[Secondary Immunodeficiency in Rheumatology]

Area of Science:

• Rheumatology
• Immunology
• Infectious Diseases

Background:

• Immunosuppressive therapies, including disease-modifying anti-rheumatic drugs (DMARDs), are crucial for managing autoimmune and autoinflammatory diseases.
• These treatments can lead to secondary immunodeficiency, compromising the immune system's ability to fight infections.

Purpose of the Study:

• To discuss the risks of secondary immunodeficiency associated with immunosuppressive therapies in rheumatology.
• To identify specific infections and pathogens linked to various immunosuppressive agents used in rheumatic disease management.

Main Methods:

• Literature review and synthesis of existing data on immunosuppressive therapies and infection risks in rheumatology.
• Analysis of specific drug classes (glucocorticoids, B-cell depleting agents, TNF-α inhibitors, JAK inhibitors) and their associated infection risks.

Main Results:

• Glucocorticoids (≥20mg/d for >4 weeks) and B-cell depleting therapies increase hepatitis B reactivation risk.
• Anti-TNF-α inhibitors are associated with tuberculosis reactivation.
• High-dose, long-term glucocorticoids, especially with other DMARDs, raise the risk of Pneumocystis jirovecii pneumonia.
• B-cell depletion, TNF-α inhibition, and JAK blockade elevate Herpes zoster risk.
• Severe immunosuppression (e.g., B-cell depletion, cyclophosphamide, JAK inhibitors, high-dose prednisone) increases the risk of severe COVID-19.

Conclusions:

• Immunosuppressive therapy in rheumatology necessitates careful monitoring for secondary immunodeficiency and associated infections.
• Risk stratification and proactive management are essential to mitigate infection complications in patients receiving potent immunosuppressants.