Regular inhaled beta-agonist treatment in bronchial asthma

Sears, Malcolm R.; Taylor, D. Robin; Print, Cristin G.; Lake, D C; Li, Q Q; Flannery, Erin M.; Yates, D M; Lucas, Melissa; Herbison, Peter

doi:10.1016/0140-6736(90)93098-a

Cited by 1,021 publications

(406 citation statements)

References 26 publications

Supporting

Mentioning

366

Contrasting

Unclassified

Order By: Relevance

“…In addition, excessive ␤-agonist use has been associated with increased asthma mortality 22 and morbidity. 23 These associations with excess ␤-agonist use are not universally found, though, and it is not known whether tachyphylaxis per se is the basis of such observations.…”

Section: Pharmacogenetics Of ␤-Agonists In Asthmamentioning

confidence: 99%

“…23 An earlier report showed deterioration in asthma control with regularly scheduled fenoterol treatment compared with as-needed treatment. During treatment with regularly scheduled fenoterol, subjects who were homozygous for Arg16 had an increase in bronchial responsivewww.nature.com/tpj ness to methacholine compared with their responsiveness when they did not receive regular treatment.…”

Section: Pharmacogenetics Of ␤-Agonists In Asthmamentioning

confidence: 99%

See 1 more Smart Citation

The pharmacogenetics of asthma: a candidate gene approach

et al. 2001

View full text Add to dashboard Cite

Section: Pharmacogenetics Of ␤-Agonists In Asthmamentioning

confidence: 99%

Section: Pharmacogenetics Of ␤-Agonists In Asthmamentioning

confidence: 99%

The pharmacogenetics of asthma: a candidate gene approach

et al. 2001

View full text Add to dashboard Cite

“…18,19 The main causes for these possible effects have not been clarified yet and are still unknown, but have been related to inhaled drugs, especially via metered dose inhaler. 20 Worsening of asthma was not proved in recent studies.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of different doses of inhaled fenoterol on methacholine-induced bronchoconstriction in asthmatic children

et al. 1998

Sao Paulo Med. J.

View full text Add to dashboard Cite

Objective: To evaluate the protective effect of different doses of inhaled fenoterol (F) on bronchoconstriction induced by methacholine (M). Design: randomized double-blind study. Setting: Referrence center. Participants: 9 children (aged from 7 to 15 years old), with mild or moderate asthma and allergic to D. pteronyssinus. Intervention: On the first day, the M concentration necessary to induce a 20% fall in the forced expiratory volume in the first second (FEV 1 ; PC 20 FEV 1 ) was determined using closed circuit inhalation (De Vilbiss 646). On subsequent days, the children inhaled a dose of F (25 or 50 or 100 or 200 mg) through the same circuit and, after 15 minutes the FEV 1 was measured, becoming the basal value. Bronchoprovocation was then initiated using the concentration prior to the PC 20 FEV 1 of the first day and continuing until there was a 20% fall in the FEV 1 . This concentration was the "new" PC 20 FEV 1 . Results: F in a dose of 25 mg protected 2 of the 9 children, in a dose of 50 mg protected 4 of the 9 and in doses of 100 and 200 mg protected all children. We did not observe any relationship between the magnitude of the bronchodilation and bronchoprotection induced by the inhalation of F. Conclusions: Our results suggest that a dose of 100 mg of F is capable of inducing bronchoprotection in children with mild/moderate asthma. Uniterms: Asthma. Children. Bronchial hyperreactivity. Beta agonists. Fenoterol. Methacholine.

show abstract

“…Asthma mortality increased with this agents' release and decreased when it was taken off the market [9][10][11] . Additional data showed that increased numbers of prescriptions of this drug and other SABA's increased the risk of mortality implying either a cause and effect relationship or that increased SABA use was a marker of poor asthma control [12][13][14] . Subsequently, Sears and colleagues showed that asthma control was worse with regular use of fenoterol 12 and the NIH Asthma Clinical Research Network Trial (ACRN) BAGS reported that asthma control did not improve with regular compared to as needed symptomatic use of the SABA albuterol 15 .…”

Section: Introductionmentioning

confidence: 99%

“…Additional data showed that increased numbers of prescriptions of this drug and other SABA's increased the risk of mortality implying either a cause and effect relationship or that increased SABA use was a marker of poor asthma control [12][13][14] . Subsequently, Sears and colleagues showed that asthma control was worse with regular use of fenoterol 12 and the NIH Asthma Clinical Research Network Trial (ACRN) BAGS reported that asthma control did not improve with regular compared to as needed symptomatic use of the SABA albuterol 15 . Finally, two more recent studies have reported an increase for asthma related mortality (SNS) 16 and respiratory deaths primarily in patients receiving LABA mono-therapy (SMART Study) 17 .…”

Section: Introductionmentioning

confidence: 99%

Pharmacogenetics of the β2-Adrenergic Receptor Gene

Ortega

Hawkins

Peters

et al. 2007

Immunology and Allergy Clinics of North America

View full text Add to dashboard Cite

Asthma is a complex genetic disease with multiple genetic and environmental determinants contributing to the observed variability in response to common anti-asthma therapies. Asthma pharmacogenetic research has focused on multiple candidate genes including the β2-adrenergic receptor gene (ADRβ2) and its effect on individual responses to beta agonist therapy. At present, knowledge about the effects of ADRβ2 variation on therapeutic responses is evolving and should not alter current Asthma Guideline approaches consisting of the use of short acting beta agonists for as-needed symptom based therapy and the use of a regular long-acting beta agonist in combination with inhaled corticosteroid therapy for optimal control of asthma symptoms in those asthmatics who are not controlled on inhaled corticosteroid alone. This approach is based upon studies showing a consistent pharmacogenetic response to regular use of short acting beta agonists (SABA) and less consistent findings in studies evaluating long acting beta agonist (LABA). While emerging pharmacogenetic studies are provocative and should lead to functional approaches, conflicting data with responses to LABA therapy may be caused by factors that include small sample sizes of study populations and differences in experimental design that may limit the conclusions that may be drawn from these clinical trials at the present time.

show abstract

Regular inhaled beta-agonist treatment in bronchial asthma

Cited by 1,021 publications

References 26 publications

The pharmacogenetics of asthma: a candidate gene approach

The pharmacogenetics of asthma: a candidate gene approach

Protective effects of different doses of inhaled fenoterol on methacholine-induced bronchoconstriction in asthmatic children

Pharmacogenetics of the β2-Adrenergic Receptor Gene

Contact Info

Product

Resources

About