eMedicine Specialties > Dermatology > Papulosquamous Diseases

Psoriatic Arthritis

Karolyn A Wanat, MD, Resident Physician, Department of Dermatology, University of Pennsylvania School of Medicine
Michael J Dans, MD, PhD, Clinical Instructor, Department of Dermatology, University of California at San Francisco; Abby S Van Voorhees, MD, Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania

Updated: Oct 30, 2009

Introduction

Background

Psoriatic arthritis is a chronic inflammatory arthritis that is commonly associated with psoriasis. At least 5% of patients with psoriasis develop psoriatic arthritis. The association between psoriasis and arthritis was first made in the mid 19th century, but psoriatic arthritis was not clinically distinguished from rheumatoid arthritis until the 1960s. Precisely defining psoriatic arthritis is still difficult because of a lack of specific biologic tests. Psoriatic arthritis is most commonly a seronegative oligoarthritis found in patients with psoriasis with less common but characteristic differentiating features of distal joint involvement and arthritis mutilans. Because 50% of patients with psoriatic arthritis have evidence of spondyloarthropathy, often HLA-B27 associated, psoriatic arthritis has also been classified among the seronegative spondyloarthropathies.

Severe psoriatic arthritis showing involvement of the distal interphalangeal joints; distal flexion deformity; and telescoping of the left third, fourth, and fifth digits due to destruction of joint tissue.

Pathophysiology

Psoriatic arthritis is an autoimmune inflammatory condition affecting the skin and the joints as well as the insertion sites of tendons, ligaments, and fascia. Overexpression of tumor necrosis factor (TNF)-alpha is thought to play a key role. Multiple HLA associations are known. Although psoriatic arthritis is sometimes seen in the absence of detectable skin lesions, it is thought to be more frequent in patients with severe cutaneous disease. However, the exact etiology is unknown and is probably multifactorial, including immune-mediated, genetic, and environmental causes. Environmental factors may include trauma, infection, and stress.

Frequency

United States

In the United States, psoriatic arthritis affects at least 5% of patients with psoriasis. Psoriatic arthritis is thought to occur in up to 1% of the general population. Prevalence rates vary widely between studies. A random telephone survey of 27,220 US residents found a prevalence rate of psoriatic arthritis to be 0.25% in the general public and 11% among patients with psoriasis, although the exact frequency remains uncertain and has been cited between 5-30%.

International

Internationally, the incidence of psoriatic arthritis is 1-40%, depending on the population studied.

Mortality/Morbidity

Psoriatic arthritis usually follows an undulating course, with flares and remissions. Significant morbidity may occur, with long-standing or mutilating disease resulting in joint destruction. Although psoriatic arthritis was originally thought to be relatively mild, as many as 40% of patients may develop erosive and deforming arthritis.

Race

The effect of race on the prevalence of psoriatic arthritis is not well studied. However, whites are known to be affected more commonly than persons of other racial groups.

Sex

Overall, men and women are affected equally by psoriatic arthritis. However, a male predominance occurs in the spondylitic form and a female predominance occurs in the rheumatoid form.

Age

Psoriatic arthritis usually develops in the fourth to sixth decades of life, but it can occur at almost any age.

Clinical

History

Psoriatic arthritis may appear in a variety of clinical patterns (see Physical).

• Psoriasis appears to precede the onset of psoriatic arthritis in 60-80% of patients. Occasionally, arthritis and psoriasis appear simultaneously. In addition, cutaneous eruptions may be preceded by the arthropathy.
• Joint stiffness, while not specific for psoriatic arthritis, can be a prominent symptom.
• In a patient who presents with musculoskeletal symptoms without a history of psoriasis, the diagnosis can be suspected based on a family history of psoriasis; the pattern of arthritis; and the presence of psoriasis in frequently overlooked areas, such as the umbilicus, the gluteal cleft, and the ears. Although the association between severe psoriasis and the development of psoriatic arthritis is clear, the severity of psoriasis does not appear to be related to the pattern of joint involvement.
• Factors that do increase the risk of a patient with psoriasis developing arthritis in their lifetime include the presence of nail lesions as well as more extensive skin involvement. A family history of psoriatic arthritis also increases the risk of developing arthritis.

Physical

Diagnosis of psoriatic arthritis can be problematic in the absence of overt skin lesions. Joint findings may include dactylitis (sausage digits), enthesopathy (reflecting inflammation of the insertion points of tendon into bone), tendonitis, and spondylitis. A careful physical examination, including evaluation of the scalp, the gluteal crease, the umbilicus, the axillae, and the nails, may aid in making the diagnosis of psoriatic arthritis.

Psoriatic arthritis showing nail changes, distal interphalangeal joint swelling, and sausage digits.

• Clinical patterns of arthritis
  • Asymmetric oligoarthritis occurs in as many as 70% of patients with psoriatic arthritis. As many as 4 large joints are affected, often with acute scattered involvement of the metatarsophalangeal, proximal interphalangeal, and DIP joints. Sausage digits due to inflammation of the flexor tendons and synovium and pitting edema of the distal extremities may be observed.
  • DIP joint involvement occurs in approximately 5-10% of patients with psoriatic arthritis. One or several DIP joints may be involved. Periarticular swelling and acute inflammation with warmth and rubor may occur. DIP joint involvement and concomitant nail involvement with acute paronychia is a characteristic picture.
  • Symmetric psoriatic arthritis of the small joints of the hands and the feet, the knees, and the elbows usually follows a mild course and is difficult to distinguish from rheumatoid arthritis. Rheumatoid factor seronegativity, a history of psoriasis, the presence of DIP involvement, and characteristic radiographic findings all support a diagnosis of symmetric polyarthritis. This form affects as many as 25% of patients.
  • Arthritis mutilans is a rare form of psoriatic arthritis occurring in 5% of patients with psoriatic arthritis. Osteolysis of the phalanges and the metacarpals causes a telescoping motion of the digits, noted as opera-glass deformity or pencil-in-cup radiographic findings. Fever may accompany arthritis mutilans.
  • Spondylitis occurs in approximately 5% of patients with psoriatic arthritis and is often asymptomatic. Radiographic evidence of sacroiliitis may be present in as many as 20% of patients. The axial spine may be involved alone or in conjunction with peripheral joints. The vertebrae are asymmetrically affected. Atlantoaxial joint involvement may lead to subluxation. Male patients are more frequently affected than female patients.
  • Psoriatic nail lesions, soft tissue thickening above the terminal phalanx, and radiologic involvement of the phalanx with periosteal reaction and bone have been described under the term psoriatic onychopachydermoperiostitis (POPP). POPP must be differentiated from other forms of psoriatic arthritis, especially the DIP joint type. A periosteal reaction of the terminal phalanx in the absence of DIP joint involvement is characteristic of POPP. In addition, pain and soft tissue thickening is more common in POPP. Nail disease is common to both POPP and DIP psoriatic arthritis. The nails of the great toes are involved in most reported cases of POPP.¹
  • Juvenile psoriatic arthritis is usually mild and often monoarticular. Tenosynovitis and nail involvement are common. Sacroiliitis is associated with HLA-B27 positivity. When unfused epiphyses are inflamed, disordered bone growth and foreshortening can result. Children have a higher frequency of simultaneous onset of psoriasis and psoriatic arthritis.
• Other associations
  • First described by Chamot et al in 1987, synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO) syndrome is characterized by variable bone changes (hyperostosis, arthritis, aseptic osteomyelitis) of the chest wall, sacroiliac joints, and long bones. Dermatologic manifestations include palmoplantar pustulosis, hidradenitis suppurativa, pustular psoriasis, dissecting cellulitis of the scalp, Sweet syndrome, and Sneddon-Wilkinson disease. Skin and osseous involvement may occur simultaneously or be separated by as long as 20 years.^2,3
  • The number of diagnosed cases of psoriasis and psoriatic arthritis has risen dramatically in sub-Saharan Africa in association with the escalating epidemic of HIV infection. Although HIV infection is not known to affect the incidence of psoriasis, it may significantly exacerbate otherwise limited disease. The evolution of mild psoriasis to erythroderma in the setting of a flare-up of psoriatic arthritis may be a sign of HIV infection.

Causes

Although the exact cause of psoriatic arthritis is unknown, genetic, environmental, immunologic, and vascular factors contribute to one's predisposition.

• Genetic factors
  • Approximately 40% of patients with psoriasis or psoriatic arthritis have first-degree relatives who are affected. The sibling occurrence risk is approximately 8%. Although concordance rates of psoriatic arthritis in twins are not yet known, a 65-72% concordance rate of psoriasis exists between monozygotic twins, compared with a 15-30% concordance for dizygotic twins. A 65-72% concordance exists between monozygotic twins compared with a 15-30% concordance for dizygotic twins.
  • The following important genetic susceptibility loci have been elucidated^4,5,6,7,8,9 :
    • Early-onset psoriasis: HLA-Cw6, HLA-B57, HLA-DR7, and HLA-B17 with HLA-Cw*0602 variant found to be highly associated
    • Psoriasis: HLA-Cw6 (or psoriasis susceptibility 1 [PSOR1] on chromosome 6) and 6 other psoriasis susceptibility loci (PSOR2, PSOR3, PSOR4, PSOR5, PSOR6, PSOR7), transcription factor RUNX1
    • Psoriatic arthritis: HLA-B7, HLA-B27, HLA-DR4, HLA-38, HLA-DR7
    • Psoriasis and psoriatic arthritis: HLA-Cw6, HLA-B13, HLA-B17, HLA-B57, and HLA-B39
    • Predictors for gene progression: HLA-B39; HLA-B27 in the presence of HLA-DR7; HLA-DQ3 in the absence of HLA-DR7
    • Protective: HLA-B22
  • The following associated gene polymorphisms are also thought to be associated with psoriasis and psoriatic arthritis^{4,6,8,10,11,12,13,14} :
    • TNF-alpha promoter
    • MHC class I-chained related gene A (MICA)
    • Caspase-activating recruitment domain (CARD) 15
    • Interleukin (IL)–12/IL-23p40 and IL-23 receptor
• Environmental factors: Although trauma and infection are thought to play a role in the etiology of psoriatic arthritis, no conclusive evidence supports this notion. Infection-mediated molecular mimicry is theorized to play a pathogenic role through immunologic factors.
• Immunologic factors: Much evidence suggests that a T-cell–mediated process drives the pathophysiology of psoriasis and psoriatic arthritis. Activated T cells may contribute to the enhanced production of cytokines found in synovial fluid. Th1 cytokines (eg, TNF-alpha, IL-1beta, IL-10) are more prevalent in psoriatic arthritis than in rheumatoid arthritis. Monocytes also play a role in psoriatic arthritis and are responsible for the production of matrix metalloproteinases, which may mediate the destructive changes in the joints of patients with psoriatic arthritis.^9,15
• Vascular factors: Slight differences exist in the vascular patterns of joints in psoriatic arthritis compared with those of rheumatoid arthritis, suggesting possible different pathogenic mechanisms of these diseases.¹⁶

Differential Diagnoses

Psoriasis, Nails
Psoriasis, Plaque
Psoriasis, Pustular

Other Problems to Be Considered

Gout
Osteoarthritis
Rheumatoid arthritis
Septic arthritis

Workup

Laboratory Studies

Psoriatic arthritis is a chronic inflammatory condition for which no specific laboratory tests are available. The diagnosis is based primarily on clinical and radiographic findings. The main differential diagnosis is rheumatoid arthritis.

Comparison of Expected Laboratory Values in Psoriatic Arthritis and Rheumatoid Arthritis

Imaging Studies

The following radiographic abnormalities are suggestive of psoriatic arthritis:

• Paramarginal erosions without osteopenia
• Fluffy periosteal bone formation
• Bony ankylosis
• Pencil-in-cup deformity
• Acro-osteolysis
• Asymmetric sacroiliitis
• Large, nonmarginal, nonconsecutive syndesmophytes

Treatment

Medical Care

The goal of treatment is to improve the patient's quality of life and range of motion, to suppress inflammation, and to minimize the eventual development of destructive joint disease. Surgical intervention in the case of severe joint involvement is occasionally necessary. Regular exercise and an adequate amount of rest are central in the management of psoriatic arthritis.

Medical treatment regimens range from nonsteroidal anti-inflammatory drugs (NSAIDs) to disease-modifying antirheumatic drugs (DMARDs) to newer biologic therapies, such as the anti–tumor necrosis factor (TNF)-alpha medications. Although traditional therapy has consisted of NSAIDs and local corticosteroid injections, with DMARDs being reserved for NSAID-resistant cases, the finding that 40% of patients may develop erosive and deforming arthritis suggests that early, more aggressive treatment with DMARDs may be warranted.

• NSAIDs are considered a first-line therapy for very mild joint disease, but early consideration should be given to DMARDs. NSAIDs may be used in combination with topical therapy for skin involvement. In some cases, NSAIDs may cause worsening of skin involvement, in which case, a different family of NSAIDs should be used. In addition, more aggressive therapy with methotrexate (MTX) or TNF-alpha inhibitors may be used as an initial therapy in order to allow for control of both psoriasis and psoriatic arthritis. TNF inhibitors also prevent the development of joint destruction in psoriatic patients with joint symptoms.
• The most widely used DMARDs are MTX, sulfasalazine, cyclosporine, and leflunomide. These are safe and effective in treating active peripheral arthritis but are not effective in treating axial disease. In addition, no controlled studies have evaluated their efficacy in preventing radiologic joint damage. Combining MTX with cyclosporine or sulfasalazine, as is seen in the treatment of rheumatoid arthritis, may be more effective in some patients.¹⁷
• Antimalarials are generally avoided in patients with psoriatic arthritis for fear of exacerbating psoriatic skin lesions. However, 2 case series describing 50 and 31 patients treated with hydroxychloroquine (Plaquenil) found that no patients had exacerbations of their skin lesions. Given the lack of controlled trials, use of this therapy is not encouraged.¹⁸
• Biologic therapy agents may include etanercept, infliximab, golimumab, adalimumab, alefacept, ustekinumab, and certolizumab, as follows: 
  • Etanercept (Enbrel), Infliximab (Remicade), and Adalimumab (Humira) are biologic agents that inhibit TNF-alpha and have similar efficacy for treating psoriatic arthritis and preventing bony erosions. Etanercept is a fusion protein of the TNF receptor bound to human immunoglobulin G1 (IgG1) Fc domain. Infliximab is a chimeric TNF-alpha monoclonal antibody. Adalimumab is a fully human monoclonal antibody. Golimumab (Simponi) is a human monoclonal antibody against TNF alpha, which was approved by the US Food and Drug Administration (FDA) for treatment of active psoriatic arthritis and ankylosing spondylitis in April 2009.^{19,20,21,22,23}
  • Alefacept (Amevive), a T-cell inhibitor via a human LFA3 Fc fusion protein that blocks the interaction between CD2 on T cells and LFA-3 on antigen-presenting cells, has also been demonstrated to improve signs and symptoms of psoriatic arthritis when used in combination with MTX. It is FDA approved for the treatment of adult patients with moderate-to-severe plaque psoriasis but not yet FDA approved for psoriatic arthritis.²³
  • Ustekinumab, a human immunoglobulin monoclonal antibody that blocks IL-12 and IL-23 by means of antibodies targeting the common p40 chains, has demonstrated efficacy in significantly reducing signs and symptoms of psoriatic arthritis and diminished lesions compared with placebo in a phase II study. It is currently approved for psoriasis in Canada and Europe, but it is still awaiting FDA approval in the United States.^24,25
  • Certolizumab, a polyethylene glycosylated Fab fragment of an anti–TNF alpha monoclonal antibody, has been approved for adult patients with Crohn disease and is thought to have efficacy in psoriatic arthritis because of its mechanism of action. However, no published data about its efficacy are currently available.¹⁴
• Mycophenolate mofetil (CellCept), an immunosuppressive agent widely used in organ transplantation and gaining favor in treating autoimmune and inflammatory skin disorders, may be effective in treating psoriatic arthritis. However, larger controlled studies are needed to prove its efficacy.^26,27
• Systemic corticosteroids are generally avoided because of possible withdrawal-induced rebound of skin disease.
• In a study completed by the Psoriatic Arthritis Study Group, beneficial effects were observed for patients with psoriasis and psoriatic arthritis on stable doses of MTX when one or more courses of intramuscular alefacept were added. Further benefit in psoriatic arthritis was apparent after a second course of alefacept, and no additional toxicity was observed.

Medication

Although indomethacin is the strongest of the available traditional NSAIDs, it is best used for short-term treatment of acute flare-ups because of its GI and CNS adverse effects and its potential to increase blood pressure.

COX-2 inhibitors may be the optimal agents in patients at risk for GI toxicity with NSAIDs.

MTX and cyclosporine are effective in treating both skin disease and joint disease, while sulfasalazine is only effective in treating joint disease. The main limitation of MTX is hepatotoxicity, but liver a biopsy may not be necessary in patients receiving very low doses of MTX. The main limitation of cyclosporine is renal toxicity.

Etanercept (Enbrel) is approved by the FDA for psoriatic arthritis. It has been available for therapy for rheumatoid arthritis for many years and has a good safety profile as to the risk of infection and malignancy. Infliximab (Remicade), adalimumab (Humira), and golimumab (Simponi) are monoclonal anti-TNF antibodies that are also now approved by the FDA to treat psoriatic arthritis. Both etanercept and infliximab are also approved for the treatment of psoriasis, which can be an advantage in patients with concurrent arthritis and skin disease.

Nonsteroidal anti-inflammatory drugs

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action may be inhibition of COX activity and prostaglandin synthesis. Other mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions, may also exist.

Ibuprofen (Motrin, Ibuprin, Advil, Excedrin IB)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Dosing

Adult

400 mg PO q4-6h, 600 mg PO q6h, or 800 mg PO q8h while symptoms persist; not to exceed 3.2 g/d

Pediatric

20-70 mg/kg/d PO divided tid/qid; start at lower end of dosing range and titrate; not to exceed 2.4 g/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; persons at high risk of bleeding

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

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Diclofenac (Voltaren, Cataflam)

Inhibits prostaglandin synthesis by decreasing activity of COX, which, in turn, decreases formation of prostaglandin precursors.

Dosing

Adult

Persistent night pain or morning stiffness: Up to 100 mg PO qhs may help to relieve pain; not to exceed total daily dose of 200 mg

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; persons at high risk of bleeding

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

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if leukopenia, granulocytopenia, or thrombocytopenia persists

Naproxen (Anaprox, Naprelan, Naprosyn, Aleve)

For relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing activity of COX, which is responsible for prostaglandin synthesis.

Dosing

Adult

250-500 mg PO bid; may increase to 1.5 g/d for limited periods

Pediatric

<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

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

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia rarely occurs, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug

Indomethacin (Indocin)

Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.

Dosing

Adult

25-50 mg PO bid/tid
75 mg SR bid; not to exceed 200 mg/d

Pediatric

1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; GI bleeding or renal insufficiency

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

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if leukopenia, granulocytopenia, or thrombocytopenia persists)

Sulindac (Clinoril)

Decreases activity of COX and, in turn, inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Dosing

Adult

150-200 mg PO bid or 300-400 qd; not to exceed 400 mg/d

Pediatric

Not established

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; patients in whom aspirin, iodides, or other NSAIDs induce hypersensitivity; GI bleed and renal insufficiency

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

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

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in preexisting renal disease or compromised renal perfusion; low WBC counts rarely occur and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if leukopenia, granulocytopenia, or thrombocytopenia persists; caution in anticoagulation defects or patients receiving anticoagulant therapy

Celecoxib (Celebrex)

For those at risk of GI toxicity with NSAIDs. Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek lowest dose for each patient.

Dosing

Adult

200 mg/d PO qd; alternatively, 100 mg PO bid

Pediatric

Not established

Interactions

Coadministration with fluconazole may cause increase in plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease plasma concentrations

Contraindications

Documented hypersensitivity

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

May cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, and conditions predisposing to fluid retention; caution in severe heart failure and hyponatremia because may deteriorate circulatory hemodynamics; NSAIDs may mask usual signs of infection; caution in the presence of existing controlled infections; evaluate therapy when symptoms or laboratory results suggest liver dysfunction

Meloxicam (Mobic)

Decreases activity of COX, which, in turn, inhibits prostaglandin synthesis. These effects decrease formation of inflammatory mediators.

Dosing

Adult

7.5 mg PO qd; may increase to 15 mg PO qd

Pediatric

Not established

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of MTX toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; active GI bleeding

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

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

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if leukopenia, granulocytopenia, or thrombocytopenia persists)

Immunosuppressant agents

These agents inhibit key factors in the immune system that are responsible for inflammatory responses.

Methotrexate (Rheumatrex)

Antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction. Adjust dose gradually to attain satisfactory response.

Dosing

Adult

2.5 mg/wk PO/IM initially; administer 3 doses over a 24-h period, then titrate to as high as 25 mg/wk depending on response

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; folic acid or its derivatives contained in some vitamins may decrease response; probenecid, NSAIDs, salicylates, procarbazine, and sulfonamides (including TMP-SMZ) can increase plasma levels; may decrease phenytoin plasma levels; may increase thiopurine plasma levels

Contraindications

Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency

Precautions

Pregnancy

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

Precautions

Monitor CBC counts monthly and liver and renal function q1-3mo during therapy (monitor more frequently during initial dosing, dose adjustments, or when risk of elevated MTX levels, eg, dehydration); has toxic effects on hematologic, renal, GI, pulmonary, and neurologic systems; discontinue if significant decrease in blood cell counts occur; fatal reactions reported when administered concurrently with NSAIDs

Cyclosporine (Sandimmune, Neoral)

Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions, such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease for a variety of organs. Demonstrated to be helpful in a variety of skin disorders, especially psoriasis.

Dosing

Adult

2.5-5 mg/kg/d PO in divided doses

Pediatric

Administer as in adults

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; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UV-B radiation in psoriasis because may increase risk of cancer

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

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 patients who cannot take PO

Biologic therapies

Postulated mechanisms include free radical–mediated oxidative damage to DNA; decreased secretion of IL-6, IL-1-beta, IL-10, and TNF-alpha reduced angiogenesis; induction of IFN-gamma; and IL-2 production by CD8 T cells.

Etanercept (Enbrel)

A fusion protein containing the human TNF receptor bound to a human IgG1 Fc domain. Acts by binding and inhibiting TNF, the cytokine that contributes to inflammatory and immune responses.
Indicated to reduce signs and symptoms of active arthritis in patients with psoriatic arthritis and to help prevent bone erosions.

Dosing

Adult

25 mg SC twice weekly

Pediatric

0.4 mg/kg SC; maximum single dose 25 mg

Interactions

None reported

Contraindications

Documented hypersensitivity; sepsis; concurrent live vaccination; reactivation of tuberculosis; possible drug-induced lupus

Precautions

Pregnancy

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

Precautions

Caution in impaired renal function and asthma; discontinue administration if a serious infection develops; adverse effects may include pain at injection site, localized erythema, rash, UTI symptomatology, GI upset, nausea, vomiting, rhinitis, and cough

Infliximab (Remicade)

Neutralizes cytokine TNF-alpha and inhibits its binding to TNF-alpha receptor. Mix in 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 psoriatic arthritis and to help prevent bone erosions.

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

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

Precautions

TNF-alpha modulates cellular immune responses; anti-TNF therapies, such as 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 psoriatic arthritis.

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 adalimumab or MTX); 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)

Golimumab (Simponi)

Tumor necrosis factor (TNF)–alpha inhibitor. Decreases inflammation caused by overproduction of TNF associated with chronic inflammatory diseases. Indicated for moderate-to-severe rheumatoid arthritis, active psoriatic arthritis, and active ankylosing spondylitis. Available as 50-mg/mL, single-dose Simponi SmartJect (Autoinjector) or a prefilled syringe.

Dosing

Adult

50 mg SC monthly with or without MTX or other nonbiologic DMARD

Pediatric

<18 years: Not established

Interactions

Higher incidence of serious infections may occur when coadministered with abatacept, anakinra, or rituximab (do not administer concurrently); may decrease humoral response to live-virus vaccines (eg, MMR)

Contraindications

Documented hypersensitivity; active infections

Precautions

Pregnancy

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

Precautions

Similar to other TNF–alpha inhibitors, may cause reactivation of tuberculosis or hepatitis B; test patients for latent tuberculosis before initiating treatment; serious infections (eg, bacterial sepsis, severe invasive fungal infections, opportunistic infections) may occur; do not initiate if infection exists, and discontinue if serious infection or sepsis develops; lymphoma incidence increased over general population; may exacerbate existing demyelinating disease or cause new onset of demyelinating disease; may worsen heart failure or may cause new onset of heart failure; common adverse effects include upper respiratory tract infection, sore throat, and nasal congestion

5-Aminosalicylic acid derivatives

These agents inhibit inflammatory reactions and pain by decreasing activity of COX, which is responsible for prostaglandin synthesis.

Sulfasalazine (Azulfidine, EN-Tabs)

Acts locally in colon to decrease the inflammatory response and systemically inhibits prostaglandin synthesis. Loading dose is not necessary.

Dosing

Adult

1 g PO tid/qid initially; titrate to 2-4 g/d in divided doses depending on response

Pediatric

<2 years: Not established
>2 years: 40-60 mg/kg/d PO in 3-6 divided doses; follow by maintenance dose of 20-30 mg/kg/d divided qid

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

Caution in patients with renal or hepatic impairment, blood dyscrasias, urinary obstruction, or G-6-PD deficiency

Follow-up

Deterrence/Prevention

Medications to avoid when possible include beta-blockers, antimalarials (although hydroxychloroquine has been shown to not exacerbate skin lesions), lithium, systemic steroids, and NSAIDs (If skin lesions worsen with an NSAID, switch to a different family of NSAID.).

Prevention includes rest and exercise. Joint protection, including splints, braces, and other supports, may be helpful. No definitive prevention exists because this is a chronic disease that can wax and wane.

Complications

Spondylitis resulting in atlantoaxial subluxation with resultant neurologic complications can occur. Therapy may limit possible disability.

Prognosis

Psoriatic arthritis is often mild, with involvement of only a few joints. Treatments with immunomodulatory medicine can be successful for patients with severe disease.

Patient Education

For excellent patient education resources, visit eMedicine's Psoriasis Center and Arthritis Center. Also, see eMedicine's patient education articles Psoriatic Arthritis, Psoriasis, Types of Psoriasis, Understanding Psoriasis Medications, and Nail Psoriasis.

Excellent information for patients can be found at the following Web sites:

• Arthritis Foundation
• The National Psoriasis Foundation
• University of Missouri Health Care
• The Merck Manual of Diagnosis and Therapy - Arthritis associated with spondylitis
• MEDLINEplus - Psoriatic arthritis

Multimedia

Media file 1: Severe psoriatic arthritis showing involvement of the distal interphalangeal joints; distal flexion deformity; and telescoping of the left third, fourth, and fifth digits due to destruction of joint tissue.

Media file 2: Psoriatic arthritis showing nail changes, distal interphalangeal joint swelling, and sausage digits.

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Keywords

psoriatic arthritis, psoriasis, seronegative spondyloarthropathy, polyarthritis, rheumatoid arthritis, oligoarthritis, chronic inflammatory arthritis, asymmetric oligoarthritis, asymmetrical oligoarthritis, symmetric oligoarthritis, symmetrical oligoarthritis, arthritis mutilans, spondylitis, DIP psoriatic arthritis, distal interphalangeal joint arthritis, juvenile psoriatic arthritis, psoriatic nail lesions

Contributor Information and Disclosures

Author

Karolyn A Wanat, MD, Resident Physician, Department of Dermatology, University of Pennsylvania School of Medicine
Karolyn A Wanat, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and American Medical Women's Association
Disclosure: Nothing to disclose.

Coauthor(s)

Michael J Dans, MD, PhD, Clinical Instructor, Department of Dermatology, University of California at San Francisco
Michael J Dans, MD, PhD is a member of the following medical societies: American Academy of Dermatology and American Medical Association
Disclosure: Nothing to disclose.

Abby S Van Voorhees, MD, Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania
Abby S Van Voorhees, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, National Psoriasis Foundation, Phi Beta Kappa, Sigma Xi, and Women's Dermatologic Society
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Genentech Honoraria Consulting; Incyte Grant/research funds Other; Warner Chilcott Honoraria Consulting; Merck Salary Management position; Abbott  Speaking and teaching

Medical Editor

Alexa F Boer Kimball, MD, MPH, Associate Professor of Dermatology, Harvard University School of Medicine; Vice Chair, Department of Dermatology, Massachusetts General Hospital; Director of Clinical Unit for Research Trials in Skin (CURTIS), Department of Dermatology, Massachusetts General Hospital
Alexa F Boer Kimball, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Managing Editor

Christen M Mowad, MD, Associate Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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