RÉSUMÉ
The inhibition of TNF has been a major advance in the treatment of chronic inflammatory diseases by acting on their local and systemic expression. However, this treatment can be responsible for serious infections, in particular reactivation of tuberculosis. Their mechanisms are now better understood. On the one hand, chronic inflammatory diseases are accompanied by a deficit in cell-mediated immunity, particularly affecting the Th1 pathway. On the other hand, TNF having a central role in the formation of granulomas, its inhibition allows the release of the tuberculosis bacillus and its rapid spread. This understanding has enabled preventive actions with screening and treatment of latent tuberculosis.
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SUMMARY
The inhibition of TNF has been a major progress in the treatment of chronic inflammatory diseases by acting on their local and systemic manifestations. However, this treatment can be responsible for severe infections, specifically reactivation of tuberculosis. The underlying mechanisms are now better understood. First, chronic inflammatory diseases are associated with a cellular mediated immune defect, especially affecting the Th1 pathway. On the other hand, TNF has a central role in granuloma formation. TNF inhibition allows the escape of tuberculosis bacteria and its fast diffusion. This understanding has allowed the implementation of prevention measures with screening and treatment of latent tuberculosis.
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Key words
TNF
Biotherapies
Infections
Pharmacovigilance
Bacterial infections
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Key-words
Tnf
Biotherapies
Infections
Drug safety
Bacterial Infections
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Copyright © 2018 National Academy of Medicine. Published by Elsevier Masson SAS All rights reserved.
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