AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 completely resolved. PsA appears to deserve its own classification; it is a chronic inflammatory arthritis that affects people with psoriasis.

Pathophysiology

As its name implies, 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 PsA is estimated at 0.1-1 %.

International

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

Mortality/Morbidity

While no direct mortality 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 PsA, but psoriasis is significantly more common in whites than in persons of other racial groups.

Sex

The male-to-female ratio is 1:1, with the exception of some subsets of patients.

• Females are more commonly affected with the symmetric 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 is usually 30-55 years. In the juvenile form, the age of onset is 9-11 years.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 usually 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 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).
• 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

PsA manifests in a variety of forms, with 5 classic patterns being originally described by Wright in 1959. Peripheral joint disease occurs in 95% of the patients, and, in the other 5%, axial spine involvement occurs exclusively.

• Asymmetric 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 asymmetric 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.
  • Sausage digits may evident upon presentation, as may pitting edema in the distal extremities.
• Symmetric 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 RA.
  • 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 symmetric 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.
  • 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 asymmetric 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).

Causes

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

• Genetic predisposition
• • 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.
• 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.
• Immunological 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 both the skin and joints.
  • The theory of immunological involvement is also supported by the fact that immunosuppressive agents are successful in treating PsA.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• No laboratory studies can confirm the presence of PsA.
• HLA testing can assist in the prognosis of disease progression.
• 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.
• 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 RA.
• 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 RA) in affected joints. 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.
  • 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 asymmetric fusiform soft tissue swelling
  • Unilateral or symmetric sacroiliitis
  • Large, nonmarginal, unilateral, asymmetric syndesmophytes (intervertebral bony bridges) in the cervical, thoracic, and lumbar spine, often sparing some of the segments
• CT scanning or 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 PsA, including the ability to differentiate synovitis and enthesitis, accurately and objectively monitor disease activity, and accurately deliver local therapy.

Histologic Findings

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

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Rehabilitation Program

Physical Therapy

The rehabilitation treatment program 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, including 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 both 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 both 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 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 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 physiatrist feels uncomfortable with prescribing some of the medications, 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

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

While symptom management should not be minimized, the advent of disease-modifying antirheumatic drugs (DMARDs) has significantly transformed the treatment of PsA. The most common medications are etanercept (Enbrel), adalimumab (Humira), and infliximab (Remicade). 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 is commonly considered the criterion to institute DMARD therapy. Systemic steroid therapy is typically avoided because of the risk of exacerbating the dermatologic component of psoriasis after withdrawal of the steroids.

Drug Category: 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.

Drug Category: Chemotherapeutic agents

Inhibit cell growth and proliferation.

Drug Category: Immunosuppressive agents

Useful because evidence indicates PsA may be immune mediated.

Drug Category: Antimalarial agents

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

Drug Category: Tumor necrosis factor inhibitors

TNF is a cytokine of which 2 forms have been identified with similar biological 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.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Patients with PsA 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 PsA 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, 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 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 Understanding Psoriasis Medications.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Given the complexity of DMARD therapy, PsA patients should be simultaneously followed by both 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.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• 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].
• Gladman DD, Antoni C, Mease P, et al. Psoriatic arthritis: epidemiology, clinical features, course, and outcome. Ann Rheum Dis. Mar 2005;64 Suppl 2:ii14-7.
• Kane D. The role of ultrasound in the diagnosis and management of psoriatic arthritis. Curr Rheumatol Rep. Aug 2005;7(4):319-24.
• Krueger JG, Bowcock A. Psoriasis pathophysiology: current concepts of pathogenesis. Ann Rheum Dis. Mar 2005;64 Suppl 2:ii30-6.
• Kyle S, Chandler D, Griffiths CE, et al. Guideline for anti-TNF-alpha therapy in psoriatic arthritis. Rheumatology (Oxford). Mar 2005;44(3):390-7.
• Levine N. Scaly red plaques on dorsal part of hand. Patient notes morning stiffness and pain. Geriatrics. Dec 2005;60(12):17.
• Nash P, Clegg DO. Psoriatic arthritis therapy: NSAIDs and traditional DMARDs. Ann Rheum Dis. Mar 2005;64 Suppl 2:ii74-7.
• Salaffi F, De Angelis R, Grassi W, et al. 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.
• Shbeeb M, Uramoto KM, Gibson LE, et al. The epidemiology of psoriatic arthritis in Olmsted County, Minnesota, USA, 1982-1991. J Rheumatol. May 2000;27(5):1247-50.
• Siannis F, Farewell VT, Cook RJ, et al. Clinical and radiological damage in psoriatic arthritis. Ann Rheum Dis. Apr 2006;65(4):478-81.
• Taylor WJ. Understanding psoriatic arthritis. Hosp Med. Mar 2005;66(3):163-7.
• 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.
• 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.
• 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.

Article Last Updated: Aug 11, 2006