axSpA.
Exclusion: • X-ray negative + < 4 features + MRI negative + no HLA-B27/compelling picture → Not axSpA.

Flowchart 1 (Sjögren's Diagnosis): Note: Included as per source material. • Step 1: Identify 'Dry eyes' (duration ≥3 months, recurring sand/gravel sensation, use of tear substitutes >3/day, dry mouth for ≥3 months, or frequent drinking of liquids) OR 'Major salivary gland involvement'. • Path A (Ocular): Unstimulated whole saliva ≤ 0.1 mL/min OR Schirmer’s ≤ 5 mm/hr on at least one eye OR Ocular surface score ≥ 5 (van Bijsterveld) or ≥ 3 (Warnherr). • Path B (Serology/Histopathology): Serum antibodies against Ro antigen OR Minor salivary gland biopsy focus score ≥ 1. • Exclusion Criteria: No diagnosis if history of head/neck radiation, active Hep B/C, AIDS, Sarcoidosis, Myxoidosis, Graft-vs-host disease, or IgG4-related disease.

Flowchart 2 (axSpA Diagnosis): For patients with chronic back pain (>3 months), insidious onset, <50 years old, and common causes ruled out: • Step 1: Is SI joint x-ray positive for definite sacroiliitis? • Yes → AS (r-axSpA). • No → Proceed to Step 2. • Step 2: Are there ≥ 4 SpA features? • Yes → Is the clinical picture compelling? • Yes → Nr-axSpA. • No → Proceed to Step 3 (Note: If no, and <4 features, likely not axSpA). • No (< 4 features) → Proceed to Step 3. • Step 3: Is MRI of SI joints positive for sacroiliitis? • Yes → Is the clinical picture compelling AND/OR is the patient HLA-B27 positive? • Yes → Nr-axSpA. • No → Not axSpA.

MANAGEMENT & TREATMENT¶

Initial Therapy: • NSAIDs: Highest tolerable dose continuously for active disease; as needed if stable. No particular NSAID is preferred.
Stepwise Escalation (if active after 4 weeks of full-dose NSAIDs): • Biologics: • TNFi: Adalimumab (40 mg SC every 2 weeks), Certolizumab pegol (200 mg SC twice/month or 400 mg SC once/month), Golimumab (50 mg SC monthly or 2 mg/kg IV at weeks 0, 4, and then every 8 weeks), Infliximab (5 mg/kg IV at weeks 0, 2, 6, then every 6 weeks). • IL-17i: Secukinumab (150 mg SC at weeks 0, 1, 2, 3, and 4; then 150 or 300 mg every 4 wks), Ixekizumab (160 mg SC once, then 80 mg every 4 wks). • JAKi: Tofacitinib (5 mg oral BID - axSpA only), Upadacitinib (15 mg daily - axSpA and nr-axSpA).
Special Considerations for Biologics: • Uveitis: TNF monoclonal antibodies preferred over soluble receptor TNFi. • IBD: IL-17 inhibitors contraindicated in active IBD; use TNF, IL-12/23i, or JAKi. • Secondary Failure: If first TNFi fails, switch to another TNFi (secondary failure) or a different class (IL-17i or JAKi).
Concomitant Medications (Table 374-5): • Sulfasalazine (up to 3 g/d) and Methotrexate (up to 25 mg/wk) for peripheral joints/entheses only.
Local Treatments: • Glucocorticoid injections for upper extremity enthesitis or intraarticular for peripheral arthritis. • Warning: Do not inject around lower limb weight-bearing entheses (risk of rupture).
Systemic Steroids: Avoid in axSpA; no efficacy shown.
Psoriatic Arthritis Management (Table 374-7): • Goal: Maximize quality of life, stop progression. • Treatment Selection: • If predominant skin disease → IL-12/23, IL-17, or IL-23 inhibitors preferred over TNFi. • If comorbid IBD → TNF, IL-12/23i, or JAKi; avoid IL-17i if active. • If comorbid uveitis → TNF monoclonal antibodies preferred. • Other Agents: • Methotrexate preferred for skin involvement. • PDE-4 or TYK-2 inhibitors may be used for skin/musculoskeletal (except axial). • Abatacept: No efficacy for skin, nail, or axial; modest for peripheral. • Topical glucocorticoids (clobetasol, retinoic acid, PUVA, cyclosporin) for skin/nail.

COMPLICATIONS & PROGNOSIS¶

• Structural Damage: Progression to 'bamboo spine' (complete ankylosis of SI joints and spine). • Functional Impairment: Reduced spinal/neck mobility due to syndesmophytes. • Systemic Complications: • Renal: IgA nephropathy, AA amyloidosis. • Cardiac: Heart blocks, aortic valve insufficiency. • Pulmonary: Fibrosis, restrictive lung disease (due to rib cage changes). • Prognosis: 50% of nr-axSpA progress to r-axSpA over 20 years; <10% develop full bamboo spine.

SPECIAL POPULATIONS¶

• Females: Often misdiagnosed with fibromyalgia due to lower prevalence of HLA-B27 and presentation of back pain/enthesitis. • IBD Patients: Use TNF, IL-12/23i, or JAKi; avoid IL-17i if IBD is active. • Uveitis Patients: Prefer TNF monoclonal antibodies.

KEY PEARLS & HIGH-YIELD POINTS¶

• Diagnosis Rule: AxSpA diagnosis relies on pattern recognition and ruling out common causes (e.g., mechanical back pain). • Imaging Timing: MRI is for early active inflammation; X-ray/CT are for structural changes. • Syndesmophytes: These are 'bridges' of bone between vertebrae, a hallmark of axSpA. • Psoriatic Arthritis (Table 374-6): CASPAR criteria require ≥3 points (e.g., Psoriasis [2], HLA-B27, Dactylitis, etc.). • ASAS Criteria (Table 374-8): Diagnosis of pSpA requires arthritis/enthesitis/dactylitis plus ≥1 of (Psoriasis, IBD, Infection, HLA-B27, Uveitis, Sacroiliitis) OR ≥2 of (Arthritis, Enthesitis, Dactylitis, IBP in past, Family history).

Reference Tables¶

TABLE 374-1 Spectrum of Spondyloarthritis CONDITION Radiographic axSpA (r-axSpA, also called ankylosing spondylitis…¶

Harrison's 22e, p.2880

SPONDYLOARTHRITIS (SPA)
AXIAL SPONDYLOARTHRITIS (axSpA)		PERIPHERAL SPONDYLOARTHRITIS (pSpA)
CONDITION	CLINICAL FEATURES	CONDITION	CLINICAL FEATURES
		Conditions commonly included under pSpA
Radiographic axSpA (r-axSpA, also called ankylosing spondylitis [AS])	Sacroiliitis grade 2 (bilateral), grade 3 or 4 (unilateral or bilateral)	Psoriatic arthritis	Skin psoriasis and nail involvement usually preceding arthritis, enthesitis, dactylitis
Nonradiographic axSpA (nr-axSpA)	Sacroiliitis grade 1 (unilateral or bilateral) or grade 2 (unilateral)	Inflammatory bowel disease–associated arthritis	Crohn’s disease or ulcerative colitis with inflammatory arthritis
		Reactive arthritis	Urethritis, history of preceding infection with Salmonella, Shigella, Yersinia, Campylobacter, and Chlamydia, mucosal ulcers, conjunctivitis, keratoderma blennorrhagica
		Undifferentiated peripheral SpA	Enthesitis, dactylitis, family history of SpA, HLA-B27, acute anterior uveitis, and not fitting in any of the other conditions mentioned above
		SAPHO syndrome
		Acne-associated arthritis
		Hidradenitis suppurativa–associated arthritis

TABLE 374-3 Grading of Sacroiliitis GRADE Grade 0 Grade 1 Grade 2 Grade 3 Grade 4 Source: Reproduced with permission…¶

Harrison's 22e, p.2883

GRADE	DESCRIPTION
Grade 0	Normal
Grade 2	Minimum abnormality (small, localized areas with erosions or sclerosis, without alterations in the joint width)
Grade 4	Severe abnormality (total ankylosis)

TABLE 374-4 Clinical Features of Inflammatory Versus Mechanical Back Pain FEATURE Age at onset Onset Morning stiffness…¶

Harrison's 22e, p.2883

FEATURE	INFLAMMATORY BACK PAIN	MECHANICAL BACK PAIN
Age at onset	Before 40–45 years	20–65 years
	Insidious
Morning stiffness	Prolonged (more than 30 min)	Less than 30 min
	Yes, usually after midnight
Exercise/activity	Improves pain and stiffness	Worsens pain
	Worsens pain and stiffness
Duration	Chronic	Acute or chronic
	More than 50% relief in 48 hours

TABLE 374-2 Modified New York Classification Criteria for Ankylosing Spondylitis (AS) Clinical Criteria 1. Low back…¶

Harrison's 22e, p.2883

Clinical Criteria
1. Low back pain >3 months
Improved with exercise
Not relieved by rest
1. Limited lumbar motion in fontal and lateral planes
1. Reduced chest expansion

TABLE 374-5 Pharmacologic Management of Axial Spondyloarthritis (axSpA) • Nonsteroidal anti-inflammatory drugs (NSAIDs)…¶

Harrison's 22e, p.2887

• Nonsteroidal anti-inflammatory drugs (NSAIDs) should be used in highest tolerable doses continuously in active disease and on an as-needed basis if the disease
is stable. No particular NSAID is preferred over any other. Side effects to monitor are gastric ulcer disease, hypertension, renal insufficiency, and cardiovascular
disease.
• Conventional synthetic DMARDs like sulfasalazine, up to 3 g/d, and methotrexate, up to 25 mg/wk, are useful for the treatment of peripheral joint and entheses
involvement, but not for axial disease in axSpA.
• If the disease remains active despite a 4-week trial of full-dose NSAIDs, treatment should be escalated to start a biologic from either the TNFi or IL-17i class.
• Before initiating therapy with biologics or JAKi, screening for latent tuberculosis, hepatitis B, and hepatitis C should be performed.
• All five TNFi agents are approved for the treatment of AS, while selective TNFis are approved for nr-axSpA in various countries.
• Soluble receptor of TNF–etanercept 50 mg subcutaneous (SC) injection once weekly.
• TNFi monoclonal antibodies:
• Adalimumab 40 mg SC every 2 weeks.
• Certolizumab pegol 200 mg SC twice a month or 400 mg SC once a month.
• Golimumab 50 mg SC once a month or golimumab 2 mg/kg intravenous (IV) at weeks 0, 4, and then every 8 weeks thereafter.
• Infliximab 5 mg/kg IV infusion at weeks 0, 2, 6, and then every 6 weeks.
• No TNFi is preferred, except in patients with concomitant uveitis or IBD in whom TNF monoclonal antibodies are preferred over soluble receptor TNFi therapy.
• In the case of primary failure of TNFi, treatment can be switched to IL-17i or JAKi. In the case of secondary failure of TNFi therapy (failing after initial benefit), an
alternative TNFi can be used.
• Two IL-17Ais are approved for the treatment of nr-axSpA and AS.
• Secukinumab 150 mg SC at weeks 0, 1, 2, 3, and 4, followed by 150 or 300 mg every 4 weeks.
• Ixekizumab 160 mg SC once, followed by 80 mg every 4 weeks.
• In case of primary failure of IL-17Ai, treatment can be switched to TNFi or JAKi. In the case of secondary failure of IL-17Ai therapy, an alternative IL-17i can be used.
• Two JAKis are approved for the treatment of AS, while only one is approved for nr-axSpA. JAKi should be used in patients who have failed TNFi.
• Tofacitinib 5 mg orally two times a day is approved for the treatment of AS only.
• Upadacitinib 15 mg once a day is approved for the treatment of AS and nr-axSpA.
• One IL-17A and IL-17F inhibitor is approved in certain parts of the world to treat both nr-axSpA and radiographic axSpA.
• Bimekizumab 160 mg SC every 4 weeks.
• Local glucocorticoid injections for upper extremity enthesitis or intraarticular injections for peripheral arthritis are indicated. Injections around lower limb weight-
bearing entheses are not recommended because of the risk of rupture.
• Systemic glucocorticoids do not have any efficacy in axSpA and should be avoided.

TABLE 374-6 Classification Criteria for Psoriatic Arthritis (CASPAR) Patients with Inflammatory Articular Disease…¶

Harrison's 22e, p.2889

CATEGORY	DESCRIPTION	POINT VALUE
Psoriasisa	Current psoriasis as determined by a rheumatologist or dermatologist	2
	Personal history of psoriasis obtained from patient or qualified health care provider	1
	A family history of psoriasis as reported by patient in a first- or second-degree relative	1
	Typical psoriatic nail dystrophy (onycholysis, pitting, and hyperkeratosis) present at assessment
Rheumatoid factor	Rheumatoid factor negative	1
	Current dactylitis or history of dactylitis recorded by a rheumatologist
Radiographic evidence	Juxtaarticular new bone formation (excluding osteophyte formation) on plain radiograph of hand or foot; appears as ill- defined ossification near joint margins	1

TABLE 374-7 Pharmacologic Management of Psoriatic Arthritis (PsA)¶

Harrison's 22e, p.2891

PRINCIPLES AND RECOMMENDATIONS
1. The primary goal of treating patients with PsA is to maximize long-term health-related quality of life through control of symptoms, abrogation of inflammation,
  prevention of structural damage, normalization of function, and social participation.
1. PsA requires multidisciplinary treatment (rheumatologist, dermatologist, psychiatrist, gastroenterologist, ophthalmologist, dietician, endocrinologist, cardiologist,
  and physical/occupational therapists), and it should be based on a shared decision-making between the patient and the rheumatologist.
1. “Treat to target” is recommended, with the target being minimal disease activity or remission. Patients should be regularly monitored, and treatment should be
  adjusted appropriately to reach the target.
1. NSAIDs may be used as an initial short-term treatment to relieve symptoms related to peripheral arthritis, enthesitis, dactylitis, and axial disease. NSAIDs alone are
  very rarely sufficient to treat PsA but can be combined with cs-, b-, or tsDMARDs.
1. Local injections of glucocorticoids should be considered for active arthritis, enthesitis, and/or dactylitis. Glucocorticoid injections around lower extremity weight-
  bearing entheses should be avoided due to the risk of tendon rupture.
1. Systemic glucocorticoids should be avoided. In rare circumstances such as acute flares of arthritis, they may be used with caution at the lowest effective dose for
  the shortest period.
1. In patients with active disease with peripheral arthritis, enthesitis, and/or dactylitis, treatment with csDMARDs, such as methotrexate, sulfasalazine, or leflunomide,
  should be considered at an early stage. Methotrexate is preferred if clinically relevant psoriasis is present.
1. PDE-4 inhibitor or TYK-2 inhibitor may be considered as the initial treatment instead of csDMARD for active musculoskeletal disease (except axial disease) or active
  skin disease.
1. In patients with predominant axial disease, csDMARDs should be avoided, and either bDMARDs or JAKi should be considered after inadequate response to
  NSAIDs.
1. I n rare circumstances, in patients with very active musculoskeletal disease (multiple swollen joints, structural damage in the presence of active inflammation, and/
  or clinically relevant extraarticular manifestations such as IBD or uveitis) or extensive skin involvement, treatment with bDMARDs can be started before csDMARDs
  at the discretion of the treating provider.
1. T he choice of initial biologic for active musculoskeletal disease (TNF, IL-12/23, IL-17, or IL-23 inhibitors) should be based on pros and cons of each therapy class,
  patients’ comorbidities, and their comfort with risks/benefit.
1. F or patients with predominant skin disease along with musculoskeletal disease, IL-12/23, IL-17, or IL-23 inhibitors are preferred over TNF inhibitors.
1. F or PsA patients with comorbid IBD, monoclonal antibodies against TNF, IL-12/23 inhibitors, IL-23 inhibitors, or JAKi therapy is preferred. IL-17 inhibitors should be
  avoided in patients with active IBD but can be used in patients with history of IBD.
1. F or PsA patients with comorbid uveitis, therapy with monoclonal antibodies against TNF is preferred.
1. J AKi should be used after failure of TNF inhibitors according to the black-box warning issued by regulatory authorities based on their CV risk. Comorbidities of
  metabolic syndrome and CV disease should be considered before JAKi treatment.
1. Combination of methotrexate with bDMARDs such as TNF inhibitors has not been shown to improve efficacy compared to bDMARDs alone.
1. Abatacept has no efficacy against the disease domains of skin, nail, and the axial skeleton. Its efficacy against peripheral arthritis is modest.
1. A gents that effectively treat skin and nail involvement (but with minimal efficacy on the musculoskeletal domains) include topical glucocorticoids such as
  clobetasol, retinoic acid derivatives, PUVA, and cyclosporin.
1. Biosimilars may be used in place of the original biologics.
1. T apering of DMARDs in a PsA patient with long-term minimal disease activity or remission should be a shared decision. Stopping DMARD therapy is not
  recommended.

TABLE 374-8 Assessment of Spondyloarthritis International Society (ASAS) Criteria for Peripheral Spondyloarthritis…¶

Harrison's 22e, p.2892

Arthritis or enthesitis or dactylitis
Plus ≥1 of: - Psoriasis - Inflammatory bowel disease - Preceding infection - HLA-B27 - Uveitis - Sacroiliitis on imaging (radiographs or MRI)	Plus ≥2 of the remaining: - Arthritis - Enthesitis - Dactylitis - IBP in the past - Positive family history for SpA