One of the major changes I have made in the past decade of evaluating psoriatic patients is to look for symptoms of psoriatic arthritis. After evaluating psoriasis for body surface area and erythema, induration, and scale (0-4), I ask if the patient has any stiffness or tenderness in the fingers and/or toes when they awaken. I then ask if they've had any symptoms or history of dactylitis (swelling of an entire digit) or enthesitis (where a ligament or tendon attaches to a bone; i.e., Achilles, plantar, costocondrol), or any symptoms of sacroiliitis.
The reason I pose these questions is because roughly one quarter of all psoriasis patients develop psoriatic arthritis. While about 10 percent of patients develop the arthritic symptoms before psoriasis and about 10 percent develop arthritic symptoms at the same time as the onset of their psoriasis, in a majority of cases skin disease typically precedes joint disease by up to 10 years. This puts the dermatologist in a perfect position to diagnose psoriatic arthritis before the joint destruction becomes irreversible.
In terms of what to look for when evaluating for psoriatic arthritis, it's worth noting that about 80 percent of patients with psoriatic arthritis have psoriatic onychodystrophy, compared to 30 percent of psoriatic patients without psoriatic arthritis. In addition, psoriatic arthritis has been associated more frequently with scalp psoriasis, intergluteal/ perianal psoriasis, as well as extra-articular manifestations, (i.e., ocular involvement: conjunctivitis, iritis, aortic incompetence [less than four percent]).1
Psoriatic arthritis clinically appears most frequently as a distal interphalangeal (DIP) joint disease pattern either oligoarticular pattern (less than five joints) in an asymmetric distribution, or polyarticular pattern (greater than five joints) in a symmetric distribution. The other two patterns are arthritis mutilans and spondyloarthritis, which affects the sacroiliac joints and apophyseal joints of the spine. A German study evaluating 1,511 patients with psoriasis found that 20 percent of patients had psoriatic arthritis. In addition, 53 percent had five or more joints involved. The most common patterns were oligoarthritis (31 percent), arthritis mutilans (five percent), DIP involvement (41 percent), dactylitis (24 percent), and asymmetric oligoarthritis (31 percent).1
Classification criteria for psoriatic arthritis consists of established inflammatory articular disease with at least three points from the following features:
- Current psoriasis (2 pts)
- History of psoriasis (1 pt)
- Family history of psoriasis (1 pt)
- Dactylitis (a combination of enthesitis of the tendons and ligaments and synovitis involving the whole digit) (1 pt)
- Juxtarticular new-bone formation (1 pt)
- RF negativity (1 pt)
- Nail dystrophy (1 pt)
Disease Course and prognosis
Psoriatic arthritis develops most often between the ages of 30 and 50 and is characterized by stiffness, pain, swelling, and tenderness of the joints and surrounding ligaments and tendons (dactylitis and enthesitis). Progression of clinical damage occurs in the majority of patients with psoriatic arthritis. In fact, approximately 20 percent of patients with psoriatic arthritis have a severe and debilitating form of arthritis.2 Another 40 to 57 percent have deforming erosive arthropathy, while 47 percent have sustained erosive damage within two years. Importantly, the severity of the skin disease and the arthritis do not correlate with each other.2
The pathogenesis in the joint is similar to the skin, insofar as there is a prominent lymphocytic infiltrate in the sublining layer stroma in the joint and inflammatory enthesis. In psoriatic arthritis, synovial tissue is characterized by a T cell infiltrated with an increased vascularity and an increase in macrophages, which results in a synovial tissue with a sublining infiltrate of B and T cells, vascular proliferation, and proliferating synoviocytes, which produce TNF, Il 17, Il 12. This induces osteoclastic activity and activation of RANK ligand whereby osteoclasts derived from TNF-activated peripheral blood mononuclear cells migrate to synovium resulting in bone erosion. There is no up-regulation of cutaneous lymphocyte antigen, suggesting a different lymphocyte population is involved than for psoriasis.2
Assessment and Treatment
In trials investigating patients with psoriatic arthritis, the American College of Rheumatology Criteria (ACR) is most commonly used. The ACR clinical response criteria are defined as percentage reduction (20% [ACR 20], 50% [ACR 50], and 70% [ACR 70]) in tender and swollen joint counts and in three of the remaining five ACR core items (patient and physician global assessments, pain, disability, and ACR).
The most reliable therapy for patients with mild to moderate psoriatic arthritis is non-steroidal anti-inflammatory drugs (NSAIDs) given by intra-articular injections.3 However, patients with moderate to severe psoriatic arthritis may require disease modifying antirheumatic drugs (DMARDs), a class that includes methotrexate, sulfasalzine, and leflunomide. However, it's worth noting that although they minimize the symptoms of psoriatic arthritis, DMARDs do not prevent the progression of joint destruction.
Because of the elevated levels of TNF-alpha in the joint, TNF inhibitors such as etanercept (Enbrel, Amgen) and adalimumab (Humira, Abbott) have been extremely helpful in the treatment of psoriatic arthritis. There may be a difference in the PASI 75 results amongst the TNF inhibitors; however, they seem to be equally efficacious in the arthritic component of psoriatic arthritis.4
One study found that patients receiving adalimumab 40mg sq qo/week had an ACR 20 score of 58 after 12 weeks of treatment.3 Those on etanercept 25mg sq two times per week had an ACR 20 score between 59 and 73 at 12 weeks. The study also looked at golimumab (Simponi, Janssen, 50mg sq for 20 weeks) and intravenous infliximab (Remicade, Janssen, 5mg/kg for 24 weeks), yielding ACR scores of 51 and 54, respectively. Another study found that patients receiving golimumab 50mg sq had an ACR score of 52, whereas patients receiving 100mg had an ACR score of 61. Possible side effects of TNF therapy include headache, sever infections, opportunistic infections, new onset demyelinating disorders, possible increased risk of lymphoma, drug-induced lupus, vasculitis, and exacerbation of CHF.
Finally, although not FDA approved for psoriatic arthritis, I have seen some improvement in arthritic symptoms in patients being treated with ustekinumab (Stelara, Janssen) for psoriasis.
As psoriatic arthritis usually follows the onset of psoriasis, dermatologists are in a unique position to diagnose and treat the arthritic component prior to the onset of joint destruction. Evaluation for signs and symptoms of psoriatic arthritis (i.e., stiffness in fingers and toes upon awakening in the morning, dactylitis, enthesitis, joint pain, and swelling) is an essential component in the caring for each psoriatic patient. Finally, when treating psoriatic arthritis, remember that the level of TNF in the joint correlates with the severity of arthritis.
Dr. Bagel has served as consultant, researcher, or speaker for Amgen, LEO, Abbott, Janssen, Galderma, and GlaxoSmithKline.
Jerry Bagel, MD, FAAD, is director of the Psoriasis Treatment Center of Central New Jersey.
- Reich K, Krüger K, Mössner R, et al. Epidemiology and clinical pattern of psoriatic arthritis in Germany: a prospective interdisciplinary epidemiological study of 1511 patients with plaque-type psoriasis. Br J Dermatol. 2009 May;160(5):1040-7.
- Fitzgerald O, Winchester R. Psoriatic arthritis: from pathogenesis to therapy. Arthritis Res Ther. 2009;11(1):214.
- Gottlieb A, Korman NJ, Gordon KB, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 2. Psoriatic arthritis: overview and guidelines of care for treatment with an emphasis on the biologics. J Am Acad Dermatol. 2008 May;58(5):851-64.
- Weger W. Current status and new developments in the treatment of psoriasis and psoriatic arthritis with biological agents. Br J Pharmacol. 2010 Jun;160(4):810-20.