β2-Adrenergic receptor Gly16Arg polymorphism and impaired asthma control in corticosteroid-treated asthmatic adults

Manoharan, Arvind; Griffin, Benjamin R.; Lipworth, Joseph; Berg, Jonathan; Andrew, Nicola; Jackson, Catherine; Lipworth, Brian J.

doi:10.1016/j.anai.2015.01.017

Cited by 4 publications

(3 citation statements)

References 10 publications

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“…The proportion of phenotypic variability accounted for by genetic variation (heritability) is estimated to be 28.5% for bronchodilator responsiveness and 50% for lung function 221 . For example, the Arg16 allele of the gene encoding the β 2 -adrenergic receptor has been shown to associate with worsening of asthma when children with the disease receive continuous SABA or LABA monotherapy 222,223 . This and other variants of the β 2 -adrenergic receptor have different effects on the disease in different ethnic populations 224 .…”

Section: Box 1 | Asthma Triggersmentioning

confidence: 99%

Asthma

Holgate

Wenzel

Postma

et al. 2015

Nat Rev Dis Primers

498

408

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Asthma is the most common inflammatory disease of the lungs. The prevalence of asthma is increasing in many parts of the world that have adopted aspects of the Western lifestyle, and the disease poses a substantial global health and economic burden. Asthma involves both the large-conducting and the small-conducting airways, and is characterized by a combination of inflammation and structural remodelling that might begin in utero. Disease progression occurs in the context of a developmental background in which the postnatal acquisition of asthma is strongly linked with allergic sensitization. Most asthma cases follow a variable course, involving viral-induced wheezing and allergen sensitization, that is associated with various underlying mechanisms (or endotypes) that can differ between individuals. Each set of endotypes, in turn, produces specific asthma characteristics that evolve across the lifecourse of the patient. Strong genetic and environmental drivers of asthma interconnect through novel epigenetic mechanisms that operate prenatally and throughout childhood. Asthma can spontaneously remit or begin de novo in adulthood, and the factors that lead to the emergence and regression of asthma, irrespective of age, are poorly understood. Nonetheless, there is mounting evidence that supports a primary role for structural changes in the airways with asthma acquisition, on which altered innate immune mechanisms and microbiota interactions are superimposed. On the basis of the identification of new causative pathways, the subphenotyping of asthma across the lifecourse of patients is paving the way for more-personalized and precise pathway-specific approaches for the prevention and treatment of asthma, creating the real possibility of total prevention and cure for this chronic inflammatory disease.

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Section: Box 1 | Asthma Triggersmentioning

confidence: 99%

Asthma

Holgate

Wenzel

Postma

et al. 2015

Nat Rev Dis Primers

498

408

View full text Add to dashboard Cite

show abstract

“…The proportion of phenotypic variability accounted for genetic variation (heritability) is estimated to be 28.5% for bronchodilator responsiveness and 50% for lung function (Lima, 2014). For example, the Arg16 allele of the gene encoding the β2-adrenergic receptor has been shown to associate with worsening of asthma when adult with the disease receive continuous SABA or LABA monotherapy (Manoharan et al, 2015). This and other variants of the β2-adrenergic receptor have different effects on the disease in different ethnic populations (Ortega et al, 2014).…”

Section: Alternative Therapeutic Approachesmentioning

confidence: 99%

Recent trends in management of bronchial asthma

goda

Sileem

El-Nahas

et al. 2021

Zagazig Journal of Pharmaceutical Sciences

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Bronchial Asthma is the most common chronic inflammatory disease of lungs. The prevalence of asthma is increasing worldwide, and the disease possesses a substantial global health and economic burden. Asthma involves both the large and the small-conducting airways, and is characterized by a combination of inflammation and structural remodeling. Disease progression occurs in the context of a developmental background in which the postnatal acquisition of asthma is strongly linked with allergic sensitization. Most asthma cases follow a variable course, involving viral-induced wheezing and allergen sensitization, that is associated with various underlying mechanisms (or endotypes) that can differ between individuals. Each set of endotypes, in turn, produces specific asthma characteristics that evolve across the life course of the patient. Strong genetic and environmental drivers of asthma interconnect through novel epigenetic mechanisms that operate prenatally and throughout childhood. Asthma can spontaneously remit or begin de novo in adulthood, and the factors that lead to the emergence and regression of asthma, irrespective of age, are poorly understood. Nonetheless, there is mounting evidence that supports a primary role for structural changes in the airways with asthma acquisition, on which altered innate immune mechanisms and microbiota interactions are superimposed. On the basis of the identification of new causative pathways, the sub-phenotyping of asthma across the life course of patients is paving the way for more-personalized and precise pathway-specific approaches for the prevention and treatment of asthma, creating the real possibility of total prevention and cure for this chronic inflammatory disease.

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“…While these drugs do cause relief of symptoms, there are a substantial proportion of patients who continue to exhibit persistent symptoms inspite of being on these medication at maximal doses. 7 Leukotriene antagonists have been a suitable choice only in those with mild persistent asthma and exercise induced asthma. Omalizumab, the first ever monoclonal antibody for asthma, is associated with anaphylactic reactions and neoplasms have occurred in clinical trials.…”

Section: Introductionmentioning

confidence: 99%