eMedicine Specialties > Dermatology > Papulosquamous Diseases

Psoriatic Arthritis: Treatment & Medication

Author: Karolyn A Wanat, MD, Resident Physician, Department of Dermatology, University of Pennsylvania School of Medicine
Coauthor(s): 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
Contributor Information and Disclosures

Updated: Oct 30, 2009

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.

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

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

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

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.

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

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

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

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.

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

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

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

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.

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

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

Documented hypersensitivity; GI bleeding or renal insufficiency

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.

Adult

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

Pediatric

Not established

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

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

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.

Adult

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

Pediatric

Not established

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

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.

Adult

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

Pediatric

Not established

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

Documented hypersensitivity; active GI bleeding

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.

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

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

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

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.

Adult

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

Pediatric

Administer as in adults

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

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

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.

Adult

25 mg SC twice weekly

Pediatric

0.4 mg/kg SC; maximum single dose 25 mg

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

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.

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

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.

Adult

40 mg SC q2wk

Pediatric

Not established

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

Documented hypersensitivity; active infection

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.

Adult

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

Pediatric

<18 years: Not established

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)

Documented hypersensitivity; active infections

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.

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

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

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

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

More on Psoriatic Arthritis

Overview: Psoriatic Arthritis
Differential Diagnoses & Workup: Psoriatic Arthritis
Treatment & Medication: Psoriatic Arthritis
Follow-up: Psoriatic Arthritis
Multimedia: Psoriatic Arthritis
References
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Further Reading

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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

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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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