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Juvenile idiopathic arthritis: Old disease, new tactics

The Journal of Family Practice. 2019 March;68(2):E8-E13
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Beyond NSAIDs and disease-modifying antirheumatic drugs are now biologic agents and anti-interleukin drugs that can augment therapy.

PRACTICE RECOMMENDATIONS

› Pair the findings of your clinical exam with the results of imaging and laboratory testing to make the diagnosis of juvenile idiopathic arthritis (JIA), as it is a diagnosis of exclusion. B

› Individualize treatment based on where the patient falls in the JIA disease spectrum to increase the likelihood that medical therapy will be effective. A

› Consider treating diagnosed JIA with an available biologic agent, which can provide a long asymptomatic period. B

Strength of recommendation (SOR)

A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series

Laboratory testing

Mandibular asymmetry secondary to condylar resorption and remodeling is the most common presenting complaint of juvenile idiopathic arthritis—not arthralgia or pain, as you might expect.

No diagnostic tests for JIA exist. Assays of acute-phase reactants, including C-reactive protein, the erythrocyte sedimentation rate, and serum amyloid-A proteins, can be utilized to demonstrate inflammation but not to confirm the diagnosis. For some classes of JIA, various tests, including rheumatoid factor, antinuclear antibody, human leukocyte antigen B-27, and cyclic citrullated peptide antibodies, can be used to confirm a specific class but, again, are not recommended for confirming JIA.6

The complete blood count, blood cultures, and tests of uric acid and lactate dehydrogenase can be ordered during treatment to monitor for complications, such as malignancy, infection, MAS, and sepsis.

 

Treatment is based on disease class

Nonsteroidal anti-inflammatory drugs (NSAIDs) and intra-articular steroids are used in all JIA classes, as an adjunct to class-specific treatment, or as induction agents.31 These therapies, although they alleviate acute signs and symptoms, such as pain, inflammation, swelling and joint contractures, are not useful for long-term treatment of JIA because they do not halt disease progression.

Systemic steroids can be utilized in exceptional cases, including chronic uveitis with arthritis or in patients with destructive arthritis and poor prognostic features, including cyclic citrullated peptide antibodies, positive RF, erosions, and joint-space narrowing.32

Other drugs. Options include traditional disease-modifying anti-rheumatic drugs (csDMARDs), such as methotrexate and leflunomide; biologic agents, such as TNF-a inhibitors (eg, etanercept, adalimumab, and infliximab); and anti-IL monoclonal antibody drugs (eg, the IL-6 inhibitor tocilizumab and IL-1 inhibitors anakinra, and canakinumab).31 Indications by class include:

  • csDMARDs as first-line therapy in persistent eoJIA and pJIA;
  • TNF-Symbolα inhibitors for refractory eoJIA and for pJIA episodes31;
  • tocilizumab, recommended for sJIA patients who have persistent systemic signs; and
  • anakinra and canakinumab for refractory SJIA patients.32

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