Psoriatic arthritis L40.5

Polyetiologic, immunologically triggered, rheumatoid factor-negative(usually CCP-AK negative), eminently chronic inflammation of the connective tissue and supporting apparatus (oligo- or polyarthritis), as a facultative manifestation of psoriasis in the musculoskeletal system. Psoriatic arthritis is characterized by an individual manifestation of a typical pattern of involvement of the joints, the visual apparatus and the bones. Synovialitis, enthesitis, tendinitis, tendosynovialitis, erosive arthritis, sacroilitis, ostitis, periostitis and dactylitis are found in varying clinical manifestations.

Remember! Most important extracutaneous manifestation of psoriasis! S.a. Psoriasis arthropathica

Men are affected in a ratio of 1:1.3 to women.

In the USA, 5-42% of patients with psoriasis vulgaris suffer from psoriatic arthritis.

In a clinical study from the UK, the prevalence of PsA was estimated to be up to 14% in patients with PsO in two large dermatology centers using the CASPAR criteria (Ibrahim G et al. 2009).

Of note, the incidence of PsA in patients with confirmed psoriasis increases steadily with the duration of the disease, with an annual incidence rate of 2.7 per 100 cases reported (Eder L et al. 2016). 40% of patients with PsA have radiologically detectable deformities and joint damage, 19% of patients have limitations in joint function.

In terms of etiopathogenesis, psoriatic arthritis is classified as an IMID (immune-mediated inflammatory disease). These are diseases that are characterized by immune-mediated mechanisms. They also include psoriasis vulgaris and rheumatoid arthritis. The etiology of psoriatic arthritis is complex and multifactorial, involving genetic, immunological and environmental factors.

• Genetic factors: Twin studies prove the relevance of genetic factors. In homozygotes there is a 35-70% concordance; first-degree relatives have a 50-fold increased risk of developing psoriatic arthritis. In psoriatic arthritis, an association with genes of the major histocompatibility complex (MHC) is associated with an increased risk. Associations are found with the HLA class I alleles HLA-B38 and HLA-B39. HLA-B27 is associated with spondyloarthritis.
• Associations of PsA with a heat shock protein-like transmembrane protein MICA (class I MHC chain-related) have been described. A further risk is found in the presence of certain GOF variants of the TNF gene, which results in increased TNF-alpha expression. No link to the PSORS1 gene locus has been established for psoriatic arthritis.
• Immunological factors: An increased humoral and cellular immune status could be proven. Serum IgG and IgA are generally elevated (correlation with disease activity), circulating immune complexes can be detected, the synovia contains increased IgG- and IgA-producing plasma cells. Activated T cells appear to play a key role. Cytokines produced by activated T cells stimulate the proliferation and activation of keratinocytes and synovial fibroblasts in vitro. Activated CD8+ cells have been detected in the synovial fluid of psoriatic arthritis patients. Skin and synovia contain mono- and oligoclonal CD8+ and CD4+ cells. Psoriatic arthritis patients show elevated serum and synovial fluid levels of TNF-alpha.
• Environmental factors:
  • Viral and bacterial infections can act as trigger factors. The HI virus has a special position here. In Zambia, in a larger study of men, 27 of 28 patients with psoriatic arthritis were tested seropositive for HIV and suffered from new joint symptoms. It is currently not fully understood whether this HIV-associated psoriatic arthritis is strictly analogous to idiopathic psoriatic arthritis, as, for example, associations with certain HLA patterns do not occur with increased prevalence in HIV-associated psoriatic arthritis.

  • Trauma and injuries: Physical injuries, such as skin injuries or joint trauma, but also banal physical-mechanical stresses in the relapse phase can act as triggers for the disease (Koebner phenomenon).

A lactovegetable diet should be used here, supported by the additional administration of unsaturated fatty acids (e.g. EPAMAX). If after 3 weeks a clear reduction of the complaints can be achieved, this therapy should be maintained.

Phytotherapeutically, Salix alba, willow bark from the ESCOP with a daily dose of 240 mg has been positively monographed for the treatment of psoriatic arthritis.

Also the use of the African devil's claw root (Harpagophyti radix), e.g. Rivoltan®, Doloteffin®^, is possible due to its anti-inflammatory, weak analgesic effect, positive monograph of the ESCOP, however not explicitly for psoriatic arthritis.

Frankincense, Boswella serrata H15, shows excellent effects in psoriatic arthritis. Numerous studies prove the anti-inflammatory effect by inhibiting the enzyme 5-lipoxygenase which induces the leukotriene synthesis. Frankincense has not been approved as a drug in Germany to date.

Chronic, relapsing, mutating, seronegative, painful polyarthritis. The main clinical symptoms are pain and synovitic swelling of the affected joints. The finger or toe end joints (distal interphalangeal joints [DIP]) are usually affected with redness and swelling. Patients mainly complain of pain in the second half of the night and morning stiffness. A typical distribution pattern is detectable (clinically or only scintigraphically recognizable). In the case of arthritic involvement of the DIP, psoriatic involvement of the corresponding fingernail is often detectable (see psoriasis of the nails below).

• Polyarthritic type (about 15% of the PSA collcetive): Peripheral manifestation (correlation with HLA-B 39, 18 and 5): Small, peripheral joints are affected, preferably hands (mostly DIP). Characteristic are the involvement "in the beam" (so-called sausage finger, sausage toe) and the transverse involvement, especially of the distal interphalangeal joints. Asymmetry of joint involvement. Compared to other arthritides, the inflammation is often not as pronounced (=dry inflammation). It often does not occur as pure arthritis but as inflammation of the surrounding structures (dactylitis, enthesiopathy, periarthritis).
• Truncal skeletal manifestation (about 5% of the PSA collective); correlation with HLA-B27): Infestation of the sacroiliac and vertebral joints (spondylarthritis; sacroiliitis). Clinically often severe, deforming arthritis. The pain symptoms occur in the majority of patients as nocturnal low back pain.
• Mono-arthritic type (asymmetric oligoarthritis-about 70% of the PSA collective): Affection of individual joints, e.g. knee or shoulder joint.
• Arthritis mutilans (about 5% of the PSA collective): clinical course with aggressively destructive joint inflammation and pronounced physical limitations.
• Extra-articular manifestations: psoriatic nail changes (see psoriatic nails below), iritis, oral ulcerations, urethritis and heel pain. Iritis is usually mild and is associated with sacroiliitis and spondylitis.

Psoriatic arthritis and fibromyalgia: Alsawy N et al. (2021) found fibromyalgia in 38.3% of 60 patients with PsA. Other studies showed that the prevalence of fibromyalgia in PsA ranges from 17% to 64%. PsA patients with fibromyalgia are predominantly female, and suffer more frequently from symmetrical polyarthritis than patients without fibromyalgia. Fibromyalgia patients also have significantly higher enthesopathy scores, poorer sleep quality, greater fatigue and lower quality of life (Littlejohn GO 2021; Ulutatar F et al. 2021). However, no differences were found between the groups in objective measures of disease activity, such as C-reactive protein, the number of swollen joints and the number of dactylitis (Littlejohn GO 2021).

Rheumatoid factors are predominantly negative (RFs are positive in 5-9% of cases).

Anti-CPA antibodies (antibodies against citrullinated peptides) are found in 10-15% of patients with psoriatic arthritis. These are absent in psoriatic patients without arthritis.

Anti-CarP autoantibodies (directed against the carbamylated protein anti-CarP) could prove to be new diagnostically relevant biomarkers for psoriatic arthritis. anti-CarP autoantibodies proved to be good predictors for the development of rheumatoid arthritis in a larger French cohort study (n=720 patients). Anti-CarP antibodies were found in about 1/3 of patients (32.6%) - including 23.6% of patients who were negative for both ACPA and RF. Anti-CarP antibodies are also positive in rheumatoid factor and ACPA negative psoriatic arthritis (Chimenti MS et al. 2015).

ESR and high CRP: A high ESR and high CRP are characteristic of psoriatic arthritis. The ESR correlates best with clinical joint scores.

The diagnosis (see table with CASPAR criteria) is made on the basis of the patient's medical history, clinic, serology and X-ray findings. Physical examination includes: number, localization, distribution of affected joints and skin findings.

Radiology: Psoriatic arthritis shows certain features not found in rheumatoid arthritis: increased osteolysis, pencil-in-cup deformity, ankylosis, spurring, calcifications at the tendon insertions.

Prominent pencil-in-cup deformity: Pencil-in-cup lesions are caused by severe osteolysis. The proximal end of the phalanges or metacarpal bones bulges, the distal end is pointed.

There are paramarginal erosions in the spine, asymmetric sacroiliitis.

An MRI can be used to assess the enthesiopathy.

Further diagnostics: skeletal scintigraphy.

The treatment goals for psoriatic arthritis are to alleviate inflammation-related musculoskeletal symptoms, maintain joint function and mobility and prevent joint destruction. Early treatment of PsA is necessary in order to achieve significantly better therapeutic results (Haroon M et al. 2015). In this respect, dermatologists in particular should be sensitively trained in the screening of PsA. Training should focus on the early signs of PsA, such as inflammatory activity in tendon attachments (enthesitis) or tendon courses (tendinitis). Studies have also shown that the proximal and distal finger joints as well as the elbow and knee joints are affected early (arthritis) and should therefore be examined more closely by the dermatologist. Persistent "back pain" should also be considered in psoriatic patients.

In principle, the treatment of PsA should generally follow the treat-to-target approach in modern management, with the treatment goal being either remission or minimal disease activity (Smolen JS et al. 2018). This goal should be defined in consultation with the patient. All treatment principles should result in long-term control of inflammatory activity and prevention of mutating joint damage that can lead to irreversible disability. This requires early and appropriate use of systemic therapies. Guidelines from the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA - Coates LC et al. 2015) and the European League Against Rheumatism (EULAR) provide detailed treatment recommendations for various manifestations of the joint and soft tissue component of psoriatic disease (Gossec L et al. 2016).

• Traditional therapy:
  • In mild cases (few joints, minor clinical symptoms), no disease-modifying drugs are indicated. Non-steroidal anti-inflammatory drugs are usually sufficient; additional physical measures; possibly intra-articular corticosteroid injections.
  • For moderate to severe additional skin involvement and moderate joint involvement: methotrexate, mycophenolate mofetil, ciclosporin A. Methotrexate is approved in a dose of 7.5 mg to 25 mg once a week for oral or parenteral administration in PsA.
  • For severe psoriatic arthritis: Continuous long-term therapy. In a meta-analysis (20 randomized clinical trials), significantly better results than placebo were achieved for the following preparations:
    • Sulfasalazine
    • azathioprine
    • Etretinate (low efficacy)
    • MTX parenterally. In one study, perorally applied MTX showed better results than intramuscularly applied gold preparations. No reliable evidence could be provided that MTX influences the long-term progression of arthritis.
    • Ciclosporin: At least one study has shown that Ciclosporin is equivalent to MTX (but significantly more toxic!).
    • Sulfasalazine: Several studies prove the efficacy of (0.5 to a maximum of 3 g/day) in PsA, although there is no formal approval for this indication.
    • Leflunomide: Standard in the treatment of rheumatoid arthritis; approved for psoriatic arthritis. In studies (59% of patients treated with leflunomide), the active substance showed a good response within 24 weeks, as well as a reduction in PASI and an improvement in quality of life.
    • Internal cortisone therapy is generally not recommended, as considerable rebound phenomena of the skin symptoms are to be expected after discontinuation.
• Extended therapy:
  • Etanercept: The active substance is approved for the monotherapy of psoriatic arthritis and plaque psoriasis (patients > 18 years). 2 studies have shown efficacy in the treatment of psoriatic arthritis with active joint and skin disease. The preparation is an effective and safe alternative in the treatment of psoriatic arthritis. Cave: Cost-intensive therapy.
  • Infliximab: The active substance is well tolerated and is approved for the treatment of psoriatic arthritis. The combination with low-dose MTX is recommended in the treatment of rheumatoid arthritis (and psoriatic arthritis) in order to prevent the formation of autoantibodies against infliximab.
  • Adalimumab: The active substance is well tolerated and is approved for the treatment of psoriatic arthritis. The combination with low-dose MTX is recommended to prevent the formation of autoantibodies against adalimumab. Can also be used as monotherapy if MTX is intolerable.
  • Certolizumab
  • Hydroxychloroquine: showed unsatisfactory clinical results in studies (dosage: 250 mg/day).
• In addition to tumor necrosis factor (TNF)-alpha blockers, there is considerable overlap in the treatment of PsO and PsA (including with IL12/23, p19-IL23, IL-17A/F cytokine blockers (ustekinumab, guselkumab, risankizumab, ixekizumab, secukinumab) (Bellinato F et al. 2020; Köhm M et al. 2020).

Psoriatic arthritis is usually a chronic disease that persists for years. It can progress in phases, with periods of remission and exacerbation. The impact of the disease on quality of life and functionality is often aggravated by the usually simultaneous presence of psoriasis vulgaris. Early diagnosis and treatment are crucial for the course and prognosis. Adequate therapy can help to alleviate the symptoms and slow down the progression of the disease. Modern therapies, including biologics and other disease-modifying anti-rheumatic drugs (DMARDs), have significantly improved treatment options. These drugs can reduce inflammation and minimize the risk of joint damage.

• Peripheral arthritis is found in 95% of patients and can be oligo- or polyarticular. About 5% have only spinal/axial involvement, between 20-50% have spinal and peripheral involvement.
• Long-term prognosis: Many patients with psoriatic arthritis can control their symptoms and achieve a good quality of life with proper treatment. However, the disease is progressive in some cases despite adequate treatment. 20% of patients develop a destructive form of arthritis and 10 years after the onset of the disease >50% of patients show 5 or >5 deformed joints.
• Psychosocial aspects: The psychosocial impact of the disease is often significant for the patient. Many patients suffer from psycho-social problems because they are impaired in their everyday habits. These affect the following components:
  • Body image and self-esteem: The visible skin changes and joint pain can have a strong influence on the self-image of those affected. Many patients feel uncomfortable in their skin, which can lead to reduced self-esteem.
  • Depression and anxiety: Studies show that people with psoriatic arthritis have a higher risk of depression and anxiety. Constantly dealing with pain and the impact of the disease on daily life can be emotionally draining.
  • Social isolation: Because of shame or discomfort about the appearance of their skin or the limitations of joint pain, sufferers may avoid social contact. This can lead to isolation and loneliness.
  • Occupational challenges: Psoriatic arthritis can significantly affect the ability to work. Pain/permanent fatigue can reduce productivity and limit the ability to perform certain tasks. This can lead to fear of job loss and financial worries.
  • Family and relationship problems: The burden of chronic illness can also put a strain on relationships with family members and partners. Problems such as a lack of understanding, frustration or excessive demands can arise in relationships and latently destroy them.
  • Stress and coping mechanisms: Constantly coping with the symptoms, the necessary treatment measures and their psychosocial effects can lead to increased stress. Some patients may develop unhealthy coping mechanisms, such as alcohol or drug abuse.
  • Access to support and information: Many patients may struggle to find the right support or information about their condition. This can increase feelings of helplessness and make coping more difficult.
  • Adherence to treatment: Psychosocial problems can also affect the willingness to adhere to treatment plans.

HIV patients often have severe courses (skin and joints). HIV infection as a possible trigger!

Psoriatic arthritis can potentially be a very serious disease that can lead to significant disability. As psoriasis vulgaris often precedes psoriatic arthritis, dermatologists are the first doctors to be contacted and it is their responsibility to diagnose and treat psoriatic arthritis at an early stage. Further treatment should be interdisciplinary and involve rheumatologists, physiotherapists, occupational therapists and orthopaedists.

There is considerable overlap in the approved drugs for the treatment of psoriasis and psoriatic arthritis (PsA) (including Methotrexate, apremilast and IL12/23, p19-IL23, IL-17A/F cytokine blockers (ustekinumab, guselkumab, risankizumab, ixekizumab, secukinumab) and tumor necrosis factor (TNF)-alpha blockers (adalimumab, etanercept, infliximab and certolizumab) (Bellinato F et al. 2020; Köhm M et al. 2020). In contrast, other treatment options used for PsA are less effective for PsO (sulfasalazine, leflunomide) or are not approved for PsO (tofacitinib, golimumab) (Köhm M et al. 2020).

If we analyze the current status of outpatient and inpatient treatment, the following picture emerges (König A et al.2023): Around one third of patients in private practices and non-university hospitals received only conventional systemic therapy such as methotrexate, non-steroidal anti-inflammatory drugs, leflunomide, systemic steroids, sulfasalazine, ciclosporin, apremilast or COX-2 inhibitors or apremilast. Treatment with biologics as monotherapy was carried out more frequently in patients in private practices and university clinics than in non-university clinics (!). The proportion of patients who received both treatments (conventional and biological) was highest in university clinics (26.8%).

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