An extracutaneous manifestation affecting 5-20% of patients with psoriasis.
A chronic inflammatory arthritis associated with psoriasis (PsO) and found in about 20 to 30% of such patients.
There are 5 types of psoriatic arthritis:
Oligoarticular arthritis which is asymmetric and involves less than five small or large joints.
The asymmetric oligoarticular pattern is the most common form on presentation of psoriatic arthritis, accounting for at least 60% of cases of psoriatic arthritis.
Classification of Psoriatic Arthritis
Inflammatory arthritis-peripheral arthritis and/or sacroiliitis or spondylitis
The presence of psoriasis
The absence of serologic tests for rheumatoid factor
CASPAR Criteria -scores
Skin psoriasis: present – 2 / previously present -1 / family history, patient not affected – 1
Nail lesions: onycholysis, pitting, hyperkeratosis – 1
Dactylitis: present or past, documented by a rheumatologist – 1
Rheumatoid factor: negative by any method except for latex – 1
Juxta-articular bone formation: distinct from osteophytes – 1
CASPAR criteria, psoriatic arthritis is considered with inflammatory arthritis who have at least 3 points; this has a specificity of 98.7% and a sensitivity of 91.4%.
Over time the majority of patients have polyarticular arthritis.
The clinical features of psoriatic arthritis are described in terms of articular and extra-articular manifestations.
Articular/periarticular manifestations of psoriatic arthritis.
Peripheral arthritis presents in an oligoarticular vs. polyarticular pattern.
Psoriatic skin disease usually presents before the onset of arthritis.
Psoriatic skin disease can occur simultaneously and even before the onset of joint disease.
Psoriatic arthritis affects approximately 30% of patients with psoriasis.
The severity of psoriatic skin disease does not correlate well with the severity of the articular disease.
Radiographic patterns in psoriatic arthritis consists of: erosive changes, gross joint destruction, joint space narrowing, and “pencil-in-cup” deformity.
Radiographic changes are related to bone destruction and pathological new bone formation.
These changes are often in the same digit or even the same joint, which is a characteristic feature of psoriatic arthritis: bone destruction with bone production.
Despite DMARDs (disease-modifying anti-rheumatic drugs), psoriatic arthritis results in radiographic damage in about 47% of patients during the first two years of the disease.
Radiological features of peripheral arthritis in hands and feet include: erosive changes, new bone formation, bony ankylosis, and joint osteolysis.
Psoriatic arthritis patients are at increased risk of death compared to the general population from cardiovascular diseases.
The Classification of Psoriatic Arthritis (CASPAR) study identified 63% of patients having polyarticular arthritis.
The frequency of radiological axial involvement in psoriatic arthritis has been found to be about 43%
The patterns of arthritis are:
oligoarticular arthritis – 14%,
polyarthritis – 40%,
distal arthritis – 12%,
arthritis mutilans – 16%,
sacroiliitis and spondylitis – 30%
Polyarticular arthritis which is usually symmetric and presents similar to rheumatoid arthritis but may involve the DIP joints, rheumatoid factor negative
Distal arthritis signified by prominent involvement of the DIP joints
The distal pattern is less common occurring in less than 20% of patients and may be present along with spondyloarthritis.
Arthritis mutilans characterized by a severe destructive joint disease with deformities especially in hands and feet.
Arthritis mutilans prevalence can range from 2 to 21%, and as the most severe form, its presentation is associated with osteolysis leading to digital telescoping, bone resorption, and sacroiliitis.
Specific features of the disease including digital telescoping, digital shortening, pencil-in-cup deformities, osteolysis, and involvement of DIP joints and other small joints of the hands.
Patients may experience the transition of one pattern of arthritis to another over time.
Spondyloarthritis pattern with sacroiliitis and spondylitis
The cumulative incidence of psoriatic arthritis in patients with psoriasis was 1.7% at 5 years, 3.1% at 10 years, 5.1% at 20 years, and 20.5% at 30 years.
Factors predictive of the development of psoriatic arthritis in patients with psoriasis include: severe psoriasis phenotype, scalp, intergluteal and perianal psoriasis, presence of nail pitting, low level of education, and uveitis.
Risk factors for psoriasis and psoriatic arthritis: an environmental trigger such as infection or mechanical stress initiates a chronic inflammatory process primarily involving the joints and skin, resulting in the production of IL-23.
IL-23 is a central cytokine in the pathogenesis of psoriatic arthritis and psoriasis.
Macrophages and dendritic cells produce IL-23.
The gastrointestinal tract may be the source of IL-23 due to disturbed barrier function or changes in the microbiota.
It is a debilitating disease requiring targeted treatment with frequent monitoring and follow-up care.
Has many clinical features with other spondyloarthropathies and also rheumatoid arthritis (RA).
It is usually seronegative.
A small percentage of patients may be positive for rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibodies (anti-CCP antibodies).
The ((14-3-3 eta)) protein is a biomarker for the detection of erosive psoriatic arthritis.
Pathogenesis involves a complex interaction between genetic and environmental factors resulting in immune-mediated inflammation involving the skin and joints and may involve other organs.
Approximately 33 to 50% of psoriatic arthritis patients have at least one first degree relative who also has psoriasis or psoriatic arthritis.
Estimated to have a prevalence of 0.05% to 0.25% in the general population and around 6% to 41% in psoriasis patients.
The prevalence of undiagnosed psoriatic arthritis might be as high as 15.5%.
Its onset is usually in the 30s and 40s.
It occurs about equally in males and females.
In 68% of patients, the onset of skin disease precedes that of arthritis.
The prevalence of type 2 DM in patients with PsA ranges from 6.1 to 20.2%, generally higher when compared to the general population.
Nails affected in the majority of patients with psoriatic arthritis.
Psoriatic arthritis nail disease is characterized by onycholysis, pitting, and splinter hemorrhages.
The severity of nail disease correlates with the severity of both skin and joint disease.
Nail disease is present in 80 to 90% of patients with psoriatic arthritis and is associated with DIP joint involvement.
In about 15% of patients, the arthritic manifestations coincide with the skin disease, and in 17% of patients, arthritis occurs before the skin manifestations.
The annual incidence of psoriatic arthritis was 1.9 to 2.7% per 100 patients with psoriatic arthritis.
Younger age of onset associated with HLA-B17 and HLA-Cw6.
May be severe and be associated with joint damage, deformities, impaired function, and early mortality.
Associated with poor quality of life.
Patients affected by PsA have a higher prevalence of type 2 DM compared with the general population.
Elevated serum levels of adipokines, including TNF-α, which inhibits the autophosphorylation of the insulin receptor and suppresses the expression of glucose transporter 4, favor insulin resistance and could partially explain the association between psoriatic arthritis and diabetes.
A higher risk of DM is reported in women with more severe forms of psoriatic arthritis.
Adiponectin and omentin, with insulin-sensitizing and anti-atherogenic properties, are decreased in patients with PsA.
Some of the treatments for PsA could affect the glucose homeostasis. Systemic corticosteroids are known to impair insulin resistance, whereas apremilast (phosphodiesterase type 4 inhibitor) and TNF-α inhibitors could exert neutral effect or reduce the insulin-resistance.
These proinflammatory cytokines recruit neutrophils which enter the synovial fluid.
IL-23 inhibitors are approved for the treatment of psoriatic arthritis and psoriasis but are not effective for rheumatoid arthritis.
It follows or is concurrent with the onset of psoriasis in more than 85% of patients.
HLA locus of the major system compatibility complex on chromosome 6 is the major locus for both psoriasis and psoriatic arthritis.
In a study of 158 patients with psoriatic arthritis and 101 patients with psoriasis and no arthritis: HLA-B13, HLA-B17, and HLA-Cw6 Were more common with psoriasis and HLA-B-17 was more common among psoriatic arthritis patients (Rahman P).
Genetic associations in psoriatic arthritis include HLA-B*08:01, HLA-B*27:05, HLA-B*38:01, HLA-B*39:01, HLA-B*57:01, and HLA-C*06:02.
The subset of patients with symmetric polyarthritis is associated with HLA-DR4.
HLA-B27 is associated with axial involvement, while HLA-B38 and HLA-B39 are associated with polyarthritis.
Axial involvement which is related to the prevalence of HLA-B27 which is higher in individuals of the White race, especially of northern European descent.
Non-HLA genes associated with psoriatic arthritis include IL-23R.
Psoriasis has a stronger association than psoriatic arthritis with HLA-B*57:01 and HLA-C*06:02.
IL-12B gene is associated with psoriasis but not psoriatic arthritis.
CD8+ T cells play a central role which is supported by the association of psoriatic arthritis with HLA Class I alleles.
Other immune cells involved in the pathogenesis include CD4+ type 17 helper (Th17) cells which produce IL-17 and IL-22, type 3 innate lymphoid (ILC3) cells which produce IL-17 and IL-22 and gamma-delta T cells which produce IL-17 and TNF-alpha.
The genetic associations with psoriatic arthritis and psoriasis are not identical.
Some genes associated with psoriatic arthritis are not associated with psoriasis, and vice versa.
Genes associated with psoriatic arthritis include: those in the HLA region which are involved in antigen presentation and immune recognition and also non-HLA genes involved in immune activation and inflammation including intracellular signaling, cytokine expression, and signaling, and T cell effector function.
Increased risk of having psoriatic arthritis includes psoriatic nail changes, scalp and intergluteal involvement.
Enthesitis, the inflammation at the site where ligaments, tendons, and joint capsules attach to the bone, is the prominent pathologic lesion in psoriatic arthritis in contrast to synovitis in rheumatoid arthritis.
Entheseal involvement: erosions and new bone formation, is characteristic in all spondyloarthropathies.
Involvement of the axial skeleton including sacroiliitis and spondylitis, includes formation of ossification of the annulus fibrosis.
In differentiating psoriatic arthritis from ankylosing spondylitis: it is asymmetric and often has a unilateral presentation of sacroiliitis.
Distal interphalangeal (DIP) joints are frequently involved in psoriatic arthritis but not so in rheumatoid arthritis because these joints have many entheses but very little synovial tissue.
Assessments by imaging include: plain radiography, CT scan, ultrasound, and MRI.
MRI and ultrasound are more sensitive than plain radiography for detecting early joint inflammation and damage and axial changes, including sacroiliitis.
Events that may precipitate the development of psoriatic arthritis in patients with psoriasis include the use of systemic corticosteroids, trauma, vaccinations, and infections (Pattison E).
50% of patients with joint involvement develop rapidly progressive joint damage with an estimated11% annual erosion rate in the first two years of disease process
Psoriasis skin rash generally occurs before joint pain so patients being seen for psoriasis should be monitotrd for the development of joint symptoms.
High association with obesity.
Ocular disease in the form of uveitis is often chronic, bilateral, and involves posterior elements.
An autoimmune disease with human leukocyte antigen (HLA) associated risk factors.
Approximately 33 to 50% of psoriatic arthritis patients have at least one first degree relative who also has psoriasis or psoriatic arthritis.
May affect ligaments, tendons, fascia, and joints.
Can develop in the absence of clinical psoriasis.
Occurs in approximately 30% of patients with psoriasis and may precede rash.
May be more frequent when skin involvement is more severe.
Significantly associated with pustular psoriasis.
Epidemiologic studies have shown an association between streptococcal infection and recent antibiotic exposure to psoriatic arthritis.
Skin trauma can induce flares of psoriatic skin lesions which is known as the Koebner phenomenon, and similarly joint trauma may induce a flare of arthritis, referred to as “internal” or “deep” Koebner phenomenon.
Tobacco, appears to be protective for psoriatic arthritis.
Approximately 1 million U.S. adults have this process.
Rate in white population ranges from .05-.24%, approximately half of that for seropositive rheumatoid arthritis.
Associated with flares and remissions.
Can involve sacroiliac joints.
Can involve spine.
About 7% require musculoskeletal surgery.
Equally affected among the genders.
Usually seen in individuals between ages 35-55 years, but can occur at any age.
No laboratory tests are specific for psoriatic arthritis.
Acute phase reactants such as ESR and CRP may become elevated as in most inflammatory processes.
ESR and CRP levels are increased in only about 40% of patients.
RF and anti-CCP antibodies are classically absent in psoriatic arthritis.
A negative rheumatoid factor is considered to be a criterion for the diagnosis of psoriatic arthritis.
There is a positive rheumatoid factor in about 2 to 10% of patients with a diagnosis of psoriatic arthritis, and approximately 5% are positive for anti-CCP antibodies.
ANA positive titer of >1:80 in 14% in patients with psoriatic arthritis.
Treatment based on disease severity, degree of joint damage, the extent of extra-articular disease, patient preference, and other co-morbidities.
Evaluation includes peripheral joints, entheses, digits, axial involvement, and skin and nails is crucial.
Various parameters used in assessing disease activity in psoriatic arthritis:
Harbingers of a severe disease course and poor prognosis: large number of actively inflamed joints or polyarticular presentation, elevated ESR, clinical or radiographic damage, loss of function, and diminished quality of life.
It is a debilitating disease requiring targeted treatment with frequent monitoring and follow-up care.
Complete symptomatic relief is achievable.
A majority of patients continue to have persistent inflammatory disease.
Features associated with severe disease course and poor prognosis include: a large number of actively inflamed joints, elevated ESR, clinical or radiographic damage, loss of function, and diminished quality of life.
It is considered to be a debilitating.
The disease requires targeted treatment with frequent monitoring.
While symptomatic relief is achievable, the majority of patients continue to have persistent inflammatory disease.
Management requires education of the fluctuating nature of the disease, and counseling of the chronic nature of psoriatic arthritis and the importance of exercise, smoking cessation, weight loss, physical therapy, and occupational therapy.
Exercise is encouraged to restore joint function.
Non-pharmacological therapies of psoriatic arthritis include: physical therapy, occupation therapy, exercise program, and smoking cessation.
The type of treatment initiated depends on the presentation: peripheral arthritis, enthesitis, dactylitis, axial disease, and skin/nail disease.
In treatment-naïve patients, NSAIDs are useful for mild peripheral arthritis.
Mild to moderate peripheral arthritis may be treated with conventional synthetic DMARDs (disease-modifying antirheumatic drug ) such as methotrexate or occasionally sulfasalazine.
Sulfasalazine is not effective for skin disease.
Severe peripheral arthritis treatment is usually with biologic DMARDs, especially TNF (tumor necrosis factor) inhibitors.
Axial disease and enthesitis are usually treated the similarly, but there is a minimal role of conventional DMARDs.
Patients who fail NSAIDs should automatically transition to biologic DMARDs.
A TNF inhibitor is usually recommended over an IL-17 inhibitor, IL-12/23 inhibitor, abatacept, or tofacitinib.
An IL-17 inhibitor is usually recommended over an IL-12/23 inhibitor, abatacept, or tofacitinib.
An IL-12/23 inhibitor is usually recommended over abatacept or tofacitinib.
In patients with severe psoriasis, an IL-12/23 inhibitor or an IL-17 inhibitor may be used instead of a TNF inhibitor.
Tofacitinib may be used instead of a TNF inhibitor in patients preferring oral medication who do not have severe psoriasis.
Guidelines recommend a TNF inhibitor over conventional synthetic DMARDs as a first-line treatment in treatment-naïve psoriatic arthritis patients.
The percentage of patients with psoriatic arthritis with a clinical response was significantly higher with who Upadacitinib than with placebo.