Adverse Effects of Nonsystemic Steroids (Inhaled, Intranasal, and Cutaneous): a Review of the Literature and Suggested Monitoring Tool

Gupta, Ratika; Fonacier, Luz

doi:10.1007/s11882-016-0620-y

Cited by 36 publications

(27 citation statements)

References 48 publications

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“…Systemic adverse effects such as growth suppression and local effects including oropharyngeal candidiasis are well recognised in association with ICS [4][5][6][7]. With recent pragmatic studies showing greater adherence to, and effectiveness of, LTRA compared to ICS [8][9][10], the prospect of increased adherence resulting in better asthma control has renewed interest in the use of LTRA as monotherapy or adjunct therapy.…”

Section: Introductionmentioning

confidence: 99%

Neuropsychiatric adverse drug reactions in children initiated on montelukast in real-life practice

et al. 2017

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@ERSpublicationsThe incidence of children on montelukast with drug cessation due to neuropsychiatric adverse events was >10% http://ow.ly/nCGG30bgjpd ABSTRACT Although montelukast is generally well tolerated, postmarketing studies have reported serious neuropsychiatric adverse drug reactions (ADRs) leading to a United States Food and Drug Administration black box warning. The objective of this study was to determine the incidence of neuropsychiatric ADRs leading to discontinuation of montelukast in asthmatic children.We conducted a retrospective cohort study in children aged 1-17 years initiated on montelukast. In a nested cohort study, children initiated on montelukast as monotherapy or adjunct therapy to inhaled corticosteroids (ICS) were matched to those initiated on ICS monotherapy. A non-leading parental interview served to ascertain the occurrence of any ADRs with any asthma medication, and circumstances related to, and evolution of, the event.Out of the 106 participants who initiated montelukast, most were male (58%), Caucasian (62%) with a median (interquartile range) age of 5 (3-8) years. The incidence (95% CI) of drug cessation due to neuropsychiatric ADRs was 16 (10-26)%, mostly occurring within 2 weeks. Most frequent ADRs were irritability, aggressiveness and sleep disturbances. The relative risk of neuropsychiatric ADRs associated with montelukast versus ICS was 12 (2-90).In the real-life setting, asthmatic children initiated on montelukast experienced a notable risk of neuropsychiatric ADRs leading to drug cessation, that is significantly higher than that associated with ICS.

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Section: Introductionmentioning

confidence: 99%

Neuropsychiatric adverse drug reactions in children initiated on montelukast in real-life practice

et al. 2017

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“…Anti‐inflammatory medications usually inhibit mast cell degranulation indirectly by modulating T‐cell activation and have an indirect effect on mast cell inhibition . Omalizumab is an anti‐IgE monoclonal antibody that binds free IgE in the serum and prevents IgE binding to the FcεRI.…”

Section: Discussionmentioning

confidence: 99%

Modulation of allergic responses by mitochondrial STAT3 inhibitors

Erlich

Sharkia

Landolina

et al. 2018

Allergy

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“…While current therapies such as anti-histamines and leukotriene antagonists reduce mast cell-mediated inflammation, these target a select few mediators and do not prevent mast cell activation. Additionally, immunosuppressive medications, such as steroids or mast cell stabilizers, have limited efficacy in a few populations and many side effects [13–14]. Novel therapeutic approaches targeting mast cell activation are needed to better treat allergic disease.…”

Section: Introductionmentioning

confidence: 99%

Didox (3,4-dihydroxybenzohydroxamic acid) suppresses IL-33-induced cytokine production in primary mouse mast cells

Caslin

McLeod

Spence

et al. 2017

Cellular Immunology

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While IgE is considered the primary mediator of mast cell activation, IL-33 contributes substantially in asthma, allergic rhinitis, and atopic dermatitis. To develop effective treatments for allergic disease, it is important to understand the role of therapeutic agents on IL-33 activation. We examined the effect of Didox (3,4-dihydroxybenzohydroxamic acid), an antioxidant and ribonucleotide reductase (RNR) inhibitor, on IL-33-mediated mast cell activation. Didox suppressed IL-6, IL-13, TNF, and MIP-1α (CCL3) production in bone marrow derived mast cells following IL-33 activation. This suppression was observed in different genetic backgrounds and extended to peritoneal mast cells. The antioxidant N-acetylcysteine mimicked the suppression of Didox, albeit at a much higher dose, while the RNR inhibitor hydroxyurea had no effect. Didox substantially suppressed IL-33-mediated NFκB and AP-1 transcriptional activities. These results suggest that Didox attenuates IL-33-induced mast cell activation and should be further studied as a potential therapeutic agent for inflammatory diseases involving IL-33.

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Adverse Effects of Nonsystemic Steroids (Inhaled, Intranasal, and Cutaneous): a Review of the Literature and Suggested Monitoring Tool

Cited by 36 publications

References 48 publications

Neuropsychiatric adverse drug reactions in children initiated on montelukast in real-life practice

Neuropsychiatric adverse drug reactions in children initiated on montelukast in real-life practice

Modulation of allergic responses by mitochondrial STAT3 inhibitors

Didox (3,4-dihydroxybenzohydroxamic acid) suppresses IL-33-induced cytokine production in primary mouse mast cells

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