eMedicine Specialties > Physical Medicine and Rehabilitation > Arthritis & Connective Tissue Disorders

Psoriatic Arthritis: Treatment & Medication

Author: Michael F Saulino, MD, PhD, Assistant Professor, Department of Physical Medicine and Rehabilitation, Thomas Jefferson University, MossRehab
Coauthor(s): Jeffrey M Heftler, MD, Interventional Physiatrist, Orthopaedic and Neurosurgical Specialists, Greenwich, CT
Contributor Information and Disclosures

Updated: Mar 24, 2009

Treatment

Rehabilitation Program

Physical Therapy

The rehabilitation treatment program for patients with psoriatic arthritis should be individualized. The treatment should be started early in the disease process. Such a program should consider use of the following:

• Rest (local and systemic) - Prolonged rest should be avoided to prevent the deleterious effects of immobility.
• Exercise (passive, active, stretching, strengthening, and endurance)
• Modalities (heat, cold)
• Orthotics (upper and lower extremities, spinal)
• Assistive devices for gait and adaptive devices for self-care tasks - These include possible modifications to homes and automobiles
• Education about the disease, energy conservation techniques, and joint protection
• Possible vocational readjustments
• Acute phase - Encourage rest as indicated. Splints may be used for rest and pain relief, especially for the hands, wrists, knees, or ankles. Cold modalities should be used to decrease inflammation and assist with pain relief. Joints should not be moved beyond the limit of pain; passive movements should be limited at this time. Education should be completed during this phase, with topics including the disease itself, the importance of rest, the exercise program, joint protection, energy conservation, and weight loss, if appropriate.
• Subacute and long-term phase - Isometric exercises are begun, with progression to active movement. Gradual range-of-motion (ROM) exercises include passive and active exercises; areas with subluxation should not be forced passively. Heating modalities, including moist heat packs, paraffin wax, diathermy, and ultrasound, can be used to decrease pain; this should be performed just prior to performance of ROM exercises. Institute gait activities with the patient bearing weight as tolerated, with or without an assistive device. Gentle stretching should be gradually introduced. If pain persists beyond 2 hours after therapies, then the intensity should be decreased. If a joint is swollen, then no resistive exercises should be performed through full ROM.

For patients with axial spine involvement, spine extension exercises help with flexibility and strength. ROM exercises should be performed, but not in patients with increased pain. If the patient has sausage toes, extra-depth shoes with a high toe box should be considered to protect the foot. With pain in the toes, such shoes should have a rocker-bottom modification to alleviate forces during the toe-off phase in the gait cycle. The patient may also benefit from arch supports if plantar fascitis is a problem.

Occupational Therapy

As in other inflammatory arthropathies, therapies for psoriatic arthritis are based on the patient's symptoms. Paraffin baths or splinting individual finger joints can be used for pain relief, but these therapies do not change the course of the disease. Stress the importance of joint protection.

Surgical Intervention

Currently, no prospective studies are addressing surgical intervention in patients with psoriatic arthritis (PsA). Patients in severe pain or with significant contractures may be referred for possible surgical intervention. Treatment should be aimed at pain relief or increasing the patient's function. Hip and knee joint replacements have been successful, for the most part, in patients with PsA. Arthrodesis or arthroplasty has been used for joints such as the thumb PIP joint. The wrist often spontaneously fuses, and this may relieve the patient's pain without surgical intervention.

• Because of the diffuse soft tissue involvement associated with the disease, high rates of recurrence of joint contractures have been noted after surgical release, especially in the hand.
• For arthritis mutilans, surgical intervention is usually directed toward salvage of the hand. Combinations of arthrodesis, arthroplasty, and bone grafts to lengthen the digits may be used. The goal is to maintain the pinch mechanism of the thumb and the first 2 fingers.

Consultations

If the patient's physiatrist feels uncomfortable with prescribing medications for psoriatic arthritis, referral to a rheumatologist with more experience with these agents may be advisable. The physiatrist may then concentrate on functional restoration of the patient. Referral to a surgeon should be considered for appropriate patients.

Other Treatment

For acute flare-ups of a small number of joints, intra-articular steroid injections may be helpful in the short term. Avoid injecting through the psoriatic lesions because they may be colonized with staphylococci or streptococci. If the only access to a joint is through a psoriatic lesion, take care to clean the skin thoroughly prior to injection.

Medication

While symptom management should not be minimized, the advent of disease-modifying antirheumatic drugs (DMARDs) has significantly transformed the treatment of psoriatic arthritis (PsA). The most common medications are etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade).⁹ The first 2 medications are injected subcutaneously, while the last medication is given by intravenous infusion.

Older DMARDs that have been reported efficacious for PsA include sulfasalazine, auranofin, methotrexate (MTX), leflunomide, cyclosporine A, and azathioprine. The utility of these agents is somewhat marginal compared with the newer DMARDs.

Traditional treatment of PsA included symptomatic relief with anti-inflammatory and analgesic medications. This therapy includes oral nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroid injections into joints and around inflamed tendons. If joint injection with corticosteroids fails to control pain after 2 injection sessions, this commonly is considered the criterion to institute DMARD therapy. Systemic steroid therapy typically is avoided because of the risk of exacerbating the dermatologic component of psoriasis after withdrawal of the steroids.

Nonsteroidal anti-inflammatory drugs

Despite the possibility of worsening psoriasis through an increase of epidermal proliferation and cutaneous inflammation by arachidonic acid and its metabolites, NSAIDs are widely used. Approximately two thirds of patients who use them have pain relief without an increase in symptoms. The NSAIDs listed below have not been reported to worsen psoriasis.

Meclofenamate (Meclomen)

Decreases activity of cyclooxygenase, which results in decreased formation of prostaglandin precursors.

Chemotherapeutic agents

Inhibit cell growth and proliferation.

Methotrexate (Folex PFS, Rheumatrex)

Acts primarily on rapidly dividing tissues like those found in PsA. May affect immune function. Ameliorates symptoms of inflammation (eg, pain, swelling, stiffness).
Adjust dose gradually to attain satisfactory response.

Immunosuppressive agents

Useful because evidence indicates PsA may be immune mediated.

Cyclosporine (Sandimmune, Neoral)

Can block an early step in T-cell activation; also has a direct anti-inflammatory activity by inhibiting release of immune mediators from tissue mast cells, basophils, and PMN leukocytes. Symptomatic improvement in skin and joint manifestations usually seen in 2-8 wk.

Antimalarial agents

Some of these agents may inhibit regulatory steps responsible for immune reactions.

Hydroxychloroquine sulfate (Plaquenil)

Inhibits chemotaxis of eosinophils, locomotion of neutrophils, and complement-dependent antigen-antibody reactions. Mechanism of action in relation to PsA unknown.
Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate.

Sulfasalazine (Azulfidine, EN-tabs)

Combination of sulfapyridine and 5-aminosalicylic acid (mesalamine). Metabolized to its active components, sulfapyridine and mesalamine, by bacteria in the colon. When given as sulfasalazine, a larger quantity of sulfapyridine and mesalamine reach the colon than when these agents are administered as single agents. Once sulfapyridine and mesalamine reach the colon, the beneficial effects result primarily from the anti-inflammatory properties of mesalamine.
The anti-inflammatory mechanism of mesalamine is believed to occur, at least in part, through the inhibition of arachidonic acid metabolism in the bowel mucosa by inhibition of cyclooxygenase. This effectively diminishes the production of prostaglandins, thereby reducing colonic inflammation. Production of arachidonic metabolites appears to be increased in patients with inflammatory bowel disease. Mesalamine also inhibits leukotriene synthesis, possibly through inhibition of lipoxygenase. This action has been suggested as a major component of the drug's anti-inflammatory effects.
Inhibition of colonic mucosal sulfidopeptide leukotriene synthesis and chemotactic stimuli for PMN leukocytes may also occur.
Enteric-coated tab may be of benefit in patients who cannot take uncoated sulfasalazine tab because of GI intolerance; as opposed to NSAIDs, a therapeutic response is not observed immediately but can be seen in 4 wk (12 wk treatment may be required in some patients).

Tumor necrosis factor inhibitors

Tumor necrosis factor (TNF) is a cytokine of which 2 forms have been identified with similar biologic properties. TNF-alpha, or cachectin, is produced predominantly by macrophages, and TNF-beta, or lymphotoxin, is produced by lymphocytes. TNF is but one of many cytokines involved in the inflammatory cascade that may contribute to symptoms.

Infliximab (Remicade)

Neutralizes cytokine TNF-alpha and inhibits its binding to TNF-alpha receptor. Mix with 250 mL normal saline for infusion over 2 h. Must use with low-protein–binding filter (<1.2 µm). Indicated to reduce signs and symptoms of active arthritis in patients with PsA.

Adalimumab (Humira)

Recombinant human IgG1 monoclonal antibody specific for human TNF. Binds specifically to TNF-alpha and blocks interaction with p55 and p75 cell-surface TNF receptors. Indicated for reducing signs and symptoms of active arthritis in PsA.

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