Tuberculosis associated with therapy against tumor necrosis factor α

Winthrop, Kevin; Siegel, Jeffrey; Jereb, John A.; Taylor, Zachary; Iademarco, Michael F.

doi:10.1002/art.21382

Cited by 103 publications

(63 citation statements)

References 19 publications

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“…Nevertheless, it seems that soluble TNFRs function primarily as anti-inflammatory components through the neutralization of TNF bioactivity (36). Soluble TNFRII is the biologically active component of etanercept (Enbrel), a therapeutic TNF inhibitor used for rheumatoid arthritis and Crohn's disease, which, among other TNF inhibitors, has also been associated with reactivations of latent M. tuberculosis infection (33,55).…”

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confidence: 99%

Mannose-Capped Lipoarabinomannan from Mycobacterium tuberculosis Induces Soluble Tumor Necrosis Factor Receptor Production through Tumor Necrosis Factor Alpha-Converting Enzyme Activation

et al. 2012

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c Primary Mycobacterium tuberculosis infection results in granuloma formation in lung tissue. A granuloma encapsulates mycobacterium-containing cells, thereby preventing dissemination and further infection. Tumor necrosis factor alpha (TNF-␣) is a host-protective cytokine during M. tuberculosis infection due to its role in promoting and sustaining granuloma formation. TNF activity is regulated through the production of soluble TNF receptors (sTNFRI and sTNFRII). Therefore, we examined the potential production of endogenous sTNFRs during M. tuberculosis infection. Using the murine model of aerosol M. tuberculosis infection, we determined that levels of sTNFR production were elevated in bronchoalveolar lavage fluid 1 month following infection. An investigation of M. tuberculosis cell wall components identified that the known virulence factor mannose-capped lipoarabinomannan (ManLAM) was sufficient to induce sTNFR production, with sTNFRII being produced preferentially compared with sTNFRI. ManLAM stimulated the release of sTNFRs without TNF production, which corresponded to an increase in TNF-␣-converting enzyme (TACE) activity. To determine the relevance of these findings, serum samples from M. tuberculosisinfected patients were tested and found to have an increase in the sTNFRII/sTNFRI ratio. These data identify a mechanism by which M. tuberculosis infection can promote the neutralization of TNF and furthermore suggest the potential use of the sTNF-RII/sTNFRI ratio as an indicator of tuberculosis disease.

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Mannose-Capped Lipoarabinomannan from Mycobacterium tuberculosis Induces Soluble Tumor Necrosis Factor Receptor Production through Tumor Necrosis Factor Alpha-Converting Enzyme Activation

et al. 2012

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“…Such persons are more likely to have false negative TST results and accordingly, a number of tuberculosis cases have occurred in individuals who had negative TST results before starting anti-TNF therapy [3]. Chest radiographs are not useful in screening for LTBI, as most latently infected individuals have normal chest radiographs [4].…”

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confidence: 99%

Tuberculous bursitis of the wrist after anti-TNFalpha treatment: a case report

et al. 2010

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“…Uno dei più gravi EA dell'inibizione del TNF è la potenziale riattivazione di una tubercolosi latente, soprattutto per il frequente ritardo diagnostico dovuto alle sue manifestazioni subdole o atipiche (extra-polmonari). Questo principalmente con l'Infliximab per la sua capacità di legarsi al TNFα di membrana e di indurre la lisi cellulare e quindi la dissoluzione del granuloma tubercolare (141,142). Questo EA, sicuramente correlato all'inibizione del TNFα, e spesso osservato nella prima fase dell'esperienza clinica post-marketing nell'AR, è quasi completamente scomparso da quando è stato reso obbliga-torio lo screening e, nel caso di un risultato positivo della Mantoux, la profilassi anti-TBC.…”

Section: Eventi Avversi Dell'inibizione Del Tnfunclassified

Biological therapy with TNF-inhibitors in pediatric rheumatology. Review of the litterature and personal experience

Gerloni¹,

Pontikaki²,

Gattinara³

et al. 2011

Reumatismo

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The therapeutic approach to JIA is sometimes very troublesome and progression to erosive polyarthritis may occur in all JIA categories. Only Methotrexate has shown efficacy and safety in a large controlled trial. Nevertheless, in many cases, drug resistance or intolerance has led to try other therapeutic options, with still debatable results. Therefore, there has been space, in the last few years, for new therapies as the TNF-inhibitors. This therapeutic approach has shown a dramatic clinical benefit in active polyarticular refractory JIA: the rate and rapidity of response have exceeded those of all other studied DMARDs. Preliminary data show that they are efficacious also for other pediatric rheumatic disease (spondyloarthropathies, autoimmune uveitis, dermatomyositis, Kawasaki syndrome and some auto- inflammatory diseases). TNF-inhibitors in JIA have demonstrated a favourable benefit-to-risk profile. However, as their use has increased worldwide, some unusual, usually not serious, adverse events have emerged. Severe infections, including TB, and deaths have been reported. Long-lasting active disease, systemic disease, concurrent and previous immunosuppressive therapies, all contribute to risk of infection and other serious AEs. Given the evidence that TNF has a primary role in the pathogenesis of JIA, particularly in joint destruction, neutralizing this cytokine early, within the window of opportunity, could halt or delay progression of joint damage and debilitating consequences of the disease. Thus, for JIA patients whose disease is not quickly controlled with MTX, TNF blockers may be considered as first-line treatment, although long-term safety data still need to be established

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Tuberculosis associated with therapy against tumor necrosis factor α

Cited by 103 publications

References 19 publications

Mannose-Capped Lipoarabinomannan from Mycobacterium tuberculosis Induces Soluble Tumor Necrosis Factor Receptor Production through Tumor Necrosis Factor Alpha-Converting Enzyme Activation

Mannose-Capped Lipoarabinomannan from Mycobacterium tuberculosis Induces Soluble Tumor Necrosis Factor Receptor Production through Tumor Necrosis Factor Alpha-Converting Enzyme Activation

Tuberculous bursitis of the wrist after anti-TNFalpha treatment: a case report

Biological therapy with TNF-inhibitors in pediatric rheumatology. Review of the litterature and personal experience

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