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Psoriasis and Psoriatic Arthritis Overview

Alan Menter, MD
     The diagnosis of PsA is made on the basis of the modified Classification Criteria for Psoriatic Arthritis (CASPAR).13,21 To confirm a diagnosis of PsA, a patient with musculoskeletal symptoms, such as arthritis, enthesitis, and/or spondylitis, must score at least 3 points using the CASPAR criteria (Table 313,21).13,21 The range of diagnostic criteria illustrates the diversity of clinical phenotypes of PsA. As an example, a patient with musculoskeletal symptoms and current psoriasis can meet the diagnostic criteria for PsA with the presence of one additional sign, such as psoriatic nail dystrophy. Conversely, a patient with musculoskeletal symptoms but no personal or family history of psoriasis can meet the diagnostic criteria by exhibiting 3 other clinical features suggestive of PsA, such as actylitis, juxtaarticular new bone formation, and rheumatoid factor negativity.13

     
Joint symptoms are the predominant complaint among patients with PsA. In the MAPP survey, nearly half of patients with PsA and psoriasis (48.1%) ranked pain and swelling of the joints as the most important factor contributing to their disease severity. Additional factors cited included itching (14.8%), location/size of psoriasis lesions (10.0%), flaking (5.6%), and scaling (3.0%).6 Delayed diagnosis and initiation of treatment of PsA are major management challenges. In the MAPP survey, patients with PsA reported a mean interval of 12.4 years between the onset of joint symptoms and the onset of skin symptoms. The median age at the time of PsA diagnosis was 44 years, compared with 37 years for psoriasis.6

     To achieve tight control of disease activity to improve joint outcomes, early detection of PsA is critical for initiating appropriate treatment.22 However, making a timely diagnosis of PsA is challenging across provider specialties. In the MAPP survey, 37.6% of dermatologists (N = 101) described differentiating PsA from other arthritic diseases as the greatest challenge in managing patients with PsA. In addition, 25.0% of rheumatologists (N = 100) cited delayed referral of patients as one of the greatest challenges in managing the population of patients with PsA. Furthermore, the majority of dermatologists (87.1%) and rheumatologists (85.0%) indicated that, because of the failure to make the connection between skin and joint symptoms, PsA is likely underdiagnosed in patients with psoriasis.6 Indeed, one recent meta-analysis found that the prevalence of undiagnosed PsA among patients with psoriasis (N = 7831) was 15.5%.22

     
To minimize the delay in diagnosing PsA, dermatologists are encouraged to screen patients with psoriasis for the signs and symptoms of PsA at every clinic visit.13,15 Screening questionnaires are useful tools for detecting rheumatologic symptoms in patients with psoriasis.22 The Psoriasis and Arthritis Screening Questionnaire, Psoriasis Epidemiology Screening Tool, and Toronto Psoriatic

Arthritis Screen can be used by dermatologists and other providers to identify patients with potential PsA who require further assessment by a rheumatologist.22,23

Differential Diagnosis

     The differential diagnoses of PsA include rheumatoid arthritis, erosive osteoarthritis, crystal arthritis (eg, gout and pseudogout), and other seronegative spondyloarthropathies, such as reactive arthritis, enteropathic arthritis, and ankylosing spondylitis.14

Comorbidities

     More than half of patients with PsA will have at least 1 comorbidity that contributes to the patient’s overall disease burden.18 It is not uncommon to diagnose multiple medical comorbidities in this patient population. In a study of 631 patients with PsA, 42% had 3 or more comorbid conditions.24

     Cardiovascular comorbidities are of particular concern for patients with PsA, given the high morbidity and mortality burden of CVD.19,20 One large population cohort study examined the incidence of CVD and major adverse cardiovascular events (MACE; defined as myocardial infarction [MI], stroke, or sudden death) in both patients with PsA (N = 7982) and in those without PsA (N = 74,583). For this analysis, CVD was defined as any diagnosis of arrhythmia, ischemic heart disease, angina, MI, stroke, pericardial disease, pulmonary hypertension, or sudden death. The rate of incident CVD was 12.8 cases per 1000 person-years among patients with PsA, or 33% higher than the rate of 9.6 cases per 1000 person-years in individuals without PsA (IRR, 1.33; 95% CI, 1.23-1.44). Patients with PsA also had a significantly higher rate of MACE. The MACE rate was 4.6 events per 1000 personyears in the PsA group and 3.5 events per 1000 personyears in the non-PsA group (IRR, 1.30; 95% CI, 1.15-1.47). Together, these findings support the association between PsA and increased risk of CVD and MACE.19

     Another recent population-based longitudinal cohort study examined the risk of MACE in patients with PsA (N = 8706), psoriasis (N = 138,424), or rheumatoid arthritis (N = 41,742) and in unaffected individuals (N = 81,573). After controlling for traditional cardiovascular risk factors, patients with PsA who were not undergoing treatment with disease-modifying antirheumatic drugs (DMARDs) were 24% more likely to experience MACE than were controls (hazard ratio [HR], 1.24; 95% CI, 1.03-1.49). By comparison, patients with PsA who were treated with DMARDs did not have a significantly increased risk of MACE (HR, 1.17; 95% CI, 0.95-1.46). These findings highlight the importance of appropriate treatment to control underlying disease activity and address excess cardiovascular risk.20

     
Additional comorbid conditions in patients with PsA can include osteoporosis, autoimmune ophthalmic diseases (uveitis), liver disease, inflammatory bowel disease, kidney disease, malignancy, and infection.18

Patient Expectations

     
The burden of PsA and its treatment can adversely affect quality of life for many patients.6 Depression and anxiety are highly prevalent among patients with PsA, particularly among those with more severe disease.18 Dissatisfaction with various aspects of PsA disease management—including treatment efficacy and tolerability, monitoring requirements, and convenience—is common.25 Importantly, patients with PsA may assess disease severity differently from providers, underscoring the need for open patient-provider communication to ensure that the patient’s treatment priorities are being addressed.6

     The burden of PsA and its treatment can adversely affect quality of life for many patients.6 Depression and anxiety are highly prevalent among patients with PsA, particularly among those with more severe disease.18 Dissatisfaction with various aspects of PsA disease management—including treatment efficacy and tolerability, monitoring requirements, and convenience—is common.25 Importantly, patients with PsA may assess disease severity differently from providers, underscoring the need for open patient-provider communication to ensure that the patient’s treatment priorities are being addressed.6

Treatment

     
The goals of treatment in PsA are to control inflammatory disease activity, manage joint pain, improve mobility, safeguard patient quality of life, and prevent joint destruction. Given that focusing on the skin disease alone will not improve joint symptoms in PsA, patient management ideally involves a multidisciplinary collaboration with input from dermatology and rheumatology. With the development of novel biologic therapies, clinicians have new options for targeting the underlying pathophysiology of PsA.13 See part 2 for a detailed overview of current and emerging PsA treatment strategies.

CONCLUSION

     Psoriasis and PsA are chronic immune-mediated diseases with high rates of cardiovascular and other comorbidities. Recent insights into the underlying pathophysiology of these diseases have revealed novel therapeutic targets. The diseases are underrecognized and undertreated in current clinical practice. Recognizing the true burdens of psoriasis and PsA and their common comorbidities is the first step to improving the prognosis for affected patients.

Author affiliation: Baylor University Medical Center, Dallas, Texas.
Funding source: This activity is supported by educational grants from Lilly and Novartis.
Author disclosure: Dr Menter has no relevant financial relationships with commercial interests to disclose.
Authorship information: Concept and design, drafting of the manuscript, and critical revision of the manuscript for important intellectual content.
Address correspondence to: amderm@gmail.com.
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