Synonyms: PsA, Psoriatic spondylitis
ICD-9 Code: Psoriatic arthritis, 696.0; cutaneous psoriasis 696.1.
ICD-10 Code: Psoriatic arthritis L40.5; cutaneous psoriasis vulgaris L40.0
What is it?
Psoriatic arthritis is an inflammatory arthropathy that occurs among patients with cutaneous psoriasis.
What causes it?
No etiologic agent or reactive process has ever been proven. Some contribution to disease by stress, trauma, heat-shock proteins, and infection with Streptococcus or Staphylococcus has been implicated because patients often attribute worsening of their signs and symptoms to such factors. Genetic associations with psoriatic arthritis are heterogeneous. Cutaneous psoriasis is associated with HLA-B13, HLA-B17, HLA-37, and HLA-Cw6. By contrast, HLA- B39 and HLA-B27 have been associated with psoriatic sacroiliitis and spondylitis. HLA-Cw6, HLA-Bw38, HLA-DR4, and HLA-DR7 have been linked with peripheral arthropathy.
Pathology: The histopathology of psoriatic synovitis is similar to that seen in other inflammatory arthritides within the spondyloarthritis group of diseases, such as AS. There are some immunologic features common to PsA and rheumatoid arthritis, but also clear distinctions.
Who gets it?
Psoriatic arthritis develops in approximately 30% of patients with psoriasis. Skin manifestations precede joint manifestations in about 85% of patients, often by a decade or longer. Age at onset is usually between 30 and 55 years. Most forms of psoriatic arthritis affect men and women equally; however, psoriatic spondylitis has a male predominance (approximately 2:1).
What are the symptoms?
Disease Subsets: Classically, five ‘variants’ of psoriatic arthritis had been described.
- Asymmetric oligoarthritis is seen in 30% to 40% of patients and involves large and small joints. Sausage digits (dactylitis) of the fingers or toes may be present. Skin disease may be minimal or overlooked.
- Distal interphalangeal arthritis is seen in 10% to 15% of patients. A strong association with nail changes (nail pitting) exists.
- RA-like polyarthritis (25%–50% of patients) with symmetric arthritis but lacks serum RF or nodules. Patients with polyarticular disease tend to have greater morbidity, less response to therapy, and a worse outcome than patients with oligoarticular disease.
- Psoriatic spondylitis is seen in approximately 20% of patients with psoriatic arthritis, 50% of whom are HLA-B27 positive.
- Arthritis mutilans, seen in <5% of patients, presents as destructive, erosive polyarthritis affecting the hands and feet. It often leads to deformity and disability.
However, these variants are not mutually exclusive, and patients may possess overlapping features. From the standpoint of therapeutic intervention and outcomes, there are essentially three distinct phenotypes: oligoarticular peripheral arthritis, polyarticular peripheral arthritis, and spondylitis.
Cardinal Findings: Psoriatic arthritis typically may have an insidious onset and a progressive course. The arthritis may manifest as axial or peripheral joint stiffness, pain, or swelling. Peripheral arthritis may present as a chronic, asymmetric oligoarthropathy, a symmetric distal interphalangeal polyarthritis, or a rheumatoid-like (metacarpophalangeal and proximal interphalangeal joints) polyarthritis. Inflammatory sausage-like swelling of the digits (dactylitis) involving the fingers or toes is common. Psoriatic spondylitis is seen in approximately 15% of patients and manifests as spinal stiffness, pain, or limited range of motion affecting the lumbosacral more than cervical spine. Enthesitis (inflammation where tendons, ligaments and synovial membranes inserts into bone) may present throughout the body; common places include the insertion of the Achilles tendon into the calcaneus the anterior chest wall, and the iliac crest. The degree of psoriatic skin disease may correlates poorly with the extent of arthritis. A careful examination of the scalp, buttocks, umbilicus, genitalia, and nails (fingers and toes) may reveal psoriatic lesions. Typical nail lesions may include pitting, onycholysis, subungual hyperkeratosis, and transverse ridging. Eye disease (conjunctivitis, anterior iritis, episcleritis, or keratoconjunctivitis sicca) occurs in as many as 30% of patients.
How is it diagnosed?
Inflammatory indices such as increases in the ESR or CRP are less commonly observed in patients with psoriatic arthritis than in patients with RA. Hyperuricemia may be found in patients with extensive skin involvement and often correlates with the severity of cutaneous psoriasis. Synovial fluid has an inflammatory picture, with typical WBC counts ranging from 2,000 to 40,000 cells/mm3, and a neutrophil predominance.
Imaging: Radiographic changes include soft tissue swelling, erosions, and periostitis. Distal interphalangeal disease or arthritis mutilans may develop a typical “pencil and cup” deformity resulting from erosive change and formation of reactive, heterotopic bone in the phalanges. Psoriatic spondylitis is characterized by asymmetric sacroiliitis and spondylitis with asymmetric, nonmarginal, “bulky” syndesmophytes (bridging osteophytes between vertebrae). Acroosteolysis, paravertebral ossification, and pericapsular calcification are uncommon.
Keys to Diagnosis: Look for psoriatic cutaneous or nail changes in association with one of the recognized articular subsets. Carefully examine scalp, ears, buttocks, nails, and umbilicus for psoriatic lesions.
Diagnostic Criteria: The CASPAR criteria are useful to classify a patient with inflammatory peripheral arthritis, inflammatory axial arthritis, or inflammatory enthesitis as having PsA (see below). They have been shown to have a sensitivity and specificity of approximately 91% and 98%
|Established inflammatory articular disease (joint, spine, or entheseal) plus 3 or more points from the following 5 categories
|Psoriatic skin or scalp disease present today as judged by a qualified health professional (2 pts)
|A history of psoriasis that may be obtained from patient, or qualified health professional
|(c) Family history
|A history of psoriasis in a first or second degree relative according to patient report
|2. Nail changes
|Typical psoriatic nail dystrophy including onycholysis, pitting and hyperkeratosis observed on current physical examination
|3. A negative test for RF
|By any method except latex but preferably by ELISA or nephlemetry, according to the local lab reference range
|Swelling of an entire digit
|A history of dactylitis recorded by a qualified health professional
|5. Radiological evidence of juxta-articular new bone formation
|Ill-defined ossification near joint margins (but excluding osteophyte formation) on plain xrays of hand or foot
Differential Diagnosis: Cutaneous psoriasis should be distinguished from seborrheic dermatitis, fungal infection, exfoliative dermatitis, eczema, Gottron papules, keratoderma blennorrhagica, and palmoplantar pustulosis. Psoriatic arthritis should be distinguished from erosive OA, gout, RA, pauciarticular juvenile arthritis, AS, and reactive arthritis.
How is it treated?
Treatment should be aimed at reducing pain, swelling, and stiffness while preserving optimal function and halting disease progression. Specific articular therapies may include
—NSAIDs: NSAIDs may modify symptoms in some, but they do not suppress disease progression. All NSAIDs are equally efficacious and possess similar toxicity profiles.
—Corticosteroids: Corticosteroid therapy is sometimes used as an intraarticular steroid injection (for uncontrolled mon- or oligoarthritis), intralesional steroid to control enthesitis (i.e., Achilles tendinitis, plantar fasciitis), or topical steroid for treatment of conjunctivitis or uveitis. Use of oral low-dose prednisone (5–10 mg/day) should be reserved for severe, uncontrolled peripheral arthritis, as withdrawal of oral steroids may incite a flare of skin disease.
—DMARDSs: Sulfasalazine and MTX have been tested and advocated for use in psoriatic arthritis, although the data supporting their utility is far more limited than for their use in RA. Leflunomide has been shown to have some efficacy for both articular and dermatologic manifestations, as has cyclosporine. The PDE4 inhibitor apremilast is approved for the treatment of PsA and skin psoriasis.
—Biologic agents: The greatest successes in treating psoriasis and psoriatic arthritis to date has been with the use of TNF inhibitors. All five available TNF inhibitors have been studied in and proven effective for PsA, with improvements across all domains of disease.
The IL-12/IL-23 inhibitor ustekinumab has been approved for several years for the treatment of psoriasis, and more recently for the treatment of PsA. The magnitude of efficacy may be greater for skin manifestations than it is for joint manifestations.
Adapted from: RheumaKnowledgy