Predicting Response to Omalizumab, an Anti-IgE Antibody, in Patients With Allergic Asthma

Bousquet, Jean; Wenzel, Sally E.; Holgate, Stephen T.; Lumry, William R.; Freeman, P. R.; Fox, Howard

doi:10.1378/chest.125.4.1378

Cited by 254 publications

(164 citation statements)

References 14 publications

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“…19,38 Although the effectiveness of omalizumab was noted across many participant characteristics, participants who had been both sensitized and exposed to cockroach allergen had the greatest benefit (a 71.2% reduction in exacerbations); the combination of sensitization and exposure may therefore serve as a criterion to be applied in targeting its use for optimal effectiveness and cost benefits. [27][28][29] Another potential approach to the same goal would be to focus the use of omalizumab on preventing seasonal peaks in asthma exacerbations; this would require studies examining a short, seasonal course of treatment in those at highest risk.…”

Section: Discussionmentioning

confidence: 99%

Randomized Trial of Omalizumab (Anti-IgE) for Asthma in Inner-City Children

Busse¹,

Morgan²,

Gergen³

et al. 2012

Survey of Anesthesiology

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Section: Discussionmentioning

confidence: 99%

Randomized Trial of Omalizumab (Anti-IgE) for Asthma in Inner-City Children

Busse¹,

Morgan²,

Gergen³

et al. 2012

Survey of Anesthesiology

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“…eosinophils, T cells, mast cells) and structural cells (airway epithelial cells, smooth muscle cells, endothelial cells, fibroblasts) 1,2 . The inflammation causes an associated increase in airway responsiveness to various stimuli 3 . Bronchoconstriction, cough, mucus production and airway hyperreactivity are the main clinical manifestations of asthma and these features correlate well with the severity of the disease.…”

Section: Introductionmentioning

confidence: 99%

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Shirole¹,

Sutariya²,

Saraf³

2013

Int. J. Res. Ayurveda Pharm.

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The present investigation aimed to elucidate the probable mechanism of antiasthmatic action of Butea monosperma. Bioactive fractionations of methanolic extract of B. monosperma (MBM) were carried out to get, ethyl acetate fraction (EBM) and butanolic fraction (BBM) of Butea monosperma. All fractions were evaluated mechanistically for its antiasthmatic actions in vitro using lipoxygenase assay. The lipoxygenase inhibitory effect of the extract followed the order BBM > MBM > EBM. Based on in vitro lipoxygenase assay BBM was selected for in vitro compound 48/80 induced mast cell degranulation assay and in vivo lipopolysaccharide induced inflammation in rats. BBM 50, 100 and 200μg/ml inhibited compound 48/80 induced mast cell degranulation. BBM exhibited dose dependent (50, 100 and 200mg/kg i.p.) inhibition of lipopolysaccharide-induced increased in total cell count, differential leukocyte count, nitrate-nitrite, total protein and albumin levels in bronchoalveolar fluid (BALF) and myeloperoxidase (MPO) levels in lungs homogenate.

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“…Several studies have tried to identify clinical or laboratory characteristics that predict a good therapeutic response to omalizumab. In a pooled analysis of two randomised placebo-controlled trials, factors indicative of more severe asthma (history of emergency treatment, low FEV 1 and high-dose ICS) were predictive of a greater relative response to add-on omalizumab (24,41). It is noteworthy that in one study the baseline total IgE could be a predictor of response (42).…”

Section: Recognising the Respondersmentioning

confidence: 96%

Severe Asthma: Anti-IgE or Anti-IL-5?

Bakakos¹,

Loukides²

2015

J Allergy Ther

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Severe asthma is a discrete clinical entity characterised by recurrent exacerbations, reduced quality of life and poor asthma control as ordinary treatment regimens remain inadequate. Difficulty in managing severe asthma derives partly from the multiple existing phenotypes and our inability to recognise them. Though the exact pathogenetic pathway of severe allergic asthma remains unclear, it is known that numerous inflammatory cells and cytokines are involved, and eosinophils represent a key inflammatory cell mediator. Anti-IgE (omalizumab) and anti-IL-5 (mepolizumab) antibodies are biological agents that interfere in different steps of the Th2 inflammatory cascade and are licensed in severe asthma. Both exhibit a favourable clinical outcome as they reduce exacerbation rate and improve asthma control and quality of life, while mepolizumab also induces an oral steroid sparing effect. Nevertheless, it is still questionable which agent is more suitable in the management of severe allergic asthma since no comparable studies have been conducted. Omalizumab's established effectiveness in clinical practice over a long period is complemented by a beneficial effect on airway remodelling process mediated mainly through its impact on eosinophils and other parameters strongly related to eosinophilic inflammation. However, it is possible that mepolizumab through nearly depleting eosinophils could have a similar effect on airway remodelling. Moreover, to date, markers indicative of the patient population responding to each treatment are unavailable although baseline eosinophils and exacerbation rate in the previous year demonstrate a predictive value regarding anti-IL-5 therapy effectiveness. On the other hand, a better therapeutic response for omalizumab has been observed when low forced expiratory volume in 1 sec, high-dose inhaled corticosteroids and increased IgE concentrations are present. Consequently, conclusions are not yet safe to be drawn based on existing knowledge, and additional research is necessary to unravel the remaining issues for the severe asthmatic population.

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Predicting Response to Omalizumab, an Anti-IgE Antibody, in Patients With Allergic Asthma

Cited by 254 publications

References 14 publications

Randomized Trial of Omalizumab (Anti-IgE) for Asthma in Inner-City Children

Randomized Trial of Omalizumab (Anti-IgE) for Asthma in Inner-City Children

Mechanistic Evaluation of Butea Monosperma Using in Vitro and in Vivo Murine Models of Bronchial Asthma

Severe Asthma: Anti-IgE or Anti-IL-5?

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