Skill Checkup: A Man With Plaque Psoriasis and Joint Pain

Medscape

29-05-2025

A 46-year-old White man with a 10-year history of moderate to severe plaque psoriasis presents with worsening joint symptoms. He has been treated with topical steroids for the past 2 years but reports that his psoriasis flare-ups have become more frequent and more severe over the past 6 months. Over the past 3 months, he has developed progressive joint pain, swelling, and stiffness primarily affecting the distal interphalangeal (DIP) joints of his hands. He notes that the stiffness is worst in the morning, lasting more than an hour, but improves with activity. He denies having recent trauma, fever, or infectious symptoms.
On physical exam, there is visible swelling of several fingers and toes (described as "sausage digits," consistent with dactylitis) and nail pitting. No tenderness or decreased range of motion is noted in the axial skeleton. Laboratory results show an elevated C-reactive protein level and erythrocyte sedimentation rate, but rheumatoid factor (RF) and antinuclear antibody are negative.
This patient's psoriasis history, DIP joint involvement, dactylitis, and nail pitting are characteristic of psoriatic arthritis (PsA). The presence of active psoriasis and nail changes strongly points to PsA as the most likely cause of this patient's joint disease as well.
In contrast, rheumatoid arthritis (RA) typically causes a symmetric polyarthritis of the hands that favors the proximal joints (metacarpophalangeal and proximal interphalangeal joints), while DIP joints are usually not involved. Positive RF or anti–citrullinated peptide (anti-CCP) antibodies are seen in most cases; the patient's asymmetric DIP joint arthritis and negative RF make RA unlikely.
Osteoarthritis (OA) can affect DIP joints, but it is a noninflammatory degenerative arthritis that usually presents at an older age with brief morning stiffness and pain that worsens with activity, often with bony enlargements (Heberden's nodes) rather than diffuse swelling; unlike PsA, OA does not often cause intense inflammation, dactylitis, or nail pitting. OA DIP joint changes are usually due to osteophytes ("bone spurs") without the psoriatic nail lesions.
Reactive arthritis (ReA) is a seronegative spondyloarthritis like PsA and can cause asymmetric oligoarthritis with enthesitis/dactylitis; however, ReA is usually triggered by a recent infection and often involves the lower extremities (knees, ankles, and toes) with extra-articular features like urethritis or conjunctivitis, which are not seen here.
PsA classically produces erosive changes with new bone formation on radiographs. In advanced disease, DIP joints can erode into a pencil-in-cup deformity, where the phalanx tapers and "cups" into an eroded adjacent bone. Though this can occur in other inflammatory diseases, it is most commonly associated with PsA. Such combined erosive and proliferative bone changes are highly suggestive of PsA and are not typically seen in RA (which shows only erosions with osteopenia) ​.
Positive anti-CCP antibody more strongly supports RA rather than PsA, as PsA is usually seronegative for RA markers, such as the RF and anti-CCP antibodies.
Uric acid crystals in joint fluid would more likely indicate gout, not PsA. While patients with PsA have been shown to experience a higher risk for gout, the presentation in this case (chronic DIP joint arthritis with nail changes) is not consistent with it.
HLA-B27 antigen is associated with PsA in those who have axial (spinal) involvement, but it is less common patients with PsA and without spine disease. The patient has no axial symptoms, so HLA-B27 testing would be of limited value. Moreover, HLA-B27 is not required to diagnose PsA.
The Classification of PsA (CASPAR) criteria is the internationally accepted standard for classifying PsA. It requires the presence of inflammatory arthritis (joints, spine, or entheses) plus a total of at least 3 points from features including: Current psoriasis (2 points) or personal/family history of psoriasis (1 point); psoriatic nail changes (pitting or onycholysis, 1 point); dactylitis (swelling of an entire digit, 1 point); negative RF (1 point); and juxta-articular new bone formation on radiography (1 point). PsA is diagnosed using the CASPAR criteria in patients with inflammatory arthritis who score at least 3 points, with the criteria demonstrating high specificity and sensitivity and serving as the preferred diagnostic tool once other differentials are excluded. This patient meets the CASPAR criteria as he has inflammatory arthritis with psoriasis, nail pitting, and dactylitis and is RF-negative.
The American College of Rheumatology and European League Against Rheumatism (ACR/EULAR) criteria are typically used for RA, not PsA, and emphasize symmetric joint involvement and RA-specific antibodies (RF/anti-CCP) and do not apply here.
The modified New York criteria are used to classify ankylosing spondylitis, focusing on axial skeletal findings (eg, sacroiliitis on radiography and low back pain), which are not the primary issue in this patient.
The Jones Criteria are designed for acute rheumatic fever diagnosis and are unrelated to PsA.
The patient is diagnosed with moderate to severe PsA, and given his dactylitis, arthritis, and skin involvement, he is given methotrexate as initial therapy owing to cost-effectiveness; however, he returns to his next appointment, and his PsA remains active.
In a patient with moderate to severe PsA that is inadequately controlled on a conventional synthetic DMARD (methotrexate), experts recommend escalating to a biologic DMARD. Tumor necrosis factor (TNF) inhibitors (such as adalimumab, etanercept, or infliximab) are a proven biologic choice for PsA, effective for both joint and skin symptoms. The latest Group for Research and Assessment of Psoriasis and PsA (GRAPPA), ACR, and EULAR guidelines endorse using a TNF inhibitor (or another biologic/targeted therapy) once conventional DMARD therapy fails to achieve remission. In this case, adding a TNF inhibitor is appropriate to control joint inflammation and prevent further damage while also improving psoriasis.
Switching to another conventional DMARD (like sulfasalazine or leflunomide) is generally less effective in patients with moderate to severe disease; this method is typically more effective in mild to moderate cases.
Oral corticosteroid are generally not recommended for routine PsA management, as they might worsen disease.
Nonsteroidal anti-inflammatory drugs (NSAIDs) can help symptomatically, but they are most appropriate in mild PsA, not moderate to severe disease. This patient has active polyarthritis and progressive symptoms, requiring disease-modifying therapy, and using NSAIDs without advancing systemic treatment would allow ongoing joint damage.
An oral phosphodiesterase 4 (PDE-4) inhibitor can be used as an alternative for patients who prefer an oral medication and want to avoid injections. Further, current GRAPPA guidelines and ACR guidelines include PDE-4 inhibitors among the recommended treatment options for active PsA. The potency of PDE-4 inhibitors (such as apremilast) are likely not as strong as Janus kinase inhibitors in moderate to severe cases of PsA. However, the latter needs to be weighed carefully against PDE-4 inhibitors due to higher risks for infection among other long-term side effects.
In moderate to severe cases of PsA, 5-aminosalicylic acid derivatives, such as sulfasalazine, are typically not very effective; they are reserved for add-on therapy in case of mild disease activity.
Calcineurin inhibitor can help severe psoriatic skin lesions, but they are not a preferred therapy for PsA joint manifestations.
Antimalarial drugs can be considered when previous DMARDs use is ineffective or if joint inflammation remains a significant concern, but they are not typically recommended in PsA as they might lead to psoriasis flare-ups.
Editor's Note: Skill Checkups are wholly fictional or fictionalized clinical scenarios intended to provide evidence-based educational takeaways.