Pulmonary miliary tuberculosis in a patient with anti-TNF-alpha treatment

Mayordomo, L; Marenco, José Luis; Gómez‐Mateos, Jesús; Rejón, E

doi:10.1080/030097402317255372

Cited by 66 publications

(28 citation statements)

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“…These effects can vary from mild opportunistic diseases to tuberculosis or even multiple sclerosis. [32][33][34] Although the effective treatment of RA through anti-TNFa therapy, it appears from these studies that deprivation of this cytokine in some cases can result in severe impairment of the immune response. It is not unthinkable that systemic cytokine blocking therapies will eventually result in systemic impairment of innate and acquired immunity, while local therapies can be less interfering with systemic processes.…”

Section: Discussionmentioning

confidence: 99%

Adenoviral delivery of IL-18 binding protein C ameliorates Collagen-Induced Arthritis in mice

Smeets¹,

Loo²,

Arntz³

et al. 2003

Gene Ther

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Section: Discussionmentioning

confidence: 99%

Adenoviral delivery of IL-18 binding protein C ameliorates Collagen-Induced Arthritis in mice

Smeets¹,

Loo²,

Arntz³

et al. 2003

Gene Ther

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“…Zinc deficiency was shown to decrease the production of tumour necrosis factor-a (TNFa) and gamma interferon (IFN-g) from peripheral mononuclear cells (Beck et al, 1997). It was also suggested that administration of anti-TNF-a to patients may lead to reactivation of TB (Mayordomo et al, 2002), and a mutation in the gene coding for the IFN-g receptor resulted in an increased susceptibility to mycobacterial infections (Newport et al, 1996). It therefore seems possible that zinc deficiency is implicated in the activation of TB.…”

Section: Discussionmentioning

confidence: 99%

Alterations in serum levels of trace elements in tuberculosis and HIV infections

et al. 2005

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Objective: To evaluate serum concentrations of trace elements in tuberculosis (TB) patients with or with out human immunodeficiency virus (HIV) coinfection before and after anti-TB chemotherapy. Subjects: A total of 155 TB patients, 74 of which were coinfected with HIV, and 31 healthy controls from Gondar, Ethiopia. Methods: Serum levels of copper, zinc, selenium and iron were determined using an inductively coupled plasma mass spectrometer from all subjects at baseline and from 44 TB patients (22 with HIV coinfection) at the end of an intensive phase of anti-TB chemotherapy. Results: Compared with the control group, the concentrations of iron, zinc and selenium were significantly lower (Po0.05) while that of copper and copper/zinc ratio was significantly higher (Po0.05) in the serum of TB patients. TB patients with HIV coinfection had significantly lower serum zinc and selenium concentrations and significantly higher copper/zinc ratio compared to that in TB patients without HIV coinfection (Po0.05). The serum concentration of zinc had significantly increased at the end of intensive phase of anti-TB chemotherapy in patients without HIV coinfection (Po0.05). An increase in serum selenium level was observed in TB patients with or without HIV coinfection after therapy. On the contrary, serum copper concentration and copper/zinc ratio declined significantly after anti-TB chemotherapy irrespective of HIV serostatus (Po0.05). Conclusions:The results indicate that TB patients have altered profile of trace elements in their sera. This warrants the need for further investigations so that strategies for trace elements supplementation can be planned in addition to their potential as diagnostic parameters in monitoring responses to anti-TB chemotherapy.

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“…TNF-␣ regulates various lymphocyte functions, such as cell proliferation and IL-2R expression (19), and is critical for the progression of rheumatoid arthritis (20). The substantial role played by TNF-␣ during inflammation led to the development of different strategies to block its activity (21), although not all patients respond to these treatments, and they could be accompanied with severe side effects, such as the induction of tuberculosis (22). In this report, we examined the ability of LX and ATL to modulate extracellular signal-regulated kinase (ERK)-dependent TNF-␣ secretion from T cells.…”

mentioning

confidence: 99%

Aspirin-Triggered Lipoxin A4 and B4 Analogs Block Extracellular Signal-Regulated Kinase-Dependent TNF-α Secretion from Human T Cells

Ariel

Chiang

Arita

et al. 2003

The Journal of Immunology

170

117

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Lipoxins (LX) and their aspirin-triggered 15-epimer endogenous isoforms are endogenous anti-inflammatory and pro-resolution eicosanoids. In this study, we examined the impact of LX and aspirin-triggered LXA4-stable analogs (ATLa) on human T cell functions. 15-epi-16-(p-fluoro)phenoxy-LXA4 (ATLa1) blocked the secretion of TNF-α from human PBMC after stimulation by anti-CD3 Abs, with the IC50 value of ≈0.05 nM. A similar action was also exerted by the native aspirin-triggered 15-epi-LXA4, a new 15-epi-16-(p-trifluoro)phenoxy-LXA4 analog (ATLa2), as well as LXB4, and its analog 5-(R/S)-methyl-LXB4. The LXA4 receptor (ALX) is expressed in peripheral blood T cells and mediates the inhibition of TNF-α secretion from activated T cells by ATLa1. This action was accomplished by inhibition of the anti-CD3-induced activation of extracellular signal-regulated kinase, which is essential for TNF-α secretion from anti-CD3-activated T cells. These results demonstrate novel roles for LX and aspirin-triggered LX in the regulation of T cell-mediated responses relevant in inflammation and its resolution. Moreover, they provide potential counterregulatory signals in communication(s) between the innate and acquired immune systems.

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Pulmonary miliary tuberculosis in a patient with anti-TNF-alpha treatment

Cited by 66 publications

References 0 publications

Adenoviral delivery of IL-18 binding protein C ameliorates Collagen-Induced Arthritis in mice

Adenoviral delivery of IL-18 binding protein C ameliorates Collagen-Induced Arthritis in mice

Alterations in serum levels of trace elements in tuberculosis and HIV infections

Aspirin-Triggered Lipoxin A4 and B4 Analogs Block Extracellular Signal-Regulated Kinase-Dependent TNF-α Secretion from Human T Cells

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