Psoriatic arthritis

I. What every physician needs to know.

Psoriatic arthritis is a chronic seronegative inflammatory arthritis associated with psoriasis. A textbook presentation is that of a patient with psoriasis who develops prolonged morning stiffness and swelling of the DIP joints that progresses to dactylitis (i.e. swelling of the entire digits, giving them a “sausage” appearance). There are several patterns of joint disease – oligoarthritis, polyarthritis, sacroiliitis, with arthritis mutilans being the most severe. The disease can have a progressive course and significant joint destruction over time.

Initially NSAIDs are used, but frequently disease-modifying antirheumatic drugs are necessary to control the inflammation. The most commonly used DMARD is methotrexate, but TNF inhibitors hold promise as preventing permanent joint damage.

II. Diagnostic Confirmation: Are you sure your patient has Psoriatic Arthritis?

CASPAR criteria for diagnosis use 7 simple criteria with reported sensitivity and specificity of 91.4% and 97.2% respectively.

Established inflammatory arthritis with => 3 points
◦ -psoriasis (2 points for current psoriasis; or 1 point for personal history of psoriasis; or 1 point for family history of psoriasis)

◦ -nail dystrophy(1 point)

◦ -negative rheumatoid factor (1 point)

◦ -dactylitis (1 point)

◦ -juxtaarticular new bone formation on plain radiography (1 point)

A. History Part I: Pattern Recognition:

A typical patient will present with psoriasis, prolonged morning joint stiffness and pain, dactylitis and nail problems.

Psoriasis precedes articular involvement and is evident in most patients. Up to 20% of patients however may have either minimal or no skin lesions, thus being initially misdiagnosed as having undifferentiated seronegative arthritis. Therefore it is important to carefully inspect the skin of the scalp, the intergluteal fold, the umbilicus, the area behind the ears, and the nails.

A simplified classification of the pattern of joint disease is:

Oligoarthritis
Polyarthritis
Axial arthritis

The original classification of Mall and Wright from 1973 consists of 5 patterns:

DIP arthritis (“sausage digits”)
Asymmetric oligoarthritis
Symmetric polyarthritis
Arthritis mutilans
Psoriatic spondylitis (spinal and sacroiliac involvement)

B. History Part 2: Prevalence:

Recently reported incidence of 9.8 per 100,000 people. The prevalence of psoriatic arthritis among patients with psoriasis is around 10%.

Risk factors include the presence of psoriasis, a family history of psoriasis or psoriatic arthritis, and the presence of HIV infection.

Trauma to a joint sometimes triggers psoriatic arthritis and is considered the articular equivalent of the Koebner phenomenon (appearance of a psoriatic plaque in the area of trauma to the skin).

C. History Part 3: Competing diagnoses that can mimic Psoriatic Arthritis.

Common mimickers:

Rheumatoid arthritis – symmetric polyarthritis of hands and feet; sparing the sacroiliac and lumbar joints; no dactylitis; positive serology for rheumatoid factor (RF) and anti-citrulinated protein antibody (anti-CCP).
Erosive osteoarthritis – no inflammation; typical radiographic appearance as osteoarthritis.
Gout – recurrent mono- or polyarticular attacks; synovial fluid diagnostic when negative birefringent crystals seen.
Ankylosing spondylitis – sacroiliac and spinal distribution only, without psoriasis.

Less common mimickers:

Reactive arthritis (Reiter’s disease) – associated with GI infection (Salmonela andCampylobacter) or GU infection (Chlamydia) – may present with dactylitis and insertionitis, and may be accompanied by conjunctivitis and urethritis.
Sarcoid dactylitis – rarely in patients with sarcoidosis.

D. Physical Examination Findings.

Psoriasis – well-demarcated plaque with erythema and silvery scaling; typically on extensor surfaces of elbows and knees, scalp, ears, and almost anywhere on body.

Nails – pitting, onycholysis, yellow-brown discoloration.

Dactylitis – AKA “sausage” fingers – swelling of the entire digit; may be difficult to appreciate the actual joint involvement because of the uniform swelling.

Peripheral arthritis with synovitis +/- joint effusions.

Enthesitis – pain in the area of tendon attachment to the bone – commonly the insertion of the Achilles tendon, the plantar fascia, and the epicondyles.

Sacroiliitis – tenderness in SI joints.

Spinal (axial) involvement – decreased ROM of spine measured by Shober test.

Rarely iritis on eye exam.

Very rarely aortic root dilatation with aortic insufficiency.

E. What diagnostic tests should be performed?

N/A

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

ESR and CRP – non-specific inflammatory markers; have no diagnostic value as can be normal; elevation can be due to either skin inflammation or polyarticular disease.

RF and anti-CCP antibody – to rule out rheumatoid arthritis.

HIV – patients with HIV+ tend to have more severe disease.

Hepatitis B serology, PPD – do not establish the diagnosis, but important if considering anti-TNF therapy.

Synovial fluid analysis – only if clinically indicated, to rule out crystal-induced disease and septic joint.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Plain X-rays of hands and feet – DIP joint erosions, periarticular new bone formation.

Plain X-ray of lumbosacral spine and sacroiliac joints – asymmetric sacroiliitis.

Magnetic resonance imaging (MRI) of SI joint – rarely indicated; can demonstrate subclinical sacroiliitis.

Joint and tendon ultrasonography – emerging diagnostic modality.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

None

III. Default Management.

Psoriatic arthritis is not a benign disease. NSAIDs could the the first-line treatment in mild disease, but one has to remember that they do not prevent bone erosions and irreversible joint damage. Disease-modifying drugs (e.g., anti-TNFs, metothrexate, cyclosporin, etc.) are introduced early if there is evidence of progressive or severe disease.

Current recommendations emphasize individualizing the treatment plan because of the variable manifestations of the disease.

A. Immediate management.

NSAIDs provide immediate relief of joint pain and stiffness. Any agent can be chosen, based on physician’s and patient’s preference and keeping in mind their potential GI and renal side effects as well as the possibility for fluid retention, heart failure exacerbation and loss of blood pressure control.

Intraarticular steroid injections – can occasionally be given to provide temporary relief of an inflamed joint. This is based on expert opinion since there is no data from clinical trials.

B. Physical Examination Tips to Guide Management.

Psoriatic arthritis is rarely the main reason for hospitalization. Assessing affected joints daily for pain, warmth, swelling, ROM, may not be a sensitive indicator since disease-modifying drugs take a few weeks before maximum effect is achieved.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Plain radiographic films of affected joints are ordered every few months or annually depending on the clinical response to treatment.

CBC and liver enzymes are followed during treatment with methotrexate.

ANA is occasionally checked because anti-TNFs can induce lupus.

Creatinine while taking NSAIDs.

D. Long-term management.

Disease-modifying antirheumatic drugs are commonly used for moderate and severe disease:

Methotrexate

Sulfasalazine

Leflunomide

Cyclosporin

TNF inhibitors

etanercept
infliximab
adalimumab
alefacept

Treatment is individualized based on the pattern of joint disease.

Peripheral arthritis
◦ NSAIDs

◦ Intraarticular steroids

◦ DMARDs (methotrexate, cyclosporin A, sulfasalazine, leflunomide)

◦ Anti-TNFs
Axial disease
◦ NSAIDs

◦ Physical therapy

◦ Anti-TNFs
Dactylitis
◦ NSAIDs

◦ Anti-TNFs
Enthesitis
◦ NSAIDs

◦ Physical therapy

◦ Anti-TNFs

E. Common Pitfalls and Side-Effects of Management.

NSAIDs – GI toxicity (gastritis, PUD, GI bleeding), kidney injury (AIN, ATN), fluid retention, worsening heart failure, elevated blood pressure.

Methotrexate – bone marrow suppression, liver toxicity, liver fibrosis and irreversible failure with high cumulative doses, pulmonary toxicity.

TNF inhibitors – reactivation of TB and Hepatitis B, severe bacterial infections, treatment-related lymphomas, lupus, demyelinating diseases.

IV. Management with Co-Morbidities.

N/A

A. Renal Insufficiency.

Avoid NSAIDs.

Methotrexate – for Cr clearance 10-50, reduce dose by 50%; CrCl < 10 – avoid methotrexate.

B. Liver Insufficiency.

Avoid methotrexate.