Arthritis


Clinical patterns


Important clinical features


Prevalence


Asymmetric oligoarthritis


≤4 joints involved


Asymmetric in distribution


Most common


~20–55% [5]


Symmetric polyarthritis


≥5 joints involved


Symmetric in distribution


Similar to rheumatoid arthritis


~20–62% [5]


Predominant DIP involvement disease


Typically DIPs are involved


May or may not have concurrent nail involvement [16]


Distribution similar to DIP OA


~<5–20% [2, 5]


Axial spondyloarthritis


Sacroiliitis as well as other areas of spinal involvement


Similar to other seronegative SpA


May or may not be associated with peripheral PsA


Can be asymptomatic


Up to 40% [1, 5]


Arthritis mutilans (destructive)


Rare


Asymmetric


Severe osteolysis of involved joints resulting telescoping of digits


Severe disease


~5% [2]


Dactylitis


Inflammation of IP joints and surrounding tendon sheath resulting in classic sausage-shaped swelling


Characteristic feature


Most common in 3rd and 4th toes


Can be acute or chronic


Often associated with severe disease with bone erosion


40–50% [1]


Enthesitis


Most commonly Achilles tendinitis and plantar fasciitis


Other less common areas: iliac crest, around the patella, epicondyles, etc.


30–50%



DIP = distal interphalangeal joints




There are no formal validated diagnostic criteria for psoriatic arthritis, but diagnosis should be suspected when a patient presents with any of the above manifestations in the setting of current or previous history of psoriasis. Plaque psoriasis (Fig. 7.1a, b), guttate psoriasis (Fig. 7.2a), inverse psoriasis (Fig. 7.2b), pustular (Fig. 7.3a), and erythrodermic psoriasis are five major types of skin psoriasis. Dactylitis (Fig. 7.4) and enthesitis are thought to be typical features of PsA and are helpful in establishing diagnosis. But these features may be absent and it can be particularly difficult to identify PsA, as patients may not be aware of their skin psoriasis (or skin disease may not be obvious on initial evaluation). Hence, a thorough skin examination must also include the umbilicus, scalp, anus, and postauricular areas. Isolated nail involvement (Fig. 7.3b) is also seen with presence of pitting, oil spots, and onycholysis, which can confirm diagnosis. Family history of psoriasis and psoriatic arthritis are often present. Presence of other extra-articular diseases, such as IBD and uveitis, also heightens suspicion.

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Fig. 7.1

(a) Plaque psoriasis along the extensor surface of elbow with erythematous base with silvery scales. (b) Plaque psoriasis involving dorsal aspects of the joints. (Photo Credit: Andrea L. Neimann, MD)


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Fig. 7.2

(a) Guttate psoriasis presents with numerous small drop-like papule with a silvery scales. (b) Inverse psoriasis presenting along the inguinal folds. Scales typical of psoriasis tends to get macerated in these moist areas of body leaving a shiny erythematous surface. (Photo Credit: Andrea L. Neimann, MD)


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Fig. 7.3

(a) Palmar pustular psoriasis presents with tiny yellowish pustules, which are sterile. (b) Nail psoriasis with numerous vertical ridges and dystrophic nails. Pitting, oil spots, onycholysis are other nail changes seen in psoriatic nail diseases. (Photo Credit: Andrea L. Neimann, MD, and Fardina Malik, MD)


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Fig. 7.4

A 33-year-old female with no evidence of skin psoriasis presented with acute painful swelling of left 2nd toe. Laboratory test showed elevation of c-reactive protein. She was also noted to be HLA B-27 positive. (Photo credit: Fardina Malik, MD)


Classification criteria for psoriatic arthritis (CASPAR) (Table 7.2) can often guide clinicians, but it is primarily intended to enroll patients in clinical studies or trials given much higher specificity (~99%) (Table 7.2).


Table 7.2

Classification criteria of peripheral psoriatic arthritis (CASPAR = classification for psoriatic arthritis)











































Patient with inflammatory articular diseases (joints, spine, or enthesitis) with ≥3 points from the following five categories:


Criterion


Points


1. Evidence of psoriasis

 

 Current psoriasis (examined by dermatologist or rheumatologist)


2


 Personal history of psoriasis (provided by patients or physician)


1


 Family history of psoriasis (1st or 2nd degree relative)


1


2. Psoriatic nail dystrophy (onycholysis, pitting, or hyperkeratosis) present currently


1


3. Negative test for RF by any test except latex (ELISA and nephelometry preferred)


1


4. Dactylitis

 

 Current dactylitis


1


 History of dactylitis (according to a rheumatologist)


1


5. Radiographic features of juxtaarticular new bone formation (ill-defined ossification near joint margin, excluding osteophytes)


1



RF = Rheumatoid Factor


Laboratory Features


There are no definitive laboratory tests for psoriatic arthritis. Inflammatory markers (i.e., erythrocyte sedimentation rate and C-reactive proteins) can be elevated on polyarticular diseases but remains normal in ~60% of patients. Absence of rheumatoid factor (RF) and cyclic citrullinated peptide (CCP) antibodies is seen in 95% of cases and is helpful to distinguish from RA, especially when PsA presents in a similar fashion. HLA-B27 is present in ~25% of patients.


Radiological Features


Plain X-Ray


Plain X-ray is considered “gold standard” to assess characteristic bony changes in PsA since two-third of these patients can have radiological changes [17]. Similar to rheumatoid arthritis (RA), X-ray shows erosions of bones and joint space narrowing but distribution tends to be more asymmetrical and erosions are marginal (Fig. 7.5a, b). Unlike RA, involvement of DIP joints in PsA with bony erosion and resorption can lead to classic “pencil-in-cup” deformity (Fig. 7.6a) in contrast with DIP joint involvement seen in osteoarthritis leads to “gull wing” changes. Another distinctive feature of PsA is pathologic new bone formation characterized by periostitis, bony ankylosis, and enthesophytes (abnormal bony projection at the entheseal sites). Axial involvement in PsA manifests on X-ray as unilateral sacroiliitis and paramarginal and vertical syndesmophytes (whereas spinal involvement in ankylosing spondylitis tends to be bilateral) [1] (Fig. 7.7a, b).

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Fig. 7.5

Focal marginal erosions seen in peripheral psoriatic arthritis (black arrows) involving. (a) DIP of hands and (b) MCPs and PIPs of left foot. (Image credit: Soumya Reddy, MD)


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Fig. 7.6

(a) Arthritis mutilans in PsA presenting with severe destruction of joints and resorption of adjacent bones (osteolysis) of the PIPs. Classic X-ray finding of “pencil-in-cup” deformity shown with asterisk. (b) T2 short-tau inversion recovery (STIR) sequence of magnetic resonance imaging (MRI) of bilateral sacroiliac joints shows acute bone marrow edema (black arrows) adjacent to the joints. (Image credit: Fardina Malik, MD)


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Fig. 7.7

Axial involvement in psoriatic spondyloarthritis. (a) Bridging syndesmophytes involving the lower cervical vertebrae leading to complete fusion. (b) Bilateral sacroiliitis with evidence of complete ankylosis of left SIJ and partial ankylosis on right. Right SIJ also shows subchondral sclerosis. (Image credit: Soumya Reddy, MD)


Musculoskeletal Ultrasound (MSKUS)


MSKUS is particularly helpful in detecting enthesitis in PsA as it shows entheseal thickening, changes in echogenicity of tendons (hypoechoic), and increased power Doppler signals indicating increased vascularity. In addition, it shows erosions and enthesophytes around the entheses. It can also show combination of synovitis and tenosynovitis that leads to dactylitic changes of a digit. Studies further suggest MSKUS is more sensitive than in clinical examination to detect synovitis [18, 19]. This could be helpful to detect subclinical or preclinical synovitis in patients with skin psoriasis.


Magnetic Resonance Imaging (MRI)


Resolution of MRI is excellent to detect bone marrow edema seen at the site of entheseal inflammation, especially in acute sacroiliitis or other areas of spinal involvement (Fig. 7.6b). MRI is also employed to detect focal bony erosions, synovitis of peripheral joints, as well as entheseal involvement (such as Achilles tendinitis and others).


Differential Diagnosis


It is important to distinguish PsA clinically as several clinical, laboratory, and radiological features can overlap with forms of arthritis (Table 7.3).


Table 7.3

Differential diagnosis of PsA and distinguishing features






















































































Clinical features


Features


PsA


RAa


ReAb


OAc


Gout


Pattern of joint involvement


Asymmetric (more common) and symmetric


Symmetric


Asymmetric


Asymmetric or rarely symmetric


Asymmetric or rarely symmetric (esp. polyarticular disease)


Number of joints involved


Oligoarticular most common. Polyarticular less common


Polyarticular


Oligoarticular


Monoarticluar or oligoarticular


Monoarticluar or oligoarticular


Unique joint involved


DIP


Proximal (never DIP)

 

DIP (associated with Heberden’s nodes)

 

Dactylitis


Unique feature (common)


Not seen


Present but uncommon


Not seen


Confused with an acute gout flare


Skin involvement


Psoriasis


Rheumatoid nodules


Keratoderma blennorrhagicum


No associated skin disease


Tophi


Axial (spinal and SIJ)


Present in ~50% cases (inflammatory)


Uncommon and never involves SIJ


Present in 100% cases (inflammatory)


Common (degenerative etiology)


Absent


Lab features


RF and CCP


Only <5% cases


Present


Absent


Absent


Absent


Hyperuricemia


Can be present as an associated comorbidity


Less common association


Less common


Comorbidity


Unique feature


Radiological features


Erosion and pathological new bone formation (enthesophytes)


Erosion but no pathological new bone information


Enthesophytes are seen


Osteophytes


Erosions (juxtaarticular)



aRA = Rheumatoid arthritis


bReA = Reactive arthritis


cOA = Osteoarthritis


Comorbidities


In addition to the skin and joint manifestations, psoriatic arthritis is associated with a variety of comorbidities that are associated with increased morbidity and excess mortality. Patients have higher prevalence of traditional cardiovascular risk factors (i.e., hypertension, hyperlipidemia, diabetes mellitus, and obesity) as well as increased prevalence of myocardial infarction and stroke that is independent of these risk factors [2023]. There is also an increased prevalence of inflammatory bowel disease (particularly Crohn’s disease) as well as ophthalmologic manifestations, uveitis being the most common [2426]. Furthermore, these patients also suffer from higher rates of depression and anxiety, which may impact psoriatic clinical outcomes [27, 28].


Pathogenesis


PsA results from a complex interplay of genetic and environmental factors. Twin studies in psoriasis showed a threefold higher concordance rate in monozygotic twins than dizygotic twins [29]. Furthermore, prevalence of psoriasis and psoriatic arthritis in first-degree relatives of patients with PsA is much higher than general population [30]. Unlike RA, psoriasis and PsA are associated with major histocompatibility complex (MHC) class I alleles. HLA-C∗w6 has been found in 60% patients with psoriasis, but the association is not strong in arthritis. Association of PsA with HLA-B∗08, B∗27, B∗38, and B∗39 have been observed. Additionally, genome-wide association studies have observed association of PsA with single nucleotide polymorphisms (SNP) of IL23 receptor (IL23R), IL12A, IL12B, nuclear factor κB (NF-κB), and protein tyrosine phosphatase (PTPN22) [3133]. These findings highlight the importance of heritability but risk is substantially lower than monogenic diseases and thereby indicates environmental role in PsA pathogenesis.


Similar to Koebner’s phenomenon observed in skin psoriasis [34], a deep Koebner’s phenomenon (trauma to deep tissues or entheses) is thought to play a role in PsA [35, 36]. Severe skin disease, nail psoriasis, genital psoriasis, and obesity are among other environmental triggers that play a role in initiation of PsA [37].


T cells, especially CD8+ and CD4+ Type 17 (Th17) play a pivotal role in PsA pathogenesis. Macrophage-/monocyte-derived tumor necrosis factor-α (TNF-α) in synovial fluid plays a critical role, as evident by therapeutic efficacy of TNF-α inhibitors in psoriasis and PsA. More recent work suggests entheseal sites being the initial sites of initial inflammation leading to synovitis of psoriatic arthritis. A novel population of T cells (CD3+CD4−CD8−) resident to entheses responds to circulatory IL23 [38] and elaborates IL17 and IL22. Synovia of PsA patients are particularly enriched with Th17 cells, and downstream complex effect of IL23/Th17 axis leads to joint inflammation and erosion [39]. A recent novel murine model (STAT3 overexpression) of PsA further highlights the role of Th17 cell types on PsA pathogenesis [40].


Similar to other subtypes of seronegative SpA, gut-joint axis plays an important role. Up to 70% patients with PsA were shown to have subclinical or microscopic gut inflammation. Moreover, intestinal microbiome is presumed to regulate immune system via Th17 pathway—a key cell population in PsA pathogenesis. Perturbation of intestinal microbiota (specifically lower relative abundance of Akkermansia and Ruminococcus) was shown to be associated with PsA [41].


Treatment


Treatment for psoriatic arthritis is based on the extent of disease and the domains that are affected in an individual patient (Table 7.4). However, the guiding principle is that early treatment leads to improved outcomes. Delays in treatment for as little as 6 months can lead to increased clinical and radiologic damage [42, 43]. Applying a treat to target approach in newly diagnosed disease also leads to improved clinical outcomes [4].


Table 7.4

Medications used in the treatment of psoriatic arthritis

















































































































Medication


Joints


Skin


Radiography


Side effects


Methotrexate [44, 45]


++


+


NA


GI upset, hepatic effects


Leflunomide [60, 61]


+



NA


GI upset, renal effects


Sulfasalazine [62, 63]


+



NA


GI upset, neutropenia


PDE4 inhibitor:


 Apremilast [46, 47]


++


+


NA


GI upset, weight loss


TNFi

       

 Adalimumab [50]


+++


++


++


Infections, demyelination, lymphoma, nonmelanoma cancer


 Certolizumab [51]


+++


++


++


Infections, demyelination, lymphoma, nonmelanoma cancer


 Etanercept [52]


+++


+


++


Infections, demyelination, lymphoma, nonmelanoma cancer


 Golimumab [49]


+++


++


++


Infections, demyelination, lymphoma, nonmelanoma cancer


 Infliximab [48, 64]


+++


+++


++


Infections, demyelination, lymphoma, nonmelanoma cancer


IL17 inhibitors

       

 Ixekizumab [54]


+++


++++


+


Candida infections, injection site reactions


 Secukinumab [55]


+++


++++


+


Candida infections


IL12/23 inhibitor:


 Ustekinumab [53]


+++


++++


+


Infections


JAK inhibitor:


 Tofacitinib [57]


+++


+


NA


Infections, zoster, increased LDL


Abatacept [58]


++


+


+


Infections, headache

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Oct 24, 2020 | Posted by in RHEUMATOLOGY | Comments Off on Arthritis
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