Psoriatic arthritis — epidemiology, diagnosis and treatment

Psoriatic arthritis (PsA) is a chronic, systemic inflammatory disease of the joints and skin characterised by the presence of dactylitis, enthesitis, nail psoriasis and spondylitis. Clinical manifestations also include skin psoriasis, distal interphalangeal (DIP) arthritis, osteoperiostitis, oligoarthritis and arthritis mutilans. It is one of a group of disorders known as the spondyloarthropathies. PsA is variable and heterogeneous in presentation and course, with patients suffering intermittent flare ups and periods of quiescence.

Prevalence and epidemiology

The prevalence of PsA varies somewhat in the literature. Rates are estimated to range from 0.05-to-2 per cent of the general population. In almost 70 per cent of patients, psoriasis precedes the onset of arthritis. PsA is uncommon in the Asian and black populations and unlike rheumatoid arthritis, which affects more females than males, PsA has a female-to-male ratio of 1:1.9.

Aetiology

The aetiology of PsA remains unclear, however, it is thought that certain immunologic, environmental and genetic factors play a role in disease onset. Evidence has been presented demonstrating an association between PsA and the human leukocyte antigen (HLA) B27 region of the major histocompatibility complex (MHC) in patients with spinal disease. The MHC is a group of genes involved in T-cell recognition for the acquired immune system. They are located on the surface of cells and bind to antigens produced by pathogens. It is reported that 15 per cent of the relatives of a PsA patient will also have PsA, plus an additional 45 per cent will have psoriasis.

Infectious agents associated with activation of PsA include Streptococcus pyogenes group A, candida albicans, human immunodeficiency virus and hepatitis C. Trauma may be an environmental trigger of the disease. The deep Koebner phenomenon refers to the development of PsA manifestations at sites of trauma or physical stress in the body and has been linked to tendinopathy in PsA patients with dactylitis.

Pathophysiology

PsA develops in a person with genetic susceptibility who is exposed to an environmental or bacterial ‘trigger’. The immune system responds by mounting a persistent attack on the body tissues. The specific pathophysiology is poorly understood, however, it is thought that in response to the trigger, CD4+, CD8+ and T lymphocytes in synovial tissue and the skin activate white blood cells called macrophages. This results in a production of a number of pro-inflammatory cytokines, including tumour necrosis factor (TNF)-alpha and activation of a cascade of inflammatory cells in the skin and synovium. As a result, fibroblast-like synoviocytes infiltrate the synovial lining, producing enzymes called matrix metalloproteinases that break down cartilage in the affected joint.

Clinical manifestations

The group for research and assessment of psoriasis and psoriatic arthritis (GRAPPA) describe six PsA disease domains; peripheral arthritis, axial arthritis, enthesitis, dactylitis, psoriasis and nail disease. Patients with PsA initially present to the rheumatology clinic with arthritis and/or arthralgia of affected joints. They may also describe early-morning stiffness of greater than 30 minutes, which is usually relieved by activity and exacerbated by rest. Joint tenderness and swelling will be evident, typically to the DIP joints, with associated nail dystrophy in the form of pitting or onycholysis due to structural proximity.

The axial spine may also be affected by PsA in the form of sacroiliitis or spondylitis, manifesting as buttock pain, typically in the latter part of the night. Many patients will describe a personal or family history of psoriasis. Most commonly affected skin sites for psoriasis include the scalp, elbows, knees, lower back and gluteal cleft. Dactylitis manifests as a swollen digit, often referred to as a ‘sausage finger’ or toe, and is present in almost 50 per cent of PsA patients. Enthesitis is inflammation of the attachment site of a tendon or ligament that causes pain on palpation, movement or weight-bearing. Typical sites of enthesopathy include the Achilles tendon and the
plantar fascia.

Diagnosis

Some patients exhibit mild disease that can respond well to first-line treatment, however, others report a debilitating, destructive disease with impaired function and poor quality-of-life.

It has been reported that up to 47 per cent of PsA patients develop erosions within two years of symptom onset. For this reason, early diagnosis and initiation of disease-modifying anti-rheumatic medications (DMARDs) and/or biological agents is vital to ensure positive patient outcomes and decrease morbidity. There are no specific biomarkers of the disease, therefore diagnosis is based on clinical assessment and radiological manifestations. Many classification criteria have been presented in the past, however, the Classification Criteria for Psoriatic Arthritis (CASPAR criteria), initially developed for clinical trial classification purposes, is the most widely used in rheumatology practice. The CASPAR criteria possess high levels of specificity (98.7 per cent) and sensitivity (91.4 per cent) for diagnosing PsA in clinical practice. To meet the CASPAR diagnostic criteria, a patient must first exhibit arthritis of the joint, spine or entheses. Then score three points or more from the following:

•   Current psoriasis (two points)/history of psoriasis (one point)/family history of psoriasis (one point).

•   Psoriatic nail dystrophy (one point).

•   Negative rheumatoid factor (one point).

•   Current or history of dactylitis (one point).

•   Radiographic evidence of juxta-articular new bone formation (one point).

Differential diagnosis

The clinical manifestations of other inflammatory joint diseases, such as rheumatoid arthritis, gout, or osteoarthritis, can mimic those of PsA and as a result, it is imperative that differentiation is made as early as possible for correct treatment initiation. Typical features of rheumatoid arthritis include symmetrical wrist, metacarpophalangeal, knee, ankle and metatarsophalangeal joint involvement in the absence of DIP joint involvement. Presentation of a psoriatic monoarthritis could be misdiagnosed as gout, however, in these patients uric acid levels are generally elevated and a diagnosis of crystal arthropathy can be made from microscopic analysis of joint aspirate. Clinically, osteoarthritis of the hands often leads to osteophytosis or the formation of solid bone spurs in the articular cartilage of affected DIP joints, known as Heberden’s nodes. These can be distinguishable from PsA-affected DIP joints, as the swelling is solid bone and not tender on palpation. 

Treatments for PsA

As with many autoimmune diseases, the goal of treatment is to achieve clinical remission, or low disease activity when remission cannot be achieved. Patients should be assessed regularly to evaluate the impact of the disease on their pain, function and quality-of-life. Treatments vary, depending on the disease manifestation and severity. International guidelines have been published to guide physicians in choosing the correct treatment, depending on the most severe element of the disease. For patients who report peripheral or axial arthritis, non-steroidal anti-inflammatory drugs (NSAIDs) are recommended but with caution due to potential side-effects. NSAIDs are also recommended as the first-line treatment for enthesitis and dactylitis.

Initiation of conventional DMARDs is recommended at an early stage for patients who have peripheral arthritis. Methotrexate is the drug of choice, especially when there is active psoriasis. If methotrexate is contraindicated or the patient does not respond, sulfasalazine or leflunomide can be prescribed. In patients who have multiple articular and extra-articular manifestations, a biological agent should be introduced, such as a tumour necrosis factor (TNF) inhibitor. Examples of TNF inhibitors include adalimumab, etanercept, certolizumab pegol and golimumab. Other biological agents can be considered in DMARD failure, such as ustekinumab, which targets the interleukin (IL)-12/23 pathway, or secukinumab, which targets the IL-17 pathway. Patients must be screened by a rheumatology specialist for active infection, tuberculosis and medication-specific contraindications prior to treatment initiation of any biological drug. If the patient has failed a number of conventional DMARDs and biological medications are not appropriate, treatment with a targeted PDE4 inhibitor such as apremilast is recommended.

Biologics should be initiated in patients who report mainly axial disease and do not respond to NSAIDs or physiotherapy. Treatment with intra-articular corticosteroids is recommended as an adjunctive therapy for peripheral arthritis and dactylitis. Systemic corticosteroids can be used, but with caution due to possible side-effects and the potential for skin disease to flare after abrupt discontinuation. It is recommended that PsA patients are screened for comorbidities such as metabolic syndrome, obesity, diabetes and cardiovascular disease.

Comorbidities

PsA is associated with many comorbidities that have compounding negative effects to patients’ health and wellbeing. PsA patients with high disease activity are more likely to develop type 2 diabetes and metabolic syndrome when compared to the general population. Uveitis is a common extra-articular manifestation of PsA and affects almost a third of patients. PsA patients are at higher risk of developing cardiovascular disease, including myocardial infarction and stroke, particularly if not treated with DMARDs when compared to population controls. Osteoporosis and inflammatory bowel disease in the form of Crohn’s disease have also been linked with PsA, but to a lesser degree.

Nursing assessment of the PsA patient

When seeing a PsA patient in the primary care setting, the nursing assessment should address the following issues:

•   Joint swelling and tenderness highlighting number and location of joints involved. Compare, look and palpate all small joints of hands, wrists, elbows, shoulders, knees, ankles, and toes.

•   Presence of psoriasis.

•   Presence of nail disease in the form of pitting, onycholysis, subungual hyperkeratosis or splinter haemorrhages.

•   Presence of dactylitis, or ‘sausage digit’, particularly of the toes.

•   Patient reporting plantar fasciitis/tennis elbow/frozen shoulder.

•   Psychosocial burden of the disease on the patient.

•   Duration of early-morning stiffness.

•   Fatigue.

Many disease assessment tools are available to assist the nurse in examining the severity of PsA, including the psoriasis area and severity index (PASI) score to measure disease severity and the dermatology life quality index, which is a self-report tool that demonstrates the impact of skin disease on the patient’s quality-of-life.

Nursing care of the PsA patient

Effective nursing care begins with good communication that lays the foundation for a trusting therapeutic relationship between the nurse and patient. The primary role of the nurse is to educate and support the PsA patient at every stage of their journey. Individualised patient education plans should be tailored to the patient’s needs and include information about the disease, treatment options and long-term outcomes. Discussion should also take place regarding employment status and in situations where patients have the physical capacity to work but have stopped working due to disease complications, a collaborative return to work plan should be formulated. The nurse must educate the patient about self-management techniques and the available support structures in the community. A holistic assessment of the patient’s physical, social and emotional needs should be performed at the initial meeting. Any issues raised should be addressed promptly, identifying barriers to recovery and methods of overcoming them.

The nurse must also ensure the patient has adequate symptom relief from joint pain, entheseal and/or skin disease. Simple analgesia such as paracetamol can be effective in the treatment of joint pain and when required, the addition of NSAIDs can be prescribed, safely providing relief of flaring disease. For a psoriatic monoarthritis, intra-articular (IA) joint injection of local anaesthetic and corticosteroid can be performed to aid recovery and maintain functional ability. Contraindications to IA injections include active infection, joint prosthesis, hypersensitivity to any of the agents, a neurological deficit, or a tendon rupture at the site. For active skin disease, there is a wide range of topical agents that can be prescribed, including corticosteroid creams, vitamin D analogues and tar preparations. Psoralen and ultraviolet A or B light treatments can also be beneficial for active psoriasis under the care of a specialist dermatology team, however, patients with destructive, erosive disease often require systemic medications to achieve symptom control, prevent functional deterioration and joint deformities.

For those who have advanced disease or joint deformities, maintenance of functional ability is paramount. Assessment of the patient’s activities of daily living should be performed and where applicable, the nurse should promote the use of aids and devices to help patients protect their joints while engaging in their day-to-day activities. The benefit of daily exercise should be highlighted to the patient at every visit, especially the importance of weight-bearing activities to promote bone health and prevent osteoporosis. Patients who have contracture deformities of the toes or who require extra arch support should be referred to podiatry and/or physiotherapy for review and intervention as necessary. The patient should be given smoking cessation advice and encouraged to engage with national health screening initiatives.

Contact should be made with the patient’s rheumatology team if there is a concern that current medications are not effective. This may be the case when a patient reports a number of flares in succession with increasing severity or duration, despite systemic treatment.

Uncontrolled severe disease

•   If the patient describes adverse effects from prescribed rheumatological medications or reports poor compliance with medication regimens for any reason.

•   Where laboratory results deviate from the patient’s normal levels due to rheumatological medication regimens.

References on request