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Early diagnosis is the key to successful management of psoriatic arthritis, and treatment of this inflammatory disease is largely dependent on which symptoms are predominant.
Early diagnosis is the key to successful management of psoriatic arthritis, and treatment of this inflammatory disease is largely dependent on which symptoms are predominant.
Although professional golfer Phil Mickelson’s diagnosis of psoriatic arthritis (PsA) in 2010 may be the event that spurred widespread awarness of the disease, he joined an estimated 520,000 people in the United States impacted by PsA.1,2
PsA is an immune-mediated disease in which the immune system attacks the skin and joints. PsA can develop slowly with mild symptoms or it can occur with a rapid and severe onset. Early recognition, diagnosis, and treatment of PsA are imperative to help limit structural joint damage that can occur with the disease.3 It is not known exactly what triggers the immunological response, but it can result from an infection, such as strep throat, that activates the immune system. There is also evidence to suggest a hereditary component, with approximately 40% of PsA patients reporting a family member with psoriasis or arthritis.4
In approximately 85% of PsA patients, the skin manifestations of psoriasis such as red, scaly patches precede joint involvement. It is imperative that patients with plaques communicate with their health care providers if they develop any joint pain. Although estimates vary widely, it is thought that up to 30% of patients with psoriasis develop PsA. However, PsA can also present in patients without skin lesions, especially in those patients who have relatives with plaque psoriasis. The onset of PsA usually occurs between the ages of 30 to 50 years, with an equal prevalence among males and females.4
PsA typically presents with 1 or more symptoms such as fatigue; pain or swelling over tendons; swollen fingers and toes; stiffness, pain, swelling, and tenderness in 1 or more joints; a reduced range of motion; morning stiffness and tiredness; toenail or fingernail changes that may mimic a fungal infection; and redness or pain of the eye. PsA may also develop in a joint after an injury and can have much of the same symptomatology of a cartilage tear. Although PsA often affects the distal joins in appendages, the lower back, wrist, knees, and ankles may also be impacted.3
Diagnosis of Psoriatic Arthritis
Diagnosis of PsA is made on a clinical basis and often follows the “classification criteria for psoriatic arthritis” (CASPAR). To be classified as having PsA, a patient must meet 3 or more of the following criteria: evidence of psoriasis including current psoriasis, personal history of psoriasis, or family history of psoriasis; psoriatic nail dystrophy; negative test for rheumatoid factor; current or past history of dactylitis (swelling of an entire digit); or radiological evidence of juxta-articular new bone formation.
PsA must be distinguished from other conditions such as rheumatoid arthritis (RA) and gout. RA generally involves joints symmetrically on both sides of the body and rheumatoid factor is normally present in RA patients where it is not typically found in those patients impacted by PsA. However, it is possible but rare to have a patient concomitantly diagnosed with PsA and RA. Patients can also be misdiagnosed with gout, particularly if their PsA symptoms present in the big toe. In addition, uric acid levels can be elevated in PsA patients due to skin cell turnover or an aspirin regimen.5
There are 5 types of PsA: symmetric PsA, asymmetric PsA, distal interphalangeal predominant, spondylitis, and arthritis mutilans (Table 1).6
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Treatment of Psoriatic Arthritis
Treatment of PsA is largely dependent on predominant symptoms and most likely involves both a dermatologist and a rheumatologist.
The skin symptoms related to psoriasis are often treated with topical medications. These topical products include topical corticosteroids to reduce inflammation and swelling along with antrhalin, synthetic vitamin D3, vitamin A, salicylic acid, and coal tar. Additional topical treatments may center on moisturizing, soothing, reducing scaling, and relieving itching and include aloe vera, jojoba, zinc pyrithione, and capsaicin. Phototherapy can also be used to treat the skin lesions that may be present with PsA. Ultraviolet light B (UVB), ultraviolet light A (UVA), psoralen plus UVA (PUVA), and laser treatments have all been used as part of a phototherapy regimen to treat psoriasis.7
Initial treatment of the arthritis component of PsA is centered on reducing the pain and inflammation. Nonsteroidal anti-inflammatories that block both cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2) such as ibuprofen, naproxen, aspirin, and nabumetone are often used to reduce joint pain and inflammation. COX-2 inhibitors that are selective for the action of COX-2, such as celecoxib, can also be used.4,6
If the arthritis and psoriasis symptoms don’t respond to the initial treatments, disease modifying anti-rheumetic drugs (DMARDs) and immunosuppressants may be used. These include sulfasalazine, methotrexate, cyclosporine, leflunomide, and azathioprine. Although labeled DMARDs, these drugs do have an impact on the autoimmune etiology of the psoriasis component as well.4,6
In addition to the DMARDs, there are biologic options for the treatment of PsA. Adalimumab (Humira; Abbott), etanercept (Enbrel; Amgen), golimumab (Simponi; Janssen), infliximab (Remicade; Janssen), certolizumab (Cimzia; UCB), and ustekinumab (Stelara; Janssen) all carry the FDA’s indication to treat PsA. These biologic drugs work to decrease the symptomatology of both the psoriatic component as well as the arthritic component and may prevent joint deterioration.8-13
Adalimumab, etanercept, golimumab, infliximab, and certolizumab are inhibitors of tumor necrosis factor-α (TNF-α). This action downregulates the signals that cause inflammation and interrupt the inflammatory cycle present in PsA. The anti-TNF agents carry a boxed warning indicating the importance of avoiding anti TNF-α agents if patients have an active serious infection or develop one during treatment. Test patients for latent tuberculosis prior to starting treatment and monitor for active tuberculosis during treatment.
There is a boxed warning indicating that lymphoma and other malignancies can occur in patients being treated with TNF blockers, so it is important to monitor patients for any signs of malignancy. It is also important to monitor for worsening or new onset heart failure when a patient is using a TNF blocker and anaphylaxis or serious allergic reactions can occur. Furthermore, exacerbations or new onset of demyelinating disease is possible, so patients with a history of multiple sclerosis should avoid TNF blockers. Patients who are hepatitis B virus (HBV) carriers should be monitored during and for several months after therapy for potential HBV reactivation. The most common adverse events with these agents are infections, injection site reactions (adalimumab and etanercept) or infusion reactions (infliximab), headache, and rash.8-12
Ustekinumab is an interleukin(IL)-12 and an IL-23 antagonist. IL-12 and IL-23 are cytokines that are involved in inflammatory and immune responses, such as natural killer cell activation and CD4+ T-cell proliferation. By disrupting this signaling pathway, the inflammatory cycle present in PsA may be reduced. Although not called out by the FDA as a boxed warning in the prescribing information, it is still important to monitor for signs and symptoms of infection or malignancies and to perform a test for latent tuberculosis prior to starting treatment and to monitor all patients for active tuberculosis during treatment.
Anaphylaxis and other hypersensitivity reactions can occur and it is important to monitor for the possibility of reversible posterior leukoencephalopathy syndrome (RPLS) as there was 1 case reported. RPLS is a neurological disorder not caused by demyelination or a known infection. It presents with headache, seizures, confusion, and visual disturbances. Similarly to the anti-TNF agents, common adverse reactions consist of increased risk of infections, headache, and fatigue.13 SPT
The above information is a selective summary of publicly available information and is accurate as of the date of writing. Please consult the sources for complete reference information. The views expressed in this article are those of the author alone and not of Managed Health Care Associates, Inc, or Diamoto Specialty Pharmacy Inc.
References
About the Author
Stacey Ness, PharmD, RPh, CSP, MSCS, AAHIVP, has worked in both national specialty pharmacy and payer organizations and has experience in clinical management, adherence and persistency programs, as well as chronic disease cost optimization strategies. Dr. Ness is active in the Consortium of Multiple Sclerosis Centers, Academy of Managed Care Pharmacy, National Home Infusion Association, National Association of Specialty Pharmacy, Specialty Pharmacy Certification Board, and Hematology and Oncology Pharmacy Association, and has served on the Minnesota Medicaid Drug Formulary Committee since 2008. She is a multiple sclerosis certified specialist, a credentialed HIV pharmacist, a certified specialty pharmacist, and currently serves as the director of specialty clinical services at Managed Health Care Associates, Inc, a health care services organization based in Florham Park, New Jersey.