Psoriatic Arthritis Medication

Updated: Oct 25, 2019
  • Author: Anwar Al Hammadi, MD, FRCPC; Chief Editor: Herbert S Diamond, MD  more...
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Medication

Medication Summary

Medical treatment regimens include the use of agents in the following classes of medication:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Immunosuppressants
  • Disease-modifying antirheumatic drugs (DMARDs).
  • Janus kinase (JAK) inhibitors
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Nonsteroidal anti-inflammatory drugs (NSAIDs)

Class Summary

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

For people who have morning stiffness, the optimal time for taking an NSAID may 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 gastrointestinal bleeding when taken for long periods. Cyclooxygenase (COX)–2 selective inhibitors are associated with a lower prevalence of gastric ulcer formation.

Indomethacin (Indocin)

Indomethacin is thought to be the most effective NSAID for the treatment of ankylosing spondylitis, although no scientific evidence supports this claim. It is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Ibuprofen (Motrin IB, Advil, NeoProfen)

Ibuprofen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Naproxen (Naprosyn, Naprelan, Aleve, Anaprox)

Naproxen is used for relief of mild to moderate pain; it inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in a decrease of prostaglandin synthesis.

Diclofenac (Zorvolex, Cambia)

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

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Immunosuppressants

Class Summary

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

Methotrexate (Trexall, Otrexup)

Methotrexate inhibits dihydrofolic acid reductase. It inhibits purine and thymidylic acid synthesis, which in turn interferes with DNA synthesis, repair, and cellular replication; cell cycle specific for S phase of cycle. Methotrexate may inhibit rapid proliferation of epithelial cells in skin.

Cyclosporine (Neoral, Gengraf)

Cyclosporine is a cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions.

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5-Aminosalicylic Acid Derivatives

Class Summary

5-Aminosalicylic acid derivatives inhibit prostaglandin synthesis and reduce the inflammatory response to tissue injury.

Sulfasalazine (Azulfidine, Azulfidine EN-tabs)

Sulfasalazine has been shown to reduce the inflammatory symptoms of psoriatic arthritis.

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DMARDs, TNF Inhibitors

Class Summary

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), that have shown considerable efficacy in the treatment of RA and other autoimmune diseases. [84]

Etanercept (Enbrel, Erelzi)

Etanercept is approved by the US Food and Drug Administration (FDA) 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 (Inflectra, Remicade, Renflexis)

Infliximab is another TNF-neutralizing agent. It has been approved for the treatment of Crohn disease, ulcerative colitis, RA (in combination with methotrexate), ankylosing spondylitis, and psoriatic arthritis (and has shown success in reducing the signs and symptoms of this disease). [65]

However, the FDA has issued safety warnings for infliximab concerning worsening heart failure in patients with moderate to severe chronic heart failure, as well as risk for opportunistic infections such as tuberculosis, histoplasmosis, listeriosis, and pneumocystosis.

Golimumab (Simponi, Simponi Aria)

Golimumab is an FDA-approved human TNF-alpha antibody that is given every 4 weeks as a subcutaneous injection at doses of 50 mg and 100 mg. It has been shown to significantly improve symptoms of psoriatic arthritis. [6, 66]

Ustekinumab (Stelara)

Ustekinumab is an anti-IL-12/23 monoclonal antibody approved for treatment of active psoriatic arthritis in adult patients. It may be administered alone or in combination with methotrexate. It is approved in doses of 45 mg or 90 mg SC given at weeks 0 and 4 and then every 12 weeks. At week 24 of the PSUMMIT 1 trial, 42% of patients receiving 45 mg and 50% of patients receiving 90 mg demonstrated at least a 20% improvement in signs and symptoms as measured by the American College of Rheumatology (ACR 20). These improvements were maintained at week 52 of the study. [67]

Certolizumab pegol (Cimzia)

Other new biologic agents in clinical trials include certolizumab pegol, a PEGylated Fab' fragment of an anti–TNF-alpha monoclonal antibody. Certolizumab pegol has shown promising results in the treatment of RA and may be applicable to the treatment of psoriasis and psoriatic arthritis in the future.

Adalimumab (Amjevita, Cyltezo, Humira, Hadlima, Hyrimoz, Adalimumab-atto, Adalimumab-adbm, Adalimumab-bwwd, Adalimumab-adaz)

Recombinant human anti-TNF-alpha IgG1 monoclonal antibody. Blocks inflammatory activity of TNF-alpha, by specifically binding to TNF-alpha and blocks its interaction with p55 and p75 cell surface TNF receptors. It is indicated for reduction of signs and symptoms, inhibition of progression of structural damage, and improvement of physical function in adults with active psoriatic arthritis. FDA approved adalimumab-atto, adalimumab-adbm, adalimumab-adaz, adalimumab-bwwd as biosimilars and not as interchangeable drugs.

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DMARDs, PDE4 Inhibitors

Class Summary

Agents which increase intracellular cyclic adenosine monophosphate (cAMP), such as PDE4 inhibitors, may have an antagonistic effect on proinflammatory molecule production.

Apremilast (Otezla)

Apremilast is an oral, small molecule inhibitor of phosphodiesterase-4 specific for cAMP, resulting in increased intracellular cAMP levels. The specific mechanism by which apremilast exerts it therapeutic action in psoriatic arthritis is not well defined. It is indicated for treatment of active psoriatic arthritis. It is indicated for active psoriatic arthritis.

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Interleukin Inhibitors

Class Summary

Various interleukins play a role in inflammatory processes.

Secukinumab (Cosentyx)

Human IgG1 monoclonal antibody that selectively binds to and neutralizes the proinflammatory cytokine interleukin 17A (IL-17A). IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. It is indicated for adults with active psoriatic arthritis.

Ixekizumab (Taltz)

Humanized monoclonal IgG4 antibody that targets interleukin-17A (IL-17A) resulting in neutralization of IL-17A’s proinflammatory effects. It is indicated for adults with active psoriatic arthritis; may be administered alone or in combination with a conventional DMARD (eg, methotrexate).

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DMARDs, Immunomodulators

Class Summary

Abatacept is a selective costimulation modulator that inhibits T-cell activation.

Abatacept (Orencia, Orencia ClickJect)

Chimeric protein which inhibits T-lymphocyte activation by binding to CD80 and CD86 located on antigen presenting cells (APC). T-cell activation is dependent on interacting with APC. Indicated for active psoriatic arthritis in adults.

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Janus Kinase (JAK) Inhibitors

Class Summary

These agents modulate the signaling pathway at the point of JAKs and preventing the phosphorylation and activation of STATs. Inhibition of JAKs also prevents cytokine- or growth factor-mediated gene expression and intracellular activity of immune cells, reduces circulating CD16/56+ natural killer cells, serum IgG, IgM, IgA, and C-reactive protein, and increases B cells.

Tofacitinib (Xeljanz, Xeljanz XR)

Tofacitinib inhibits JAK enzymes, which are intracellular enzymes involved in stimulating hematopoiesis and immune cell function through a signaling pathway. In response to extracellular cytokine or growth factor signaling, JAKs activate signal transducers and activators of transcription (STATs), which regulate gene expression and intracellular activity. Inhibition of JAKs prevents cytokine- or growth factor-mediated gene expression and intracellular activity of immune cells, reduces circulating CD16/56+ natural killer cells, serum IgG, IgM, IgA, and C-reactive protein, and increases B cells. Indicated for active psoriatic arthritis (PsA) in patients who have had an inadequate response or intolerance to methotrexate or other DMARDS.

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