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

Psoriatic Arthritis

Michael F Saulino, MD, PhD, Assistant Professor, Department of Physical Medicine and Rehabilitation, Thomas Jefferson University, MossRehab
Jeffrey M Heftler, MD, Interventional Physiatrist, Orthopaedic and Neurosurgical Specialists, Greenwich, CT

Updated: Mar 24, 2009

Introduction

Background

Baron Jean Luis Alibert first described psoriatic arthritis (PsA) in 1818. Since then, a variety of terms have been used to describe this type of arthritis. Much time and effort have been invested in determining whether PsA is truly a separate entity from other arthropathies, and the debate has not yet been resolved completely. PsA appears to deserve its own classification; it is a chronic inflammatory arthritis that affects people with psoriasis.^1,2,3 (See image below and Image 1.)

Psoriatic arthritis involving the distal phalangeal joint.

Pathophysiology

As its name implies, psoriatic arthritis (PsA) is a disease that affects the joints in patients with psoriasis. PsA is a chronic inflammatory arthritis that affects the synovium, but it also may be associated with the skin manifestations that accompany psoriasis and with occasional ocular symptoms.

Frequency

United States

Approximately one third of psoriatic patients develop joint manifestations. Because psoriasis affects 1-3% of the US population, the overall prevalence is psoriatic arthritis is estimated to be 0.1-1%.

International

The prevalence of psoriatic arthritis is 1-40%, depending on the population studied. One Italian study reported a prevalence of 0.4 %.

Mortality/Morbidity

While no direct mortality linked to psoriatic arthritis has been identified, significant morbidity is associated with the loss of function because of pain and deformity.

Race

No significant data are available on the effect of race on the prevalence of psoriatic arthritis, but psoriasis is significantly more common in whites than in persons of other racial groups.

Sex

The male-to-female ratio for psoriatic arthritis (PsA) is 1:1, with the exception of some subsets of patients.

• Females are more commonly affected with the symmetrical polyarthritis that resembles rheumatoid arthritis (RA) and the juvenile form.
• A preponderance of males has been noted in the type of PsA that affects the axial spine, for which the male-to-female ratio is 3:1.

Age

Age of onset for psoriatic arthritis is usually 30-55 years. In the juvenile form, the age of onset is 9-11 years.

Clinical

History

• Psoriasis precedes arthritis in 60-80% of patients.
• The duration between the onset of psoriasis and the onset of arthritis is usually less than 10 years, but it can vary.
• In most patients, the musculoskeletal symptoms are insidious in onset, but an acute onset has been reported in one third of all patients.
• In those patients who present without obvious skin manifestations, a positive family history of psoriasis may be a key to making the diagnosis of psoriatic arthritis (PsA). In such cases, the clinician should search for hidden signs of psoriasis in areas of the skin that are not readily visible, such as the scalp, ears, umbilicus, and anus.
• Symptoms consist of joint pains, morning stiffness, and onychodystrophy (ie, oncolysis, pitting of the nails). (See image below and Image 2.)

Left, typical appearance of psoriasis, with silvery scaling on a sharply marginated and reddened area of skin overlying the shin. Right, thimblelike pitting of the nail plate in a 56-year-old woman who had suffered from psoriasis for the previous 23 years. Nail pitting, transverse depressions, and subungual hyperkeratosis often occur in association with psoriatic disease of the distal interphalangeal joint. Courtesy of Ali Nawaz Khan, MBBS.

• One third of patients may develop inflammatory ocular symptoms reminiscent of reactive arthritis (previously termed Reiter disease).
• Evidence indicates that PsA is more frequent in patients with severe psoriasis than in those with milder cases. While this is true, no evidence indicates that the severity of the psoriasis relates to the pattern of joint involvement.
• Elderly onset (>60 y) PsA has a more severe onset and more destructive outcome than PsA that affects younger subjects.

Physical

Psoriatic arthritis (PsA) manifests in a variety of forms, with 5 classic patterns originally being described by Wright in 1959. Peripheral joint disease occurs in 95% of the patients, and, in the other 5%, axial spine involvement occurs exclusively. (See images below and Images 8, 9.)

Lateral radiograph of the cervical spine shows posterior element fusion. Courtesy of Bruce M. Rothschild, MD.

Lateral radiograph of the cervical spine shows syndesmophytes at the C2-3 and C6-7 levels, with zygapophyseal joint fusion. Courtesy of Bruce M. Rothschild, MD.

• Asymmetrical oligoarthritis
  • This is the best-known pattern of PsA; it occurs in up to two thirds of all patients with PsA.
  • It is characterized by asymmetrical involvement of fewer than 4 joints.
  • The most common manifestation of this condition is involvement of a large joint (eg, the knee), with scattered involvement of the distal interphalangeal (DIP), proximal interphalangeal (PIP), or metatarsophalangeal joints. (See images below and Images 3, 6, 7.)

Asymmetrical arthritis pattern of psoriatic arthritis (fixed flexion deformity).

Swelling and deformity of the metacarpophalangeal and distal interphalangeal joints in a patient with psoriatic arthritis.

Psoriatic arthritis involving the distal phalangeal joint.

• Sausage digits may be evident on presentation, as may pitting edema in the distal extremities.
• Symmetrical polyarthritis
  • This is also called referred to as the distal predominant form of arthritis.
  • It involves the wrists, small joints of the hands and feet, ankles, knees, and elbows and is very difficult to distinguish from rheumatoid arthritis. (See image below and Image 4.)

Comparison of sites of involvement in the hands and feet in psoriatic arthritis and rheumatoid arthritis.

• This form occurs in approximately 25% of patients with PsA and is slightly more common in females than in males.
• Test findings for rheumatoid factor (RF) generally are negative, which helps to differentiate this form of PsA from other conditions.
• If a patient has psoriasis and symmetrical polyarthritis, look for the characteristic clinical features of PsA (eg, dactylitis, enthesis, DIP or sacroiliac joint involvement) or radiologic evidence to make the diagnosis.
• Arthritis mutilans
  • This is a rare form of PsA that occurs in 1-5% of patients.
  • Osteolysis of the phalanges and metacarpals occurs, resulting in telescoping of the digits or opera-glass deformity. Redundant skin over resorbed joints may be present. (See image below and Image 5.)

Arthritis mutilans (ie, "pencil-in-cup" deformities).

• This type of arthritis can be extremely disabling, especially with destruction of the digits.
• Juvenile PsA
  • This form of PsA is a chronic inflammatory arthritis that occurs before age 16 years and is accompanied by the skin manifestations of psoriasis.
  • Making a definitive diagnosis may be difficult because the arthritis may precede any rash.
  • Approximately 50% of patients with PsA have a family history indicating a familial incidence of the condition, which may aid in making the final diagnosis.
  • Usually, 1-5 joints are affected in an asymmetrical pattern.
  • The median age of onset is 4.5 years in girls and 10 years in boys.
  • The most commonly affected joints are the large joints, followed by the PIP joints of the hands and feet and then the DIP joints.
• Spondylitis
  • This occurs in up to 40% of patients with PsA. Spondylitis often does not cause symptoms, but it may manifest as mild back pain despite significant findings on radiographs.
  • Random involvement of the axial spine is characteristic, unlike with ankylosing spondylitis, which affects the lumbar spine first and then progresses toward the cervical spine.
  • Spondylitis may follow 1 of 2 patterns, as follows:
    • The first type is characterized by involvement of the axial spine alone. Radiologic evidence shows sacroiliitis and nonmarginal and asymmetrical syndesmophytes. The lumbar spine is the most commonly affected area. Enthesopathic erosions also may be observed, often at the insertion of the Achilles tendon into the calcaneus.
    • The second type of spondylitis is characterized by an overlap of involvement of the spinal and peripheral joints.
• Extra-articular features associated with PsA
  • The typical skin lesion is a well-demarcated, erythematous plaque with silver white scales; however, such lesions may lack silvery scales on flexor surfaces. Typically, the skin lesions of psoriasis are present for approximately 10 years prior to the onset of the arthropathy.
  • Nail changes include pitting, onycholysis, hyperkeratosis, yellowing, and transverse ridging (Beau lines); fungal nail diseases should be excluded. Nail changes are seen in up to 87% of patients with PsA, compared with 40-45% of patients with psoriasis alone.
  • Eye disease is associated with PsA. Conjunctivitis occurs in 20% of patients; iritis occurs in 7% (more with axial involvement).

Extra-articular features associated with PsA were the subject of a 2009 study that, looking at almost 1,600 patients with psoriasis, found evidence that scalp lesions, nail dystrophy, and intergluteal/perianal psoriasis could be linked to a greater likelihood of PsA in these individuals.⁴ The hazard ratios associated with these predictors were 3.89, 2.93, and 2.35, respectively.

Causes

At this time, no single causative agent has been identified to account for the findings associated with psoriatic arthritis (PsA). The following theories attempt to explain the causes of this condition.

• Genetic predisposition^5,6
  • Evidence suggests that PsA may be affected by genetic factors, but it follows a polygenetic inheritance pattern. This theory is supported by the strong family history of psoriasis seen in patients.
  • Note that a 70% concordance rate is recognized between monozygotic twins, indicating that other factors are at play besides the genetic component.
  • Certain HLA antigens have been found to be predicative of disease progression.²
• Environmental factors
  • Because some evidence suggests that infectious agents (eg, streptococci, staphylococci) may have a role in the pathogenesis of psoriasis, they also may be involved in PsA.
  • The theory of environmental factors playing a role involves a process of superantigens reacting with autoantigens.
• Immunologic components
  • Increasing evidence points to the activation of lymphocytes as a key component of disease pathogenesis. These cells secrete cytokines, which begin a cascade of reactive changes in the skin and joints.
  • The theory of immunologic involvement is also supported by the fact that immunosuppressive agents are successful in treating PsA.

Differential Diagnoses

Rheumatoid Arthritis

Other Problems to Be Considered

Lupus erythematosus: This condition can produce a rash similar to a psoriatic rash. Usually, the arthritis associated with lupus is not as deforming as that associated with psoriasis arthritis
Rheumatoid arthritis
Secondary syphilis: This can cause rash similar to a psoriatic rash. An arthropathy can be associated with syphilis, but this entity occurs years after the skin lesions have cleared in an untreated patient.
Ankylosing spondylitis: This condition can produce back pain similar to that associated with PsA but without the associated peripheral arthropathy or skin lesion.

Workup

Laboratory Studies

• No laboratory studies can confirm the presence of psoriatic arthritis (PsA).⁷
• HLA testing can assist in the prognosis of disease progression.^2,5
• Nonspecific elevation of the erythrocyte sedimentation rate may occur. Elevated serum uric acid levels have been observed in 10-20% of patients, especially those with severe skin disease.
• Rheumatoid factor (RF) findings may be positive in up to 13% of PsA patients. Testing for RF can aid in diagnostic considerations, but it does not definitively differentiate PsA from rheumatoid arthritis.
• Synovial fluid analysis typically reveals inflammatory cells with an increased number of neutrophils, usually 2,000-15,000/µL. Much higher counts can be seen in persons with larger effusions.

Imaging Studies

• Radiography - This shows a combination of erosion (unlike in ankylosing spondylosis) and bone growth (unlike in rheumatoid arthritis [RA]) in affected joints.⁸ The following changes may be seen:
  • Pencil-in-cup deformity: This is tapering of the proximal phalanx as a result of bony erosion and bone growth in the distal phalanx. (See image below and Image 5.)

Arthritis mutilans (ie, "pencil-in-cup" deformities).

• Joint-space narrowing in the interphalangeal joints, possibly with ankylosis
• Increased joint space in the interphalangeal joints as a result of destruction
• Fluffy periostitis
• Bilateral asymmetrical fusiform soft tissue swelling
• Unilateral or symmetrical sacroiliitis
• Large, nonmarginal, unilateral, asymmetrical syndesmophytes (intervertebral bony bridges) in the cervical, thoracic, and lumbar spine, often sparing some of the segments (See image below and Image 9.)

Lateral radiograph of the cervical spine shows syndesmophytes at the C2-3 and C6-7 levels, with zygapophyseal joint fusion. Courtesy of Bruce M. Rothschild, MD.

• Computed tomography (CT) scanning or magnetic resonance imaging (MRI) of the joints
  • These imaging tests may be useful for detecting early signs of joint synovitis.
  • MRI is particularly sensitive for detecting sacroiliitic synovitis, enthesis, and erosions; it can also be used with gadolinium to increase the sensitivity.
  • MRI may show inflammation in the small joints of the hands, involving the collateral ligaments and soft tissues around the joint capsule, a finding not found in persons with RA.
• Ultrasonography - This has a somewhat undefined but emerging role in the diagnosis and management of psoriatic arthritis, including the ability to differentiate synovitis and enthesitis, accurately and objectively monitor disease activity, and accurately deliver local therapy.

Histologic Findings

Histologic findings from patients with psoriatic arthritis are similar to those found in patients with rheumatoid arthritis. They reveal synovium hyperplasia, polymorphonuclear infiltration early in the disease, and then mononuclear cells later, with cartilage erosion and pannus formation.

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.

Dosing

Adult

Mild to moderate pain: 50 mg PO q4-6h, not to exceed 400 mg/d
RA: 200-400 mg/d PO divided tid/qid

Pediatric

<14 years: Not established
>14 years: Administer as in adults

Interactions

Aspirin decreases effects; decreases effects of diuretics; increases toxicity of warfarin and MTX

Contraindications

Documented hypersensitivity; active GI bleeding, ulcer disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Diarrhea may occur (reduce dose or discontinue use)

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.

Dosing

Adult

5-25 mg PO q7d

Pediatric

Not established

Interactions

Oral aminoglycosides may decrease absorption and blood levels of concurrent oral MTX; charcoal lowers levels; coadministration with etretinate may increase hepatotoxicity of MTX; folic acid or its derivatives contained in some vitamins may decrease response to MTX
Coadministration with NSAIDs may be fatal; indomethacin and phenylbutazone can increase plasma levels; may decrease phenytoin serum levels
Probenecid, salicylates, procarbazine, and sulfonamides (including TMP-SMZ) may increase effects and toxicity; may increase plasma levels of thiopurines

Contraindications

Documented hypersensitivity; chronic liver disease; preexisting blood dyscrasia

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause GI intolerance, oral ulcers, alopecia, leukopenia, and hepatotoxicity; careful monitoring of CBC count and liver function recommended; folic acid (1 mg/qd) recommended to limit adverse hematologic effects

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.

Dosing

Adult

2-5 mg/kg PO may be effective while limiting adverse effects

Pediatric

Not established

Interactions

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase toxicity; acute renal failure, rhabdomyolysis, myositis, and myalgias increase when taken concurrently with lovastatin

Contraindications

Documented hypersensitivity; concomitant treatment with psoralen plus UV-A light or UV-B therapy, MTX, or other immunosuppressive agents; coal tar or radiation therapy; abnormal renal function; uncontrolled hypertension; malignancy

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause nephrotoxicity, which is dose related; hypertrichosis; gingival hyperplasia; evaluate renal and liver functions often by measuring BUN, serum creatinine, serum bilirubin, and liver enzyme levels; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO

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.

Dosing

Adult

200-400 mg PO q24h

Pediatric

Not established

Interactions

Serum levels increase with cimetidine; magnesium trisilicate may decrease absorption

Contraindications

Documented hypersensitivity; psoriasis; retinal and visual-field changes attributable to 4-aminoquinolines

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Eye examinations recommended q6mo because of possible retinal pigmentation (if this occurs, discontinue medication); caution in hepatic disease, G-6-PD deficiency, psoriasis, and porphyria; not recommended for long-term use in children; perform periodic (q6mo) ophthalmologic examinations; test periodically for muscle weakness

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).

Dosing

Adult

0.5-1 g/d PO for first wk; increase by 500 mg/d each wk to a maintenance dose of 2 g/d, which may be given in 2-3 divided doses; consideration can be given to increase daily dose of enteric coated tab to 3 g/d PO if clinical response is inadequate after 12 wk

Pediatric

Not established

Interactions

Decreases effects of iron, digoxin, and folic acid; conversely, increases effect of oral anticoagulants, oral hypoglycemic agents, and MTX

Contraindications

Documented hypersensitivity to sulfa drugs or any component; GI or GU obstruction

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Careful monitoring recommended for doses > 2 g/d; oligospermia, infertility, abnormal sperm forms, and impaired sperm motility have occurred in men during sulfasalazine therapy but are reversible upon stopping sulfasalazine; caution in patients with renal or hepatic impairment, blood dyscrasias, or urinary obstruction

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.

Dosing

Adult

5 mg/kg IV infusion at 0, 2, and 6 wk as induction regimen; then, 5 mg/kg q8wk for maintenance
IV infusion must be administered over at least 2 h; must use infusion set with in-line, sterile, nonpyrogenic, low-protein–binding filter (pore size <1.2 µm)

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

TNF-alpha modulates cellular immune responses; anti-TNF therapies (eg, infliximab) may adversely affect normal immune responses and allow development of superinfections; more cases of lymphoma were observed in TNF-alpha blockers compared with control groups; may increase risk of reactivation of tuberculosis in patients with particular granulomatous infections

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.

Dosing

Adult

40 mg SC q2wk

Pediatric

Not established

Interactions

May interfere with immune response to live virus vaccine (MMR) and reduce efficacy; MTX decreases clearance (available data do not support adjusting dose of either drug); coadministration with anakinra (an interleukin 1 antagonist that also blocks TNF) may cause additive adverse effects, particularly development of serious infections

Contraindications

Documented hypersensitivity; active infection

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Causes immunosuppression; may reactivate tuberculosis infection; increases risk for lymphoma development; associated with CNS demyelination (rare); discontinue if serious infection develops; autoantibody development may occur, causing lupuslike syndrome; may cause hypersensitivity reactions, including anaphylaxis and adverse hematologic effects (ie, pancytopenia, aplastic anemia)

Follow-up

Further Inpatient Care

• Patients with psoriatic arthritis who have severe destruction of their joints may require surgical intervention and hospitalization, especially if total joint replacement of the hip and/or knee is performed. The inpatient care varies with each individual case and course of hospitalization.

Further Outpatient Care

• Specific outpatient follow-up care is required for individuals with psoriatic arthritis who undergo surgical repair of their joints. In most cases, conservative treatment is successful and completed in an outpatient setting. Physical and/or occupational therapy is usually recommended, in addition to medications, to minimize pain and stiffness (see Rehabilitation Program).

Prognosis

• Prognosis is generally good for psoriatic arthritis, with most symptoms controlled with medications, but 25% of patients may have progressive disease.

Patient Education

• Education is an important component of the patient's treatment plan because he or she must be able to manage the symptoms of psoriatic arthritis (PsA) and be comfortable with self-treatment strategies. Physical therapists provide education and an exercise program developed for each individual patient. Completing the wrong kind of exercise or overexertion can be harmful for patients with PsA.
• Instructing patients with PsA in methods of joint protection is necessary and becomes part of the therapy process. Patients need to pace themselves and take adequate rest breaks from activity. Other examples of joint protection may include wearing splints on the affected joints, using proper body mechanics and lifting techniques, and assistive devices or adaptive equipment incorporated into activities of daily living.
• For excellent patient education resources, visit eMedicine's Psoriasis Center and Arthritis Center. Also, see eMedicine's patient education articles Psoriatic Arthritis, Psoriasis, and Psoriasis Medications.

Miscellaneous

Medicolegal Pitfalls

• Given the complexity of DMARD therapy, patients with psoriatic arthritis should be followed simultaneously by a rheumatologist and physiatrist. In addition, consultation with an orthopedic surgeon is warranted for individuals who may benefit from joint replacement, arthrodesis, or contracture release.

Multimedia

Media file 1: Psoriatic arthritis involving the distal phalangeal joint.

Media file 2: Left, typical appearance of psoriasis, with silvery scaling on a sharply marginated and reddened area of skin overlying the shin. Right, thimblelike pitting of the nail plate in a 56-year-old woman who had suffered from psoriasis for the previous 23 years. Nail pitting, transverse depressions, and subungual hyperkeratosis often occur in association with psoriatic disease of the distal interphalangeal joint. Courtesy of Ali Nawaz Khan, MBBS.

Media file 3: Asymmetrical arthritis pattern of psoriatic arthritis (fixed flexion deformity).

Media file 4: Comparison of sites of involvement in the hands and feet in psoriatic arthritis and rheumatoid arthritis.

Media file 5: Arthritis mutilans (ie, "pencil-in-cup" deformities).

Media file 6: Swelling and deformity of the metacarpophalangeal and distal interphalangeal joints in a patient with psoriatic arthritis.

Media file 7: Psoriatic arthritis involving the distal phalangeal joint.

Media file 8: Lateral radiograph of the cervical spine shows posterior element fusion. Courtesy of Bruce M. Rothschild, MD.

Media file 9: Lateral radiograph of the cervical spine shows syndesmophytes at the C2-3 and C6-7 levels, with zygapophyseal joint fusion. Courtesy of Bruce M. Rothschild, MD.

References

1. Guttman-Yassky E, Krueger JG. Psoriasis: evolution of pathogenic concepts and new therapies through phases of translational research. Br J Dermatol. Dec 2007;157(6):1103-15. [Medline].

2. Fitzgerald O, Winchester R. Psoriatic arthritis: from pathogenesis to therapy. Arthritis Res Ther. Feb 12 2009;11(1):214. [Medline].

3. Gladman DD. Psoriatic arthritis. Dermatol Ther. Jan-Feb 2009;22(1):40-55. [Medline].

4. [Best Evidence] Wilson FC, Icen M, Crowson CS, et al. Incidence and clinical predictors of psoriatic arthritis in patients with psoriasis: a population-based study. Arthritis Rheum. Feb 15 2009;61(2):233-9. [Medline].

5. Nograles KE, Brasington RD, Bowcock AM. New insights into the pathogenesis and genetics of psoriatic arthritis. Nat Clin Pract Rheumatol. Feb 2009;5(2):83-91. [Medline].

6. Duffin KC, Chandran V, Gladman DD, et al. Genetics of psoriasis and psoriatic arthritis: update and future direction. J Rheumatol. Jul 2008;35(7):1449-53. [Medline].

7. Qureshi AA, Dominguez P, Duffin KC, et al. Psoriatic arthritis screening tools. J Rheumatol. Jul 2008;35(7):1423-5. [Medline].

8. Siannis F, Farewell VT, Cook RJ, et al. Clinical and radiological damage in psoriatic arthritis. Ann Rheum Dis. Apr 2006;65(4):478-81. [Medline].

9. [Best Evidence] Saad AA, Symmons DP, Noyce PR, et al. Risks and benefits of tumor necrosis factor-alpha inhibitors in the management of psoriatic arthritis: systematic review and metaanalysis of randomized controlled trials. J Rheumatol. May 2008;35(5):883-90. [Medline].

10. Gelfand JM, Gladman DD, Mease PJ, et al. Epidemiology of psoriatic arthritis in the population of the United States. J Am Acad Dermatol. Oct 2005;53(4):573. [Medline].

11. Gladman DD, Antoni C, Mease P, Clegg DO, Nash P. Psoriatic arthritis: epidemiology, clinical features, course, and outcome. Ann Rheum Dis. Mar 2005;64 Suppl 2:ii14-7. [Medline].

12. Kane D. The role of ultrasound in the diagnosis and management of psoriatic arthritis. Curr Rheumatol Rep. Aug 2005;7(4):319-24. [Medline].

13. Krueger JG, Bowcock A. Psoriasis pathophysiology: current concepts of pathogenesis. Ann Rheum Dis. Mar 2005;64 Suppl 2:ii30-6. [Medline].

14. Kyle S, Chandler D, Griffiths CE, Helliwell P, Lewis J, McInnes I, et al. Guideline for anti-TNF-alpha therapy in psoriatic arthritis. Rheumatology (Oxford). Mar 2005;44(3):390-7. [Medline].

15. Levine N. Scaly red plaques on dorsal part of hand. Patient notes morning stiffness and pain. Geriatrics. Dec 2005;60(12):17. [Medline].

16. Nash P, Clegg DO. Psoriatic arthritis therapy: NSAIDs and traditional DMARDs. Ann Rheum Dis. Mar 2005;64 Suppl 2:ii74-7. [Medline].

17. Salaffi F, De Angelis R, Grassi W. Prevalence of musculoskeletal conditions in an Italian population sample: results of a regional community-based study. I. The MAPPING study. Clin Exp Rheumatol. Nov-Dec 2005;23(6):819-28. [Medline].

18. Shbeeb M, Uramoto KM, Gibson LE, O'Fallon WM, Gabriel SE. The epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991. J Rheumatol. May 2000;27(5):1247-50. [Medline].

19. Taylor WJ. Understanding psoriatic arthritis. Hosp Med. Mar 2005;66(3):163-7. [Medline].

20. Taylor WJ, Zmierczak HG, Helliwell PS. Problems with the definition of axial and peripheral disease patterns in psoriatic arthritis. J Rheumatol. Jun 2005;32(6):974-7. [Medline].

21. Winterfield LS, Menter A, Gordon K, Gottlieb A. Psoriasis treatment: current and emerging directed therapies. Ann Rheum Dis. Mar 2005;64 Suppl 2:ii87-90; discussion ii91-2. [Medline].

22. Zangger P, Esufali ZH, Gladman DD, Bogoch ER. Type and outcome of reconstructive surgery for different patterns of psoriatic arthritis. J Rheumatol. Apr 2000;27(4):967-74. [Medline].

Keywords

psoriatic arthritis, arthritis, psoriasis, psoriatic, inflammatory arthritis, arthritis psoriasis, chronic inflammatory arthritis, arthritic psoriasis

Contributor Information and Disclosures

Author

Michael F Saulino, MD, PhD, Assistant Professor, Department of Physical Medicine and Rehabilitation, Thomas Jefferson University, MossRehab
Michael F Saulino, MD, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Coauthor(s)

Jeffrey M Heftler, MD, Interventional Physiatrist, Orthopaedic and Neurosurgical Specialists, Greenwich, CT
Jeffrey M Heftler, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Rajesh R Yadav, MD, Assistant Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas at Houston
Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

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Clinical guidelines:
Guidelines of care for the management of psoriasis and psoriatic arthritis: section 1. overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. American Academy of Dermatology - Medical Specialty Society.  2008 May.  25 pages.  NGC:006435

Guidelines of care for the management of psoriasis and psoriatic arthritis: section 2. psoriatic arthritis: overview and guidelines of care for treatment with an emphasis on the biologics. American Academy of Dermatology - Medical Specialty Society.  2008 May.  14 pages.  NGC:006436

Clinical trials:
Remicade® Rheumatology Registry Across Canada (Study P02843)
Single Dose PG102 in Patients With Active Psoriatic Arthritis
Study Evaluating Epidemiology of Rheumatoid Arthritis, Psoriatic Arthritis and Ankylosing Spondylitis in Australia

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