eMedicine Specialties > Rheumatology > Spondyloarthropathies

Psoriatic Arthritis: Treatment & Medication

Author: Anwar Al Hammadi, MD, FRCPC, Consultant Dermatologist, Assistant Clinical Professor of Dermatology, University of Sharjah, Dubai, United Arab Emirates
Contributor Information and Disclosures

Updated: Apr 29, 2009

Treatment

Medical Care

The treatment of psoriatic arthritis is directed at controlling the inflammatory process. Although no clear correlation exists between the skin and joint inflammation in every patient, the skin and joint aspects of the disease often must be treated simultaneously.

Initial treatment includes nonsteroidal anti-inflammatory drugs (NSAIDs) for joint disease and topical therapies for the skin. In many patients, this approach is sufficient to control disease manifestations, although some patients have a worsening of psoriasis with NSAIDs. In these patients, a drug belonging to a different family of NSAIDs should be used.

  • Intra-articular injection of entheses or single inflamed joints with corticosteroids may be particularly effective in some patients.  
    • Use disease-modifying drugs in individuals whose arthritis is persistent. If the skin disease is well controlled with topical medication, the joint disease can be treated with a variety of second-line or cytotoxic drugs.
    • Intramuscular administration of gold has been used in the past but has been supplanted by newer disease-modifying antirheumatic drugs.
  • In patients with severe skin inflammation, medications such as methotrexate (MTX), retinoic-acid derivatives, and psoralen plus UV light should be considered. These medications have been shown to work for both skin and joint manifestations.
  • Sulfasalazine and cyclosporine are 2 second-line agents that have received particular attention in the management of psoriatic arthritis. Although these drugs may control the acute inflammation in persons with psoriatic arthritis, they have not been helpful in arresting the progression of clinical and radiologic damage. Thus, the disease must be treated earlier or better drugs are necessary to prevent the damage that may ensue as a result of psoriatic arthritis.  
    • Cyclosporine appears to be an effective agent for the treatment of psoriasis and psoriatic arthritis.
    • The major concern with cyclosporine is its toxicity, especially nephrotoxicity and hypertension. Combination therapy (eg, MTX/sulfasalazine, MTX/cyclosporine) may be more efficacious in some patients.
  • The use of biologic response modifiers that target TNF and other cytokines represents an advance in the treatment of several diseases involving autoimmune mechanisms. Several such agents have been developed, in the form of either soluble fusion proteins (eg, etanercept) or monoclonal antibodies (eg, infliximab, adalimumab), which have shown considerable efficacy in the treatment of rheumatoid arthritis (RA) and other autoimmune diseases.
  • Etanercept is approved by the US Food and Drug Administration for (1) treating adult patients (age >18 y) with chronic, moderate-to-severe plaque psoriasis; (2) reducing the symptoms and signs of moderate-to-severe polyarticular-course juvenile RA and ankylosing spondylitis; and (3) reducing the signs and symptoms and inhibiting the progression of structural damage associated with psoriatic arthritis. Therefore, etanercept may be an effective and safe alternative monotherapy for the treatment of psoriatic arthritis.
  • Infliximab (Remicade) is another TNF-neutralizing agent that has been approved for the treatment of Crohn disease, ulcerative colitis, RA (in combination with MTX), ankylosing spondylitis, and psoriatic arthritis. It has shown successful results in reducing the signs and symptoms of psoriatic arthritis. However, the Food and Drug Administration issued safety warnings for infliximab concerning worsening heart failure in patients with moderate-to-severe congestive heart failure and opportunistic infections such as tuberculosis, histoplasmosis, listeriosis, and pneumocystosis.
  • The effects of other anti-TNF medications on psoriasis and psoriatic arthritis are being studied.
  • In a study completed by the Psoriatic Arthritis Study Group, patients with psoriasis and psoriatic arthritis who were receiving stable doses of methotrexate were found to benefit from the addition of one or more courses of intramuscular alefacept. Further benefit in psoriatic arthritis was apparent after a second course of alefacept, and no additional toxicity was observed.2
  • A recent randomized 6-month study by Scarpa et al (2007) showed the early use of MTX in patients with early psoriatic arthritis markedly improved tender and swollen joints and/or entheses; however, no significant difference was found after 3 months of treatment with NSAIDs or MTX.3 These results suggest that other therapeutic approaches capable of modifying the early course of the disease should be used.
  • Several other modalities have been tried in persons with psoriatic arthritis, including vitamin-D3, bromocriptine, peptide T, and fish oils, but their efficacy remains to be proven.
  • Antimalarials, particularly hydroxychloroquine (Plaquenil), are usually avoided in patients with psoriasis for fear of precipitating exfoliative dermatitis or exacerbating psoriasis. Two studies showed that these reactions did not occur in patients treated with hydroxychloroquine; therefore, it is occasionally used to treat psoriatic arthritis.
  • Systemic corticosteroids are usually avoided because of possible rebound of the skin disease upon withdrawal.

Surgical Care

Arthroscopic synovectomy has been effective in treating severe chronic monoarticular synovitis. Because of the enhanced tendency for fibrosis associated with this therapy, anti-inflammatory and physical therapy measures aimed at improving range of motion are important adjuncts to this intervention. Joint replacement and forms of reconstructive therapy are occasionally necessary.

Diet

For people who have morning stiffness, the optimal time for taking an NSAID might be after the evening meal and again upon awakening. Taking NSAIDs with food can reduce stomach discomfort. Any NSAID can damage the mucous layer and cause ulcers and GI bleeding when taken for long periods. Cyclooxygenase (COX)–2 selective inhibitors are associated with a lower prevalence of gastric ulcer formation.

Activity

  • Exercise
    • Exercise is an important part of the total treatment to limit the pain and swelling of arthritis, which can make joints stiff and hard to move.
    • A directed exercise program can improve movement, strengthen muscles to stabilize joints, improve sleep, strengthen the heart, increase stamina, reduce weight, and improve physical appearance.
  • Rest
    • Generally, a normal amount of rest and sleep is sufficient to decrease fatigue and reduce joint inflammation.
    • In a very few people, psoriatic arthritis may cause extreme fatigue.

Medication

The treatment of psoriatic arthritis usually begins with NSAIDs. These include enteric-coated acetylsalicylic acid, naproxen, indomethacin, ibuprofen, diclofenac, tolmetin, meloxicam, or other NSAIDs. Enteric-coated acetylsalicylic acid and ibuprofen require frequent administration, whereas meloxicam and slow-release indomethacin may be administered in a once-daily routine, which may be preferred by some patients.

Indomethacin is the strongest of the available traditional NSAIDs, although it has significant adverse GI and CNS effects and a potential to increase blood pressure. It is best used for short-term (eg, acute) flares.

NSAIDs clearly control the mild inflammatory features of psoriatic arthritis; however, some NSAIDs may aggravate the skin psoriasis.

Nonsteroidal anti-inflammatory drugs

Have analgesic, anti-inflammatory, and antipyretic activities. Mechanism of action may be inhibition of COX activity and prostaglandin synthesis. Others may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.


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, or 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 200 mg/d

Pediatric

>12 years: Administer as in adults
<12 years: 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; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, 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 persistent leukopenia, granulocytopenia, or thrombocytopenia develops


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 occurs rarely, 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 divided PO 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 persistent leukopenia, granulocytopenia, or thrombocytopenia develops)


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 occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia develops; 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 celecoxib plasma concentrations because of inhibition of celecoxib metabolism; coadministration with rifampin may decrease celecoxib 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 persistent leukopenia, granulocytopenia, or thrombocytopenia develops)

Immunosuppressant agents

Inhibit key factors in the immune system 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 plasma levels of thiopurines

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

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Monitor CBC counts qmo 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 drop in blood cell counts occurs; 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 UVB 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 enzymes; may increase risk of infection and lymphoma; reserve intravenous use only for patients who cannot take PO

5-Aminosalicylic acid derivatives

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 inflammatory response and systemically inhibits prostaglandin synthesis. Loading dose 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

Tumor necrosis factor (TNF) 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.


Etanercept (Enbrel)

Acts by binding and inhibiting TNF, the cytokine that contributes to inflammatory and immune responses. 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.

Adult

25 mg SC twice weekly

Pediatric

0.4 mg/kg SC; maximum single dose 25 mg

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

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

Caution in impaired renal function and asthma; discontinue 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-cc normal saline for infusion over 2 h. Must use with low-protein-binding filter (1.2 micron or less). Indicated to reduce signs and symptoms of active arthritis in patients with psoriatic arthritis.

Adult

5 mg/kg IV infusion at 0, 2, and 6 wks 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 microns)

Pediatric

Not established

Pregnancy

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

Precautions

TNF alpha modulates cellular immune responses; anti-TNF therapies, 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 to controlled groups; may increase risk of reactivation of tuberculosis in patients with particular granulomatous infections


Adalimumab (Humira)

Recombinant human IgG1 monoclonal antibody specific for human tumor necrosis factor (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 HUMIRA 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 lupus-like syndrome; may cause hypersensitivity reactions including anaphylaxis and hematologic adverse effects (ie, pancytopenia, aplastic anemia)


Golimumab (Simponi)

TNF-alpha inhibitor. Decreases inflammation caused by overproduction of TNF associated with chronic inflammatory diseases. Indicated for moderate-to-severe RA, 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 methotrexate 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

More on Psoriatic Arthritis

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

References

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Further Reading

For additional information, see Medscape’s Psoriasis Resource Center and Arthritis Resource Center.

Keywords

psoriatic arthritis, spondylitic psoriatic arthritis, rheumatoid psoriatic arthritis, psoriasis, arthritis, skin disease, bone disease, rheumatism, rheumatoid arthritis, psoriatic arthropathy, arthritis mutilans, arthropathia psoriatica, psoriatic spondylitis, asymmetrical seronegative oligoarticular arthritis, dactylitis, sausage digits, pencil-in-cup radiograph, opera-glass hand, asymmetrical oligoarticular arthritis, symmetrical polyarthritis, distal interphalangeal arthropathy, juvenile psoriatic arthritis, sacroiliitis

Contributor Information and Disclosures

Author

Anwar Al Hammadi, MD, FRCPC, Consultant Dermatologist, Assistant Clinical Professor of Dermatology, University of Sharjah, Dubai, United Arab Emirates
Anwar Al Hammadi, MD, FRCPC is a member of the following medical societies: American Academy of Dermatology, Canadian Dermatology Association, Royal College of Physicians and Surgeons of Canada, and Skin Cancer Foundation
Disclosure: Nothing to disclose.

Medical Editor

Kristine M Lohr, MD, MS, Program Director, Professor, Department of Internal Medicine, Division of Rheumatology and Women's Health, University of Kentucky School of Medicine
Kristine M Lohr, MD, MS is a member of the following medical societies: American College of Physicians, American College of Rheumatology, and American Medical Women's Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Elliot Goldberg, MD, Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine
Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD, Professor of Medicine, Temple University School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital
Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa
Disclosure: medifocus Honoraria Review panel membership; health dialogs Honoraria Consulting; West Penn Allegheny Health System None Board membership

 
 
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