Tumour necrosis factor-α inhibitors: Difference between revisions
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== Background == |
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* TNF-α is a cytokine involved in the inflammatory response to infection |
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* Has soluble and transmembrane forms |
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* Produced by macrophages, NK cells, granulocytes, fibroblasts, and T cells |
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* Receptors for TNF-α (TNFR1 and TNFR2) are found on most human cells, and are involved in cell activation and proliferation, cytokine production, and granuloma formation |
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== Medications == |
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* [[Adalimumab]] |
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* [[Infliximab]] |
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* [[Certolizumab pegol]] |
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* [[Etanercept]] |
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== Contraindications == |
== Contraindications == |
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* Active bacterial infection, active tuberculosis or untreated LTBI, active herpes zoster infection, active invasive fungal infection, infected skin ulcers, acute hepatitis B or C, untreated chronic hepatitis B, or chronic hepatitis B or C with Child-Pugh B or C |
* Active bacterial infection, active tuberculosis or untreated LTBI, active herpes zoster infection, active invasive fungal infection, infected skin ulcers, acute hepatitis B or C, untreated chronic hepatitis B, or chronic hepatitis B or C with Child-Pugh B or C |
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== Safety == |
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* Baseline [[TST]], ±CXR, prior to starting medications, with patients identified as having [[LTBI]] being offered prophylaxis |
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** Cutoff for TST is 5 mm |
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=== Adverse Effects === |
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==== Infections ==== |
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* Bacteria: [[septic arthritis]], [[Listeria monocytogenes]], [[Legionella]], [[Nocardia]], [[Actinomyces]], [[Salmonella]] |
* Bacteria: [[septic arthritis]], [[Listeria monocytogenes]], [[Legionella]], [[Nocardia]], [[Actinomyces]], [[Salmonella]] |
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* Mycobacteria: [[Mycobacterium tuberculosis]], [[Mycobacterium avium]], [[Mycobacterium bovis]], BCG |
* Mycobacteria: [[Mycobacterium tuberculosis|'''Mycobacterium tuberculosis''']], [[Mycobacterium avium]], [[Mycobacterium bovis]], BCG |
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* Fungi: [[Aspergillus fumigatus]], [[Histoplasma capsulatum]], [[Coccidioides]], [[Cryptococcus neoformans]], [[Candida albicans]] |
* Fungi: [[Aspergillus fumigatus]], [[Histoplasma capsulatum]], [[Coccidioides]], [[Cryptococcus neoformans]], [[Candida albicans]] |
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* Parasites: [[Toxoplasma gondii]] |
* Parasites: [[Toxoplasma gondii]] |
Revision as of 00:36, 17 March 2022
Background
- TNF-α is a cytokine involved in the inflammatory response to infection
- Has soluble and transmembrane forms
- Produced by macrophages, NK cells, granulocytes, fibroblasts, and T cells
- Receptors for TNF-α (TNFR1 and TNFR2) are found on most human cells, and are involved in cell activation and proliferation, cytokine production, and granuloma formation
Medications
Contraindications
- Active bacterial infection, active tuberculosis or untreated LTBI, active herpes zoster infection, active invasive fungal infection, infected skin ulcers, acute hepatitis B or C, untreated chronic hepatitis B, or chronic hepatitis B or C with Child-Pugh B or C
Safety
- Baseline TST, ±CXR, prior to starting medications, with patients identified as having LTBI being offered prophylaxis
- Cutoff for TST is 5 mm
Adverse Effects
Infections
- Bacteria: septic arthritis, Listeria monocytogenes, Legionella, Nocardia, Actinomyces, Salmonella
- Mycobacteria: Mycobacterium tuberculosis, Mycobacterium avium, Mycobacterium bovis, BCG
- Fungi: Aspergillus fumigatus, Histoplasma capsulatum, Coccidioides, Cryptococcus neoformans, Candida albicans
- Parasites: Toxoplasma gondii
- Viruses: hepatitis B virus, hepatitis C virus, varicella-zoster virus
- Screening prior to use should be done for LTBI (TST or IGRA), hepatitis B, hepatitis C, and HIV