Safety of Anti‐TNF Therapies in Immune‐Mediated Inflammatory Diseases: Focus on Infections and Malignancy

Pereira, Rui; Lago, Paula; Faria, Raquel; Torres, Tiago

doi:10.1002/ddr.21285

Cited by 50 publications

(35 citation statements)

References 83 publications

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“…In a national registry study [11 & ] and a literature-based review [13], there was no signal noted between TNFi and malignancy incidence. However, a single center study by Berghen et al [17] noted that malignancies (both solid tumor and hematologic) after starts of anti-TNF treatment were found to be higher than normal population.…”

Section: Key Pointsmentioning

confidence: 96%

“…A comprehensive literature review examining studies between 2004 and 2014 noted that background risk without biological therapy is two-fold higher for rheumatoid arthritis and found supporting evidence that that registries do establish an increased incidence of serious infections ranging from 1.2 to 2.78 times that of the control MTX populations [12 & ]. Similarly, Pereira et al [13] reviewed literature from all diseases where biologic therapies are applied and found an increased risk of infection in patients treated with anti-TNF biologics.…”

Section: Introductionmentioning

confidence: 96%

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Infection, malignancy, switching, biosimilars, antibody formation, drug survival and withdrawal, and dose reduction

Ianculescu

Weisman²

2016

Current Opinion in Rheumatology

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TNFi agents have made their powerful impact on management of patients with rheumatoid arthritis, but questions remain: what is their true infection and malignancy risk in the evolving populations using these drugs today; are we able to maintain their benefit with a reduced schedule (and presumed less cost) and yet recapture their benefit if we guess wrong; are biosimilars just as good, or even better with less cost; are there data to inform us about how to achieve successful switching among different mechanism of action TNFi agents? Finally, are we going to face the specter of cost containment causing change from innovator to biosimilars over which we have no control?

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Section: Key Pointsmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 96%

Infection, malignancy, switching, biosimilars, antibody formation, drug survival and withdrawal, and dose reduction

Ianculescu

Weisman²

2016

Current Opinion in Rheumatology

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“…However, anti-TNF agents are very expensive and have many serious side effects, such as infectious and malignant complications [27]. IL-1β is a major proinflammatory cytokine that possesses similar biological activity to TNF-α.…”

Section: Discussionmentioning

confidence: 99%

Isoliquiritigenin Ameliorates Indomethacin-Induced Small Intestinal Damage by Inhibiting NOD-Like Receptor Family, Pyrin Domain-Containing 3 Inflammasome Activation

et al. 2018

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Activation of the NOD-Like Receptor Family, Pyrin Domain-Containing 3 (NLRP3) inflammasome, which consists of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and pro-caspase-1, triggers pro-caspase-1 cleavage promoting the processing of pro-interleukin (IL)-1β into mature IL-1β, which is critical for the development of non-steroidal anti-inflammatory drug (NSAID)-induced enteropathy. We investigated the effects of isoliquiritigenin, a flavonoid derived from the roots of Glycyrrhiza species, on NSAID-induced small intestinal damage and the inflammasome activation. To induce enteropathy, mice were administered indomethacin by gavage with or without isoliquiritigenin pretreatment. Some mice received an intraperitoneal injection of recombinant murine IL-1β in addition to isoliquiritigenin and indomethacin. Indomethacin induced small intestinal damage and increased protein levels of cleaved caspase-1 and mature IL-1β in the small intestine. Treatment with 7.5 and 75 mg/kg isoliquiritigenin inhibited indomethacin-induced small intestinal damage by 40 and 56%, respectively. Isoliquiritigenin also inhibited the indomethacin-induced increase in cleaved caspase-1 and mature IL-1β protein levels, whereas it did not affect the mRNA expression of NLRP3, ASC, caspase-1, and IL-1β. Protection against intestinal damage in isoliquiritigenin-treated mice was completely abolished with exogenous IL-1β. NLRP3^–/– and caspase-1^–/– mice exhibited resistance to intestinal damage, and isoliquiritigenin treatment failed to inhibit the damage in NLRP3^–/– and caspase-1^–/– mice. Isoliquiritigenin prevents NSAID-induced small intestinal damage by inhibiting NLRP3 inflammasome activation.

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“…[13][14][15] Because TNF signaling has been implicated in the pathogenesis of many diseases, the clinical use of anti-TNF antibodies opened important perspectives for the treatment of inflammatory diseases, such as rheumatoid arthritis. [16][17][18] However, the administration of anti-TNF and p52, resulted from the processing of p105 and p100 in their C-terminal portion, respectively. IκB proteins contain ankyrin-repeat motifs (ANK) in their C-terminal region (also found on p100 and p105) which interact with the RHD of NF-κB proteins, preventing their nuclear translocation.…”

Section: Canonical Nf-κb Pathwaymentioning

confidence: 99%

Nuclear Factor κB Activation Pathways During Infection

Andrade¹,

Amaral²

2017

CCI

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ABSTRACT:The interactions between pathogens and host cells and the way by which the immune response is modulated during this process ultimately dictate the fate of infection. Host phagocytes exposed to Mycobacterium tuberculosis (M. tuberculosis) sense microbial-associated molecular patterns and activate a series of signaling pathways. In this setting, activation of the nuclear factor κB (NF-κB) initiates transcription of several key genes involved in orchestration of antimycobacterial effector functions. This review describes these major pathways that govern the outcome of host phagocytes infected with M. tuberculosis. Furthermore, we highlight evidence of how M. tuberculosis modulates activation of NF-κB pathways to evade the host antimycobacterial defense.

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Safety of Anti‐TNF Therapies in Immune‐Mediated Inflammatory Diseases: Focus on Infections and Malignancy

Cited by 50 publications

References 83 publications

Infection, malignancy, switching, biosimilars, antibody formation, drug survival and withdrawal, and dose reduction

Infection, malignancy, switching, biosimilars, antibody formation, drug survival and withdrawal, and dose reduction

Isoliquiritigenin Ameliorates Indomethacin-Induced Small Intestinal Damage by Inhibiting NOD-Like Receptor Family, Pyrin Domain-Containing 3 Inflammasome Activation

Nuclear Factor κB Activation Pathways During Infection

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