Managing patients with psoriatic disease: the diagnosis and pharmacologic treatment of psoriatic arthritis in patients with psoriasis

Abstract

Psoriatic arthritis (PsA) is a chronic, systemic inflammatory disease. Up to 40 % of patients with psoriasis will go on to develop PsA, usually within 5-10 years of cutaneous disease onset. Both conditions share common pathogenic mechanisms involving genetic and environmental factors. Because psoriasis is typically present for years before PsA-related joint symptoms emerge, dermatologists are in a unique position to detect PsA earlier in the disease process through regular, routine screening of psoriasis patients. Distinguishing clinical features of PsA include co-occurrence of psoriatic skin lesions and nail dystrophy, as well as dactylitis and enthesitis. Patients with PsA are usually seronegative for rheumatoid factor, and radiographs may reveal unique features such as juxta-articular new bone formation and pencil-in-cup deformity. Early treatment of PsA with disease-modifying anti-rheumatic drugs has the potential to slow disease progression and maintain patient quality of life. Optimally, a single therapeutic agent will control both the skin and joint psoriatic symptoms. A number of traditional treatments used to manage psoriasis, such as methotrexate and cyclosporine, are also effective for PsA, but these agents are often inadequately effective, temporary in benefit and associated with significant safety concerns. Biologic anti-tumour necrosis factor agents, such as etanercept, infliximab and adalimumab, are effective for treating patients who have both psoriasis and PsA. However, a substantial number of patients may lose efficacy, have adverse effects or find intravenous or subcutaneous administration inconvenient. Emerging oral treatments, including phosphodiesterase 4 inhibitors, such as apremilast, and new biologics targeting interleukin-17, such as secukinumab, brodalumab and ixekizumab, have shown encouraging clinical results in the treatment of psoriasis and/or PsA. Active and regular collaboration of dermatologists with rheumatologists in managing patients who have psoriasis and PsA is likely to yield more optimal control of psoriatic dermal and joint symptoms, and improve long-term patient outcomes.

Fig. 1

Shared attributes of cutaneous psoriasis and psoriatic arthritis [–14]. AP activator protein, CPII C-propeptide of type II collagen, C2C collagen fragment neoepitopes Col2-3/4C_{long mono}, HLA human leukocyte antigen, hsCRP highly sensitive C-reactive protein, IFN interferon, IL interleukin, IL-12B interleukin 12 beta, IL-23r interleukin 23 receptor, MAPK mitogen-activated protein kinase, MMP matrix metalloproteinase, NF nuclear factor, OPG osteoprotegerin, pDC precursor dendritic cell, RANK receptor activator of NF-κB, TNF tumour necrosis factor

Fig. 2

Mechanisms of systemic, chronic inflammation in psoriasis and psoriatic arthritis. From Nestle et al. [1]. Copyright © 2009, Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society. CCL chemokine (C-C motif) ligand, CXCL chemokine (C-X-C motif) ligand, Th T helper, TNF tumour necrosis factor

Fig. 3

European League Against Rheumatism (EULAR) recommended treatment algorithm for management of psoriatic arthritis. The recommendations have been divided into four phases. Small fonts within the ellipses in phases II and III refer to dose modifications or an alternative therapy, as detailed within the body of the recommendations. ^aBecause of the variable nature of the disease, not all situations can be covered by this figure; therefore, it is important to consult the full text to which the numbers or letters in parentheses refer; dotted lines refer to situations where deleting a phase is recommended. ^bActive disease: ≥1 tender and inflamed joint and/or tender enthesis point, and/or dactylitic digit, and/or inflammatory back pain; adverse prognostic factors: ≥5 active joints; or high functional impairment due to activity; or damage; or past glucocorticoid use. ^cThe treatment target is clinical remission or, if remission is unlikely to be achievable, at least low disease activity; clinical remission is the absence of signs and symptoms. Reproduced from Gossec et al. [89]. Copyright © 2012 with permission from BMJ Publishing Group Ltd. DMARD disease-modifying anti-rheumatic drug, MTX methotrexate, TNF tumour necrosis factor