Revue des maladies respiratoires · 2025
[TNF-α blockers: Its indications and potential toxicity in pulmonology].
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Elhani I, Bourgarit A
Аннотация
INTRODUCTION: As a key cytokine in inflammation and granuloma formation TNF-α plays a central role in several pulmonary diseases, including sarcoidosis, tuberculosis and the acute respiratory distress syndrome. Although widely used in treatment of chronic inflammatory diseases, anti-TNF-α biotherapies have few indications in pulmonology.
STATE OF THE ART: In therapeutic trials, the efficacy of anti-TNF-α drugs in treating lung diseases has yet to be proven, and they are not currently recommended as first-line treatments. Possible immunization against the treatment could be counteracted by the addition of another immunosuppressant, particularly methotrexate. While anti-TNF-α drugs are associated with an increased risk of tuberculosis, discontinuing their administration in patients with tuberculosis could lead to paradoxical worsening, and the benefit-risk balance of resuming these treatments calls for debate. Lastly, occurrence of granulomatosis in a patient receiving anti-TNF-α therapy should raise the possibility of anti-TNF-α-induced granulomatosis, and the continuation of treatment should likewise be debated.
PERSPECTIVES: The development of compounds selectively targeting the TNFR1 receptor could improve efficacy and reduce adverse effects. The criteria for discontinuing or continuing anti-TNF-α therapy entailing paradoxical reactions or induced granulomatosis require clarification. The conditions calling for systematic addition of methotrexate to prevent immunization likewise need to be determined.
CONCLUSION: Although anti-TNF-α agents have transformed the treatment of inflammatory diseases, their place in pulmonology remains marginal. The development of targeted therapies could extend their use while minimizing side effects.
STATE OF THE ART: In therapeutic trials, the efficacy of anti-TNF-α drugs in treating lung diseases has yet to be proven, and they are not currently recommended as first-line treatments. Possible immunization against the treatment could be counteracted by the addition of another immunosuppressant, particularly methotrexate. While anti-TNF-α drugs are associated with an increased risk of tuberculosis, discontinuing their administration in patients with tuberculosis could lead to paradoxical worsening, and the benefit-risk balance of resuming these treatments calls for debate. Lastly, occurrence of granulomatosis in a patient receiving anti-TNF-α therapy should raise the possibility of anti-TNF-α-induced granulomatosis, and the continuation of treatment should likewise be debated.
PERSPECTIVES: The development of compounds selectively targeting the TNFR1 receptor could improve efficacy and reduce adverse effects. The criteria for discontinuing or continuing anti-TNF-α therapy entailing paradoxical reactions or induced granulomatosis require clarification. The conditions calling for systematic addition of methotrexate to prevent immunization likewise need to be determined.
CONCLUSION: Although anti-TNF-α agents have transformed the treatment of inflammatory diseases, their place in pulmonology remains marginal. The development of targeted therapies could extend their use while minimizing side effects.