Psoriatic arthritis (PsA) is a chronic, autoimmune, inflammatory form of arthritis that affects 5-25% of patients afflicted by the skin condition psoriasis. In almost 60% of PsA cases, it presents in a few joints (1-4) but becomes polyarticular as the disease progresses. Polyarthritis affects both sides symmetrically and in one out of three PsA patients, it is often associated with dactylitis and enthesopathy.
Up to 40% of patients eventually develop deformities of the affected joints that, however, remain functional. Severe joint damage is predicted by increase in the number of joints with swelling, high ESR, and duration of arthritis.
The management of psoriatic arthritis begins with making the right diagnosis. Apart from the clinical symptoms, diagnosis of PsA usually involves laboratory testing using ELISA or other testing methods to confirm the seronegative status of a patient with psoriasis. However, sometimes the arthritis precedes skin lesions. In such cases, the classifications of psoriatic arthritis (CASPAR) criteria are used to diagnose PsA in a patient, though early signs and symptoms are difficult to detect.
The CASPAR criteria are highly sensitive and specific and are currently being validated for universal diagnosis and classification of PsA.
A questionnaire designed to screen psoriasis patients for such a condition is also helpful in making an early diagnosis. Radiological evidence of joint damage is typically present late in the course of the disease. For this reason, the patients must be tested with sensitive methods of screening such as ultrasound, CT, MRI, and isotope scans.
Since PsA does not have a cure, it is important to control inflammation in the affected joints to relieve pain and provide relief that may help minimize final joint disability. Diagnosing the disease before joint damage occurs is a key factor in preventing adverse outcomes, especially with the emergence of newer drugs.
Treatment for PsA involves
- Pain reduction
- Improving functional ability and reducing the mortality rate
- Physical rehabilitation and physical therapy
The drugs used to treat PsA target various immunologic cells, such as the antigen- presenting cells (APCs) and T cells, as well as some cytokines.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit prostaglandin synthesis and COX-2 enzyme, to reduce inflammation. They are used to relieve joint pain and inflammation and reduce bone damage in mild PsA cases. However, this drug shows no difference between treated and untreated patients when administered longer term. These drugs are known to have side effects such as gastritis, liver and kidney disease, and at times cardiac problems. NSAIDs are, therefore, used only in low doses and for shortest periods.
Intra-articular corticosteroid injections may be used in mild PsA involving one or a few joints, i.e. less than four, to alleviate joint inflammation and pain.
Disease-modifying anti-rheumatic drugs (DMARDs) are prescribed to prevent rapid progression of the condition that may lead to permanent joint damage. They include several immunosuppressants and other drugs which are not chemically related. They are used to treat moderate to severe PsA that does not respond to NSAIDs. The criteria to use DMARD in PsA are: (i) one or more affected joints with swelling and tenderness, (ii) factors indicating poor prognosis such as high acute phase reactants, radiologic evidence of damage, and signs of involvement of other systems.
DMARDs are not effective in PsA cases where the pelvic bone or peripheral synovial fluids are involved. While these drugs may cause some benefit in PsA, the side effects may be serious, including hepatic damage, immunosuppression and severe infection. This is especially so with immunosuppressant drugs such as cyclosporine and azathioprine. Patients must be closely monitored for baseline blood counts, liver function, and renal function every three months while being treated with DMARDs.
Tumor necrosis factor (TNF)-alpha inhibitors are among the newest class of drugs for the treatment of PsA. They reduce the formation of the potent inflammatory cytokine TNF-alpha. TNF-alpha inhibitors such as humanized monoclonal antibodies have been found to induce remission and significantly reduce pain and stiffness as well as joint swelling and joint tenderness. They also reduce disease manifestation in the skin and nails, soft tissues around the joints, and other systemic features such as heart or vascular disease. It is extremely effective in about 50-70% of cases.
TNF-alpha inhibitors are prescribed for adults with moderate to severe active disease specified as involving three or more joints with pain and swelling, for six months or more, as well as intolerance to NSAIDs and DMARDs over three months.
However, some of the side effects of TNF-alpha inhibitors are nausea or diarrhea, alopecia, and susceptibility to serious infections such as tuberculosis and other granulomatous disorders. Both the efficacy and the toxicity of these drugs are believed to be regulated partially via genetic factors.
Other biologics include various interleukin antagonists, anti-CD20, and inhibitors of other cytokines and receptors which mediate the inflammatory process. Some of the drugs that are presently prescribed to treat psoriasis skin plaques reduce PsA symptoms as well.
Bisphosphonates are also occasionally used to reduce bone breakdown in PsA.
Surgical procedures such as joint replacement surgery may be necessary if the joint has been irreparably damaged, impairing normal function.
The management of PsA is gradually improving but many factors are yet to be determined, including the contribution of immune and non-immune mechanisms to the disease, the possible effects of combining different types of biologics, as part of therapy and so on. Research is now focusing on methods to combat non-immune mechanisms of PsA in an attempt to reverse disease manifestations and halt the progress of joint impairment that may lead to physical disabilities.