Psoriatic Arthritis

Meet the patient

A 34-year-old teacher arrives with a hot, swollen right second toe she cannot get a shoe over — the classic sausage digit — and a scaly plaque on her left elbow she has had for years and never mentioned. Her heels hurt so much on first standing that she shuffles to the bathroom on the edges of her feet.[1]

Her nails are pitted like a thimble, two are lifting off the bed, and she has never once connected the rash, the nails and the toe. Her RF is negative; her CRP is 24. She is tired, her father has psoriasis, and she thinks it is "just the weather".[1]

Two exam questions are now live, and everything below exists to answer them: is this psoriatic arthritis? (the CASPAR score settles it in 30 seconds) and is that hot swollen toe septic? (only a needle settles that). Hold both questions and the topic falls into place.[1]

What psoriatic arthritis actually is — the enthesis runs the whole show

The enthesis is the lesion that explains everything. It is the insertion of tendon, ligament or capsule into bone — a mechanically stressed transition zone — and in PsA it is where the disease lives. Enthesitis spills into the adjacent synovium (arthritis), the overlying skin (psoriasis) and the nail matrix (nail dystrophy), which is why one patient turns up with a swollen toe, a plaque and a pitted nail at the same visit.[1]

"Seronegative" is the word that does the sorting. Both rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA) are absent, which separates PsA from rheumatoid arthritis at the blood tube. Add psoriasis, asymmetry, lower-limb predominance, DIP involvement, dactylitis and enthesitis and the pattern is unmistakable.[1]

The skill is pattern recognition, then treat-to-target. Once you see it, escalate from NSAIDs through conventional DMARDs to biologics to stop the destructive, paradoxical bone remodelling that is unique to this disease — erosions and pathological new bone in the same joint. That duality is why PsA deforms where RA merely erodes.[1][4]

The family — five cousins, one lesion

PsA is one of the seronegative spondyloarthropathies (SpA): a family unified by HLA-B27, inflammatory back pain, asymmetric lower-limb oligoarthritis, enthesitis, dactylitis and RF and ACPA negativity. The enthesis is the shared lesion; the paradoxical bone remodelling is the shared X-ray.[1]

The five members, in the order examiners expect:[1]

1. Ankylosing spondylitis — the axial prototype.
2. Psoriatic arthritis — this topic.
3. Reactive arthritis — one to four weeks after a GU or GI infection (the classic triad of arthritis, urethritis, conjunctivitis).
4. Enteropathic arthritis — arthritis with inflammatory bowel disease (Crohn disease, ulcerative colitis).
5. Undifferentiated spondyloarthropathy — features of SpA that fit no named subset.[1]

The discriminator that earns marks: sacroiliitis is bilateral and symmetric in AS, but asymmetric in PsA, reactive and IBD disease. Read one sacroiliac film and you can move a patient between family members.[1]

The CASPAR score — three points and you are in

CASPAR (ClASsification criteria for Psoriatic ARthritis) is a clinical score, not a blood test. The entry requirement is established inflammatory articular disease — peripheral or axial — or entheseal disease. Then collect at least 3 points from the items below.[2]

The arithmetic examiners love: current psoriasis alone is 2 points, so a single further feature — one field of nail pitting, an RF in negative titre, one sausage digit, one fluff of periostitis — completes the score. This is why you examine every nail and every hidden skin fold in any inflammatory arthritis.[2]

The classic trap — arthritis preceding psoriasis. In 10 to 15 percent the skin is bare when the joints present, the RF is negative, and only family history, dactylitis, enthesitis, nail dystrophy and juxta-articular new bone earn the points. CASPAR was built to catch exactly these patients — current psoriasis is not required.[1][2]

The five Moll and Wright patterns — name the shape, name the prognosis

Moll and Wright drew five patterns in 1973, still taught because each behaves differently and shapes treatment. Etymology for viva gold: the Moll and Wright 1973 paper is the citation examiners want when they ask you to classify a PsA hand — name the year and you name a century of teaching behind it.[1]

1. Asymmetric oligoarthritis — the commonest (about half of patients; up to 70 percent in some series). Fewer than five joints, lower limbs, with dactylitis, enthesitis and DIP involvement. Often the presenting pattern; many evolve into polyarthritis.
2. Symmetric polyarthritis — about 25 percent. RA-like but RF negative, with more DIP and nail disease and a generally less erosive course.
3. DIP-predominant arthritis — about 5 percent. Strongly linked to nail disease; the one most easily confused with osteoarthritis — distinguish by inflammation, nails and psoriasis.
4. Arthritis mutilans — about 1 to 5 percent, the most destructive. Osteolysis and telescoping digits — the opera-glass hand. Often combined with spondylitis; function is devastated.
5. Predominant spondylitis or sacroiliitis (axial) — about 5 to 20 percent, frequently with peripheral disease. Inflammatory back pain, asymmetric sacroiliitis, and bulky asymmetric non-marginal syndesmophytes (parasyndesmophytes) — the opposite of the delicate marginal bamboo of AS. HLA-B27 is more frequent here.[1]

Etymology for viva gold: opera-glass hand — the telescoped fingers of arthritis mutilans push in and out like the collapsible lenses of 19th-century theatre glasses. One look and the diagnosis is made.[1]

Stem — which Moll and Wright pattern? (answer)

A 42-year-old man with psoriasis has an asymmetric swollen left knee, a sausage right second toe and pitted fingernails. Pattern: asymmetric oligoarthritis (the commonest) with dactylitis and nail dystrophy. CASPAR: current psoriasis (2) plus dactylitis (1) plus nail dystrophy (1) equals 4 points — positive.[1]

Epidemiology — who, when, and the 15-percent trap

About 2 to 3 percent of us have psoriasis, and 15 to 30 percent of those will develop PsA — so every psoriasis patient is asked about joints and screened with the PEST (Psoriasis Epidemiology Screening Tool), where a score of 3 or more triggers rheumatology referral. Population prevalence of PsA is about 0.3 to 1 percent — roughly half as common as RA, still one of the commonest inflammatory arthritides.[1]

Peak onset is 30 to 50 years (later than AS, earlier than RA) and the sex ratio is roughly equal — unlike the female predominance of RA or the male predominance of AS.[1]

The 70-15-15 rule of onset ordering. Psoriasis precedes arthritis in about 70 percent; both appear together in about 15 percent; and arthritis precedes psoriasis in 10 to 15 percent — the trap. No visible skin, and the diagnosis hangs on family history, dactylitis, enthesitis, RF negativity and nail changes.[1]

Genetics splits skin from spine. HLA-Cw6 drives the skin disease (and early-onset, erosive PsA); HLA-B27 drives axial disease (but in only 25 to 40 percent of axial-PsA patients, far lower than the 90 percent of AS). ERAP1 risk is amplified in HLA-Cw6 carriers — a textbook gene-environment interaction — and IL23R, TNFAIP3, RUNX3 reinforce the IL-23 / Th17 story.[1]

Triggers to name at viva: the Koebner phenomenon (plaques in scratch, scar, tattoo or sunburn lines — etymology: Heinrich Koebner, 1876, the isomorphic response), streptococcal pharyngitis (guttate psoriasis), stress, obesity and smoking, and the drugs — lithium, beta-blockers, antimalarials, NSAID withdrawal, rapid systemic-corticosteroid taper. Obesity is both a risk factor and a predictor of poor biologic response; weight loss improves drug efficacy.[1]

[1]

Paradoxical bone — erosions AND new bone in the same joint

Pathophysiology — the cytokines are the drugs

Genes plus triggers converge on the enthesis and switch on IL-23. Activated dendritic cells in skin, gut and enthesis release IL-23 and TNF; IL-23 drives Th17 cells and type-3 innate lymphoid cells to secrete IL-17A, IL-17F and IL-22 — a self-amplifying loop alongside TNF-alpha. The same cytokines hit three tissues at once — enthesis, synovium, epidermis — which is why the phenotype is multi-domain.[1]

This biology is the formulary. TNF inhibitors were first (and remain first-line); then IL-17 inhibitors (secukinumab, ixekizumab, bimekizumab), IL-23 inhibitors (guselkumab, risankizumab) and IL-12/23 inhibitors (ustekinumab) — each plugs into a node of this cascade.[1][3][4]

The duality on X-ray is the IL-23 / Th17 signature. Enthesitis first erodes bone at the insertion, then — as the Wnt and beta-catenin osteoproliferation pathway (braked by DKK-1 and sclerostin) is released when inflammation settles — drives pathological new bone. That is the mechanism behind paradoxical remodelling, and it is why anti-inflammatory control can leave a joint fused.[1]

[1]

Clinical presentation — read the skin, nails, joints, entheses, spine, eyes

The arthritis is inflammatory, and the pattern is asymmetric, lower-limb and DIP-favoured. Pain and stiffness are worse in the morning and with rest, better with activity, with morning stiffness over 30 minutes. Against RA, reach for: asymmetry, lower-limb predominance, DIP involvement, dactylitis, enthesitis, RF and ACPA negativity.[1]

Dactylitis — the sausage digit. Diffuse swelling of an entire digit from simultaneous synovitis and flexor-tendon entheseal inflammation. One of the most specific features of the whole SpA family, and a CASPAR point. It is painful, persistent, and a marker of more severe disease.[1]

Enthesitis — heel pain on first standing. The Achilles insertion and plantar fascia origin (both at the calcaneus) are the classic sites; also the patellar tendon at the tibial tuberosity, quadriceps insertion, iliac crests, ischial tuberosities and costosternal junctions. Often the first symptom of PsA, sometimes by years.[1]

Nail disease — present in up to 80 percent of PsA (versus about 30 percent of psoriasis alone) and the feature most strongly associated with joint disease. Examine every nail. Look for pitting (parakeratosis of the proximal matrix), onycholysis (plate lifts off the bed), subungual hyperkeratosis, the oil-drop or salmon-patch discolouration, and onychorrhexis or crumbling in severe disease.[1]

Everyone forgets the hidden psoriasis sites — examine all of them. Extensor elbows and knees, scalp (especially the retro-auricular margin), umbilicus, gluteal and natal cleft, genitals, perianal skin, flexures. One missed plaque is a missed CASPAR point. Patterns to name: chronic plaque (commonest), guttate (teardrop plaques after strep), palmoplantar pustular, erythrodermic (a medical emergency), inverse or flexural.[1]

Read the systems — the cardiometabolic duty is real. Chronic inflammation drives a cluster of obesity, hypertension, dyslipidaemia, insulin resistance and type 2 diabetes, NAFLD and metabolic syndrome, and excess cardiovascular mortality is the leading cause of death. IBD overlap (Crohn, UC) needs gastroenterology; depression, anxiety and fatigue are common and undertreated.[1]

Differential diagnosis — six mimics and the one-line discriminator

[1]

The discriminator line: DIP involved with erosions AND new bone, RF negative, dactylitis, enthesitis, nail dystrophy — that is PsA; DIP spared with purely marginal erosions and RF positive — that is RA. One sentence, full marks.[1]

Do not miss the dangerous mimics. Septic arthritis (hot joint, systemically unwell — aspirate and culture), gout and CPPD (crystals on microscopy, hyperuricaemia for gout), and HIV-associated arthritis (an explosive, treatment-resistant SpA-like picture in advanced HIV — check serology before immunosuppression).[1]

Investigations — confirm nothing, exclude everything

CASPAR is the test. No single investigation confirms PsA. Bloods and imaging support the pattern, exclude mimics, stage disease and prepare for drugs.[1]

RF is negative — the key discriminator and a CASPAR point. But up to 13 percent of PsA patients are RF positive in low titre — a low-positive RF does not exclude PsA when the pattern dominates. ACPA is negative and more specific than RF for RA, so a negative result is reassuring. CRP and ESR are often raised in active disease (they may be normal) — baseline and on-treatment values track response. HLA-B27 is requested when axial disease dominates.[1]

Before DMARDs and biologics: full blood count, urea and electrolytes, liver function, hepatitis B and C, HIV; baseline CRP. Aspirate any hot joint: PsA fluid is inflammatory (2,000 to 50,000 per microlitre, neutrophilic), sterile and crystal-negative; check serum urate to exclude gout, which can coexist.[1]

The X-ray hallmarks — hands, feet, pelvis: the pencil-in-cup deformity at DIP joints, fluffy periostitis (the CASPAR "juxta-articular new bone"), marginal erosions coexisting with new bone (the paradox), bony ankylosis, sausage-digit soft-tissue swelling with acro-osteolysis, asymmetric sacroiliitis, bulky asymmetric parasyndesmophytes, and the destructive osteolysis of arthritis mutilans.[1]

MRI is the early-disease cornerstone. STIR and T2 fat-saturated sequences show bone-marrow oedema at entheses and sacroiliac joints — the earliest lesion, years before the plain film — plus synovitis, tenosynovitis (the flexor sheath in dactylitis) and erosions. Bedside musculoskeletal ultrasound with power Doppler detects synovitis, enthesitis and nail disease and guides injections. DEXA screens for the osteoporosis of chronic inflammation.[1][3]

The disease-activity numbers (answer)

DAPSA = tender joint count (68) plus swollen joint count (66) plus patient pain (0 to 10) plus patient global (0 to 10) plus CRP in mg per dL — remission under 4, low activity 4 to 14, moderate 14 to 28, high over 28. The treat-to-target endpoint is Minimal Disease Activity (MDA): 5 of 7 of tender joint count under 1, swollen joint count under 1, PASI under 1 (or BSA under 3), patient pain under 15 mm, patient global under 20 mm, HAQ under 0.5, tender entheseal points under 1. The PASI scores skin severity.[3][4]

Management — domain by domain, treat to target

Modern care is domain-driven and treat-to-target, shared between rheumatology and dermatology (plus gastroenterology, ophthalmology, psychology). The target is minimal disease activity (MDA) or remission across every active domain — peripheral joints, axial skeleton, entheses, dactylitis, skin, nails.[1][3][4]

GRAPPA 2021 and EULAR 2023 agree on the spine of it: treat every active domain, escalate if the target is missed, screen and manage comorbidity. EULAR adds the guardrails — NSAIDs only for mild and short-term, no oral glucocorticoids, methotrexate preferred among csDMARDs.[3][4]

Step 1 — NSAIDs (mild peripheral and mild axial)

NSAIDs at full anti-inflammatory dose are first-line for mild peripheral disease and mild axial symptoms; EULAR 2023 limits monotherapy to mild PsA, short term. Try two different NSAIDs over 2 to 4 weeks before calling failure.[3][4]

Step 2 — local glucocorticoid injection

Intra-articular or intralesional triamcinolone acetonide 40 mg settles a focal swollen joint or stubborn enthesis (a recalcitrant DIP, a single hot Achilles). Oral glucocorticoids are NOT recommended — ineffective for axial disease, toxic long-term, and rapid withdrawal flares psoriasis.[4]

The classic trap — reaching for a prednisolone course for axial PsA is the recurring trainee error. It does not work for the spine, and tapering it sets the skin on fire. If you must bridge a peripheral flare, keep it short and plan the exit before you write the prescription.[4]

Step 3 — conventional synthetic DMARDs (moderate-to-severe peripheral)

csDMARDs treat peripheral arthritis; they do NOT treat axial disease or enthesitis. EULAR 2023 wants rapid initiation, methotrexate preferred.[4]

Step 4 — biologic DMARDs

A biologic for axial, refractory, or csDMARD-failed disease. EULAR 2023: initiate without preference among modes of action for peripheral disease; skin-predominant disease leans to IL-23p40, IL-23p19 or IL-17A and IL-17AF inhibitors; uveitis or IBD leans to a monoclonal TNF inhibitor.[4]

TNF inhibitors are the most-used class, effective across peripheral, axial, entheseal, dactylitic, skin and nail disease. The ADEPT trial (Mease 2005) showed adalimumab improved joints and skin, inhibited radiographic progression, and improved function and quality of life in moderate-to-severe PsA.[5]

IL-17 inhibitors are outstanding for peripheral, axial, entheseal, dactylitic and especially skin and nail disease. The classic trap — IL-17 inhibitors may trigger or worsen inflammatory bowel disease, so avoid them when bowel disease coexists.[3][4]

IL-23 and IL-12/23 inhibitors are excellent for peripheral and skin-predominant disease, enthesitis and dactylitis — but NOT effective for axial PsA. That gap is the single most examinable fact in modern PsA prescribing.[3][4]

Oral small molecules. EULAR 2023 positions JAK inhibitors mainly after a bDMARD has failed, weighing risk factors (venous thromboembolism, malignancy, cardiovascular disease, age over 65). Tofacitinib 5 mg orally twice daily; upadacitinib 15 mg once daily; filgotinib 200 mg once daily (not available in the USA). Class cautions: VTE, herpes zoster, and lipid and LFT monitoring. The PDE4 inhibitor apremilast — 30 mg orally twice daily (titrate up from 10 mg to limit GI upset) — helps oral ulcers, mild skin and mild peripheral disease, with no requirement for TB screening.[3][4]

Pre-biologic screen — TB, hepatitis, vaccines before you immunosuppress

Before any biologic or JAK inhibitor: latent-TB screen with IGRA (QuantiFERON-TB Gold) and chest X-ray, treating latent TB — isoniazid 300 mg once daily for 6 to 9 months, or rifampicin plus isoniazid for 3 to 4 months — before the TNF inhibitor; hepatitis B and C serology (HBsAg, anti-HBc, anti-HBs, anti-HCV); HIV where appropriate; full blood count, liver function, renal function, lipids, blood pressure, pregnancy test.[3][4]

Vaccinate before immunosuppression (pneumococcal, influenza, hepatitis B, COVID-19, HPV, recombinant herpes zoster) and avoid live vaccines during therapy. Reactivation TB is a preventable disaster — that is the whole point of the screen.[3][4]

Three guidelines, one ladder

The trial names that score marks. ADEPT (Mease 2005) — adalimumab improved joints and skin and halted radiographic progression. FUTURE 1 and 2 — secukinumab proved IL-17A blockade works across peripheral, axial, entheseal, dactylitic and skin disease. PSUMMIT 1 and 2 — ustekinumab showed IL-12/23 blockade effective for peripheral and skin disease. DISCOVER 1 and 2 — guselkumab proved selective IL-23 blockade works for peripheral disease and skin but not for axial disease, the gap that shaped domain-driven prescribing. SELECT-PsA 1 and 2 — tofacitinib effective for peripheral PsA.[3][4][5]

Adjuncts and the cardiometabolic duty

Physiotherapy and exercise (non-negotiable, especially in axial disease), smoking cessation (improves skin, joints and biologic response — smokers have worse disease), weight loss (raises biologic efficacy and cuts cardiovascular risk), and cardiovascular risk modification — statins, antihypertensives, glycaemic control — because cardiovascular disease is the leading driver of mortality. Occupational therapy, splints for dactylitis, and psychological support for depression and anxiety complete the package.[1][3]

Special populations

Pregnancy and lactation. NSAIDs are safe in the first and second trimester but avoided after 28 to 30 weeks (premature ductus-arteriosus closure, oligohydramnios). Sulfasalazine is safe throughout (supplement folic acid 5 mg once daily). Low-dose prednisolone (under 10 mg) is acceptable where needed. Among biologics, certolizumab is preferred (no Fc region, no placental transfer); adalimumab and infliximab are continued through the first and second trimesters and stopped in the third. Methotrexate and leflunomide are teratogenic and contraindicated — stop methotrexate at least 3 months before conception in both sexes, and use cholestyramine washout for leflunomide. Avoid JAK, IL-17 and IL-23 inhibitors in pregnancy and lactation (limited data).[3][4]

Juvenile psoriatic arthritis is an asymmetric large-joint oligoarthritis with nail pitting, dactylitis, or psoriasis in the child or a first-degree relative; treat as juvenile idiopathic arthritis — NSAIDs and intra-articular steroids first, then methotrexate and biologics (etanercept, adalimumab). Screen for uveitis with slit-lamp every 6 to 12 months.[1]

Elderly. Late-onset PsA carries more metabolic comorbidity and mimics osteoarthritis or polymyalgia rheumatica; NSAID and methotrexate toxicity is higher — adjust doses for renal function and polypharmacy. Biologics are effective and generally well tolerated in selected older patients.[3]

Immunocompromised or on-biologic host. Vaccinate before starting the biologic and avoid live vaccines during it; monitor for infection (TB, opportunistic) with a low threshold for culture; coordinate with infectious diseases if latent TB is treated, hepatitis B reactivates, or HIV coexists.[3][4]

Complications — the preventable-harm list

• Missing PsA because the psoriasis is hidden — always examine scalp, umbilicus, natal cleft, genitals and nails[1]
• Mislabelling PsA as RA because the RF happened to be low-positive — re-examine for DIP, dactylitis, enthesitis and nails; check ACPA[1]
• Aspirating a hot joint as "a flare" without culturing — septic arthritis coexists; always culture[1]
• Using systemic corticosteroids for axial disease — ineffective and toxic; rapid withdrawal flares psoriasis[4]
• Forgetting pre-biologic TB and hepatitis screening — reactivation TB is a preventable disaster[3]
• Choosing an IL-17 inhibitor in IBD — may worsen bowel disease; choose a monoclonal TNFi[4]
• Choosing an IL-23 inhibitor for isolated axial disease — it does not work; use an NSAID, TNFi or IL-17i[4]

Prognosis

Variable by nature — some patients ride NSAIDs for decades, others reach arthritis mutilans within years. Early treat-to-target has transformed outcomes, cutting radiographic progression and disability.[1][3]

The poor-prognostic markers: polyarticular or axial disease at presentation, raised CRP and ESR, HLA-B27 / HLA-DR4 / HLA-Cw6, erosions on the baseline X-ray, dactylitis, young age at onset, family history, obesity, smoking, and delay in starting DMARD or biologic therapy. Mortality is modestly raised (standardised mortality ratio about 1.3 to 1.6), driven by cardiovascular disease; untreated, 20 to 40 percent develop significant functional impairment.[1]

Refer all suspected PsA to rheumatology; coordinate with dermatology (skin), ophthalmology (uveitis), gastroenterology (IBD) and cardiology (cardiovascular risk). Review disease activity, drug toxicity and comorbidity at least every 3 to 6 months.[3]

The mantra, the mnemonic, the confession

[2]

The mantra: aspirate the hot joint, examine the nails, choose the drug by the domain — never the steroid for the spine, never the IL-17 in IBD, never the IL-23 for the axis.[1][4]

A consultant confession: when the picture is mixed and the RF comes back low-positive, I do not argue with the pattern. DIP involvement, a sausage digit, heel pain on first standing and nail pitting trump a borderline titre every time — re-examine the patient, check the ACPA, and let the bedside settle what the tube could not.[1]

Ward-round test

Stem 1 — the sausage toe (answer)

A 34-year-old with a hot, swollen right second toe, a scaly elbow plaque, heel pain on first standing and pitted nails. RF negative, CRP 24. What is the diagnosis, the score, and the first procedure? Model: Psoriatic arthritis, asymmetric oligoarthritis pattern with dactylitis, enthesitis and nail dystrophy. CASPAR: current psoriasis (2) plus dactylitis (1) plus nail dystrophy (1) equals 4 — well over 3. But a single hot joint is aspirated first to exclude septic arthritis before any NSAID or steroid; only a needle settles that question. Then start a full-dose NSAID and refer to rheumatology.[1][2]

Stem 2 — biologic by domain (answer)

A 45-year-old with PsA has recurrent uveitis and mild Crohn disease, uncontrolled on methotrexate. Which biologic, and which two must you avoid? Model: A monoclonal TNF inhibitor (adalimumab, infliximab or certolizumab) — effective for both uveitis and IBD. Avoid etanercept (worse for uveitis) and avoid IL-17 inhibitors (may worsen IBD). IL-23 inhibitors help IBD but not uveitis, and do nothing for the axis — not the right tool here.[4][5]

Stem 3 — arthritis before the rash (answer)

A 29-year-old man has an asymmetric swollen knee and a sausage finger, RF negative, normal skin examination — but his mother has psoriasis. How do you make the diagnosis? Model: Arthritis preceding psoriasis (10 to 15 percent of PsA). Apply CASPAR without current psoriasis: family history (1) plus current dactylitis (1) plus RF negative (1) equals 3 — CASPAR positive. Examine the nails, hidden skin sites and request a hand/foot X-ray for juxta-articular new bone to confirm. Do not wait for the rash.[1][2]

Stem 4 — the hot joint in a known PsA (answer)

A 52-year-old with established PsA on adalimumab presents with a single exquisitely hot, swollen knee and a fever. What is your first action, and what is the trap? Model: Aspirate before you treat. A hot monoarthritis in an immunosuppressed patient is septic arthritis until proven otherwise — PsA and sepsis coexist. Send synovial fluid for cell count, Gram stain, culture and crystals. The trap is labelling it "a flare" and injecting steroid before the culture is back; that is how a septic joint is missed and destroyed.[1]

References

1. [1]Ritchlin CT, Colbert RA, Gladman DD. Psoriatic Arthritis N Engl J Med, 2017.PMID 28273019
2. [2]Taylor W, Gladman D, Helliwell P, Marchesoni A, Mease P, Mielants H; CASPAR Study Group. Classification criteria for psoriatic arthritis: development of new criteria from a large international study Arthritis Rheum, 2006.PMID 16871531
3. [3]Coates LC, Soriano ER, Corp N, et al. Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA): updated treatment recommendations for psoriatic arthritis 2021 Nat Rev Rheumatol, 2022.PMID 35761070
4. [4]Gossec L, Kerschbaumer A, Ferreira RJO, et al. EULAR recommendations for the management of psoriatic arthritis with pharmacological therapies: 2023 update Ann Rheum Dis, 2024.PMID 38499325
5. [5]Mease PJ, Gladman DD, Ritchlin CT, et al. Adalimumab for the treatment of patients with moderately to severely active psoriatic arthritis: results of a double-blind, randomized, placebo-controlled trial Arthritis Rheum, 2005.PMID 16200601