Treatment of juvenile idiopathic arthritis

Symptomatic and hormonal therapy

At initial stages or to provide relief for the patient, fast-acting drugs are used, but their impact on the disease outcome is limited.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used exclusively to relieve pain syndrome and active inflammation. They do not possess a disease-modifying effect, meaning they are unable to stop the pathogenetic cascade and prevent joint deformation.

Glucocorticoids (GCs) possess a potent immunosuppressive effect, but their use has strict boundaries:

• Oral administration in most JIA patients should be completely avoided due to the high risk of systemic side effects.
• Preferred routes of administration: drugs (e.g., methylprednisolone) are administered intra-articularly or in the format of intravenous pulse therapy.
• Pulse therapy regimen: high doses (10–15 mg/kg) are administered by intravenous drip once daily in a short course lasting 3–4 days.
• Systemic therapy: is prescribed exclusively for life-threatening conditions. In such cases, the course must be short (maximum 2–3 weeks), and the dosage should not exceed 0.5 mg/kg per day.

Conventional synthetic disease-modifying antirheumatic drugs (csDMARDs)

This is a fundamental group of drugs possessing a disease-modifying effect. They intervene directly in the pathogenesis of JIA, slow down disease progression, and protect joints from destruction.

• Methotrexate. Recognized as the primary drug and the "gold standard" of treatment. Being an antimetabolite, it suppresses the synthesis of pro-inflammatory cytokines.
• Dosage: 10–15 mg/m² strictly once a week.
• Route of administration: preferably parenterally (subcutaneously or intramuscularly) to increase bioavailability.
• Characteristics: the effect is delayed, developing after 3–5 weeks.
• Toxicity: requires the mandatory intake of folic acid (1 mg/day) on all days, except the day of methotrexate injection.
• Sulfasalazine. Indicated for the enthesitis-related and oligoarticular variants of JIA. The daily dose is 30–40 mg/kg, divided into two intakes.
• Cyclosporine A. Has a narrow, specific indication—used in JIA associated with the development of rheumatoid uveitis. Prescribed at a dose of 3.5–5.0 mg/kg per day.

Biologic disease-modifying antirheumatic drugs (bDMARDs)

The advent of these high-tech agents has radically changed the prognosis for JIA patients, allowing the majority to achieve sustained remission. These are monoclonal antibodies and soluble receptors that selectively block specific links of the immune response.

TNF-α inhibitors:

1. Etanercept. An artificial soluble receptor that competitively inhibits tumor necrosis factor alpha and beta. Approved for children from 2 years of age. Administered subcutaneously (0.8 mg/kg) once a week. Used in polyarticular, oligoarticular, enthesitis-related, and psoriatic variants.
2. Adalimumab. A recombinant human monoclonal antibody (IgG1) that neutralizes both membrane-bound and free TNF-α. Approved from 2 years of age, administered subcutaneously (0.24 mg/m²) once every 2 weeks. Acts as the drug of choice in rheumatoid uveitis.

T-cell response modulators:

• Abatacept. Interrupts the immune cascade at an early stage by selective blockade of T-lymphocyte co-stimulation. Prescribed for active moderate to severe polyarticular JIA in children older than 6 years. Administered intravenously according to a special schedule (10 mg/kg).

IL-6 blockers:

• Tocilizumab. A humanized antibody (IgG1) that specifically inhibits soluble and membrane-bound interleukin-6 receptors. Used in systemic JIA in children from 2 years of age (intravenously once every 2 weeks, as monotherapy or with methotrexate).
• Dosing logic: children with a body weight of less than 30 kg require a higher dose—12 mg/kg; for a weight over 30 kg, the dose is reduced to 8 mg/kg.

Safety monitoring and management in severe cases

Specific immunosuppression during the use of bDMARDs creates risks of infectious complications. The greatest danger is the reactivation of latent tuberculosis infection. Patients require strict screening every 6 months: tuberculin skin tests and computed tomography (CT) of the chest organs.

Aggressive therapy in systemic inflammation: If the patient is in the acute phase of systemic JIA with threatening clinical and laboratory activity, and previous therapy (NSAIDs, antibiotics) has not produced an effect, emergency intervention is required.

In such a situation, a wait-and-see approach, the use of oral prednisolone, or NSAID monotherapy is erroneous. Drugs of choice become intravenous immunoglobulins (IVIG) in strict combination with glucocorticoid pulse therapy (methylprednisolone) to immediately suppress the systemic response.

Class and exam questions

What else to study on this topic

• Pathogenetic rationale for glucocorticoid pulse therapy
• Calculation of methotrexate dosage based on body surface area
• Features of tocilizumab dosing in children under and over 30 kg
• Screening protocol for latent tuberculosis infection before prescribing bDMARDs
• Management tactics for severe systemic JIA resistant to NSAIDs

Other topics of «Chapter 9. Rheumatic Diseases»

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.