Abatacept Bone Effects in Psoriatic Arthritis With Bone Biomarker

Evaluate Bone Changes in Patients With PsA

Psoriatic arthritis; Bone

Observation has pointed out, that osteitis present in the MRI scans, predicts bone erosion and that this in accordance with the concept by underlining the importance of bone marrow involvement in arthritis \[Krabben A, 2013\]. Abatacept with its favourable safety profile preferentially interrupts activation of naïve T cells and perhaps makes the strongest case for exploiting co-stimulatory blockade during the earliest detectable phase of the adaptive immune response at a time when predisposition to autoimmune disease can be detected.

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis that occurs in individuals with psoriasis. It is estimated that 1% to 3% of the general population have psoriasis.1,2,3 In Europe the prevalence of psoriasis ranges up to 6.5%.4 Between 10% and 30% of subjects with Psoriasis develop arthritis. As a result, PsA is the second most common inflammatory arthropathy, following rheumatoid arthritis (RA). 1,2,3 Psoriatic arthritis, a seronegative spondyloarthropathy, is a complex disease involving peripheral and axial joints and periarticular structures resulting in enthesitis and dactylitis. Without appropriate management, the number of joints affected by PsA and the severity of joint damage increase over time, which can lead to marked restriction of daily activities and to substantially compromised quality of life. There is evidence that active PsA is associated with accelerated atherosclerosis, obesity, metabolic syndrome and cardiovascular disease. Other co-morbidities such as pulmonary fibrosis, uveitis, and, less commonly, aortic insufficiency, also contribute to the complexity of PsA.5 Unlike RA, effective treatment options are limited for PsA. Responses to the traditional disease-modifying anti-rheumatic drugs (DMARDs) have been suboptimal.6 There is a significant unmet medical need for more effective and safe therapies in PsA, especially for reducing the arthritic signs and symptoms as well as inhibiting progression of structural damage in joints. About 20% of subjects with PsA will develop a severe destructive disabling form of arthritis.7 In the absence of definitive therapy, more than 50% of subjects with PsA will develop 5 or more deformed joints within 10 years of the onset of disease.8 TNFi therapies are efficacious for both skin and joint diseases and have been shown to inhibit structural damage, but approximately 40% of subjects treated with TNFi agents do not reach a minimal improvement \[American College of Rheumatology \[ACR) 20\]9,10,11,12.13,14,15,16,17 In addition, serious adverse events (SAEs) including infections and injection site reactions have been associated with the use of TNFi therapies. Although in some studies a small percentage of patients previously exposed to TNFi were included, these studies were not powered to demonstrate efficacy in that sub-population. Thus, in subjects who experience inefficacy or intolerance of TNF blockade, there is still medical need for new options. Therefore, there is still need in PsA for therapies that provide significant improvement in arthritis and a risk benefit profile that is acceptable. Therapies directed at novel targets (IL-12/23, PDE4-Antagonist) are also approved since 2014. 18, 19, 20, 21 Joint involvement, is clearly the most prominent example for the systemic nature of psoriasis. Notably, the burden of joint disease in patients with psoriasis may be even higher, given that not all psoriasis patients experiencing musculoskeletal complaints fulfill the classification criteria of PsA22. If present, PsA is a severe disease associated with impaired function and reduced life quality life.

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