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Psoriatic arthritis (PsA) is a chronic, relapsing joint inflammation that occurs in 5-25% of patients with psoriasis. It comes under the group of inflammatory diseases collectively known as seronegative sphondyloarthropathy indicating that PsA can be distinguished from rheumatoid arthritis by the absence of rheumatoid factor (RF) in serum. It affects men and women equally with an incidence ranging from 0.1/100,000 in Japan to as high as 23.1/100,000 in Finland. The overall global prevalence of PsA is 1–3%.
While genetic factors are strongly associated with PsA, environmental factors also play a role. PsA can be triggered by injuries, infections, medications, alcohol, smoking, and some endocrine disorders. In PsA, damage to the joints is caused by an immunological imbalance whereby kinins are released. These kinins cause inflammatory lesions in the tissues surrounding the joints. However, PsA takes a few months to manifest clinically.
The pathogenesis of PsA has been explained in two ways, (i) A variety of inciting factors such as trauma, infection, or even medications may precipitate immunological cell activation resulting in the release of a cascading array of cytokines. Tumor necrosis factor-alpha (TNF-α) and interferon-gamma play prominent roles in this pathway. (ii) Another more common theory is the inflammatory process of proteins that causes dysregulation of cell-to cell signaling, as well as changes in the levels of several inflammatory mediators, triggering the inflammatory process within the joints.
Psoriasis is of two types; Type I (early onset) and Type II (late onset). Type I psoriasis is more common and severe, with most affected individuals genetically predisposed to this disease type.
PsA mainly affects the skin, synovial membrane, tendons, and ligaments of the joints, as well as the cartilage and joint bones. Moreover, it is typically found to occur in the joints of the axial skeleton. PsA that affects the skin is primarily related to T-cell activation. The initial lesions in the synovial membrane within the joints are also composed of memory T cells.
PsA also leads to marked alteration of joint contour. Radiographical evidence shows the cartilage to have narrowed down with reduced joint space. The joint c capsules, tendons, and ligaments are inflamed. It usually presents as arthritis of one or only a few joints (oligoarthritis).
Moll and Wright described five clinical forms of PsA:
PsA is diagnosed by the presence of psoriasis and is confirmed by imaging. Radiography is useful only during the late phases of the disease when there are signs of bone destruction. However, ultrasound imaging, computed tomography (CT), and magnetic resonance imaging (MRI) are used to enable early diagnosis as well as to monitor the effects of treatment and subsequent prognosis. Radiologically, PsA is classified using the Psoriatic Arthritis Rating Score (PARS) that takes into account destructive lesions of the joints along with proliferative lesions. In the event of a suspicious lesion, isotope examination should be performed along with ultrasound of the joint and hand X-ray. MRI or CT scan is carried out when ultrasound findings are unclear or when lesions involve the axial skeleton.
Treatment is most effective when initiated early, i.e., before active joint destruction. Treatment involves relieving the pain and preventing further bone destruction, whilst facilitating independent activity as well as lowering the risk of death. Psychological support and counseling are essential during the entire treatment period.
Initial therapy starts with non-steroidal anti-inflammatory agents (NSAIDs) for mild PsA cases while intra-articular corticosteroid injections may be prescribed for oligoarthritis.
Disease-modifying anti-rheumatic drugs (DMARDs) are prescribed for long-term control of the disease and include leflunomide, gold salts, and cyclosporine, among a host of others agents. Monoclonal antibodies are biologics used to treat moderate to severe PsA cases in adults who cannot tolerate NSAIDs or DMARDs for more than three months. Monoclonal antibodies act against TNF-α and other inflammatory molecules. Six months after diagnosis of PsA, efficacy of the prescribed treatment is monitored by carrying out ultrasound scans for the affected joints as well as for joints suspected to be affected by PsA.
Early PsA diagnosis and treatment intervention, involving clinical, physical, and psychological well-being, is vital in improving and maintaining patient outcome.