***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND AND OBJECTIVE There seems to be a strong causal relationship between allergy and the origins of asthma . Susceptibility to both is determined by a combination of genetics and environment acting through a complex network of cytokines . Nearly 90 % of affected children have positive skin tests indicating the presence of specific immunoglobulin E ( IgE ) , with sensitivity to house dust mite , Alternaria , cockroach , cat , and dog most closely linked to the disease . Greater exposure to house dust mite during infancy leads to earlier onset of wheezing , and elevated serum IgE levels correlate with the appearance of asthma symptoms . Specific IgE binds to high-affinity ( FcepsilonRI ) receptors on mast cells and basophils . The IgE-mediated reactions that follow exposure of sensitized mast cells to an allergen are design ated early- and late-phase asthmatic responses ( EAR and LAR ) . EAR is characterized by release of histamine and other preformed mediators within 1 hour of allergen exposure . It is often followed by LAR , an infiltration of the airways by inflammatory cells associated with an episode of more prolonged , and usually more severe airflow obstruction , 4 to 8 hours after antigen exposure . Chronic airway symptoms result from persistent LAR caused by continuous allergen exposure . IgE antibodies are capable of passive transfer of both EAR and LAR sensitivity . IgE-mediated mast cell activation contributes to chronic tissue eosinophilia and airway remodeling , with permanent loss in pulmonary function .  Omalizumab ( rhuMAb-E25 ) is a recombinant , humanized , monoclonal anti-IgE antibody of mouse origin developed for the treatment of IgE-mediated diseases . Omalizumab binds to free IgE at the same site as the high-affinity receptor . Although it attaches to free IgE , it does not bind to IgA , IgG , or cell-bound IgE. It therefore does not induce cross-linking of cell-bound IgE , which would lead to the release of allergic mediators . It has been reported to decrease serum IgE levels in a dose-dependent manner , inhibit EAR and LAR , and cause a down-regulation of FcepsilonRI receptors on basophils . Omalizumab has been reported to be safe and effective in improving asthma control and reducing the requirement for oral and inhaled corticosteroids . This double-blind , r and omized , placebo-controlled study evaluated the safety , steroid-sparing effects , and impact on disease exacerbations of omalizumab in the treatment of childhood asthma . Methods . Participants were 334 males and premenarchal females aged 6 to 12 years , with moderate to severe allergic asthma requiring treatment with inhaled corticosteroids .  During a run-in phase , all children were switched to equivalent doses of beclomethasone dipropionate ( BDP ) , and the dose was adjusted to assure maintenance of asthma control achieved with previous corticosteroid treatment . Children were r and omized to subcutaneously administered placebo ( N = 109 ) or omalizumab ( N = 225 ) at a dose based on body weight and initial serum IgE ( 0.016 mg/kg/IgE [ IU/mL ] per 4 weeks ) . BDP dose ( initial range 168 - 420 microg/d ) was kept stable for 16 weeks ( stable-steroid phase ) , reduced over 8 weeks to the minimum effective dose ( steroid-reduction phase ) , and maintained constant for the final 4 weeks . RESULTS More participants in the omalizumab group decreased their BDP dose , and their reduction was greater than that of the placebo group ( median reduction 100 % vs 66.7 % ) . BDP was withdrawn completely in 55 % of the omalizumab group versus 39 % of the placebo group . The incidence and the frequency of asthma exacerbations requiring treatment with doubling of BDP dose or systemic corticosteroids were lower in the omalizumab group . The treatment differences were statistically significant during the steroid-reduction phase , during which fewer participants in the omalizumab group had asthma exacerbation episodes ( 18.2 % vs 38.5 % ) , and the mean number of episodes per patient was smaller than with placebo ( 0.42 vs 2.72 ) . Five asthma exacerbations requiring hospitalization all occurred in the placebo group . Participants ' and investigators ' global evaluations of treatment effectiveness were more favorable for omalizumab than placebo .  Investigators rated effectiveness excellent for 31.5 % of the omalizumab group versus 16.3 % of the placebo group and good for 44.7 % of the omalizumab group versus 32.7 % of the placebo group . There was little change in asthma symptom scores or spirometry measurements during either the stable-steroid or steroid dose-reduction phase , with minimal differences between the treatment groups . The requirement for rescue medication in the omalizumab group during both the stable-steroid and steroid dose-reduction phases was consistently lower than at baseline . At week 28 , the median number of puffs of rescue medication taken daily was 0 in the omalizumab group and 0.46 in the placebo group . The change from baseline was significant in favor of omalizumab . ( ABSTRACT TRUNCATED OBJECTIVE To evaluate the long-term effects of the anti-IgE antibody omalizumab in children with asthma . METHODS This was a 28-week , double-blind , r and omized , placebo-controlled trial with a 24-week open-label extension . In the core trial 225 children ( ages 6 to 12 years ) with moderate-to-severe allergic asthma requiring inhaled beclomethasone dipropionate ( BDP ) received omalizumab every 2 or 4 weeks , and 109 received placebo .  BDP dosage was stable for weeks 1 to 16 , then reduced during weeks 17 to 24 using strict safety criteria . The lowest dose for optimal asthma control was maintained for 4 more weeks . During the 24-week extension , all patients ( n = 309 ) received open-label omalizumab in addition to other asthma medications . One-year safety data were analyzed . RESULTS The incidence of adverse events in patients treated with omalizumab for 52 weeks was similar to those treated for 28 weeks in the core trial , which was generally comparable with placebo . In the 52-week omalizumab group , upper respiratory tract infection and headache were the most frequently reported adverse events ( 47.1 % and 42.7 % , respectively ) . Eleven patients ( 4.9 % ) reported urticaria , which resolved spontaneously or with antihistamine , except for 1 patient who was discontinued because of severe urticaria . No anaphylactic reactions or adverse events suggestive of serum sickness or immune complex formation occurred . No anti-omalizumab antibodies were detected in any of the children . There is no evidence that new or more serious adverse events occur with long-term omalizumab treatment . CONCLUSIONS Long-term treatment with omalizumab is safe and well tolerated in children with allergic asthma Background : Omalizumab has been shown to suppress responses to inhaled allergens in allergic asthma patients with pretreatment immunoglobulin E ( IgE ) ≤700 IU/ml . To extend current dosing tables , we evaluated the potential of high omalizumab doses to block allergen-induced bronchoconstriction in patients with higher IgE levels . Methods : Asthmatic adults ( 18–65 years ; body weight 40–150 kg ) were divided into groups according to screening IgE ( group 1 : 30–300 IU/ml ; group 2 : 700–2,000 IU/ml ) and r and omized 2:1 to omalizumab/placebo every 2 or 4 weeks for 12–14 weeks . Allergen bronchoprovocation ( ABP ) testing was performed before treatment and at weeks 8 and 16 . The primary efficacy endpoint , the early-phase allergic response ( EAR ) , was defined as the maximum percentage drop in forced expiratory volume in 1 s during the first 30 min after ABP . Serum free IgE was determined as a pharmacodynamic endpoint , and the exhaled fractional concentration of nitric oxide ( FENO ) was an exploratory endpoint . Results : Fifty patients were included in the study . Omalizumab  improved EAR ; at week 8 , EAR was 23.1 % for placebo , 9.3 % in group 1 ( p = 0.018 versus placebo ) and 5.6 % in group 2 ( p < 0.001 ) . At week 16 , EAR was 20 % , 11.8 % ( p = 0.087 ) and 5.1 % ( p < 0.001 ) , respectively . Free IgE decreased in groups 1 and 2 and remained < 50 ng/ml in all patients during weeks 6–16  . Omalizumab  completely suppressed FENO increases after ABP in both groups . Conclusions : Omalizumab blocked early asthmatic responses over a broad range of IgE/body weight combinations . Extending the dosing tables enables omalizumab to benefit a wider range of patients BACKGROUND In a 1-year , r and omized , open-label study in patients with moderate-to-severe allergic ( immunoglobulin E (IgE)-mediated ) asthma , adding omalizumab to best st and ard care ( BSC ) significantly improved efficacy outcomes compared with BSC alone ( control ) . We assessed the efficacy of omalizumab in the subgroup of patients with inadequately controlled severe persistent allergic asthma despite high-dose inhaled corticosteroids ( ICS ) plus a long-acting beta(2)-agonist ( LABA ) , which reflects the European Union ( EU ) label population . METHODS Efficacy outcomes included annual asthma exacerbation rate , annual asthma deterioration-related incident ( ADRI ) rate , % predicted forced expiratory volume in 1 s ( FEV(1 ) ) , asthma symptoms ( Wasserfallen score ) and quality of life ( Mini Asthma Quality of Life Question naire ( Mini-AQLQ ) ) , which were compared in the omalizumab and control groups . Outcomes were also determined for omalizumab-treated patients judged to have responded to therapy ( > or = 0.5-point improvement in Mini-AQLQ overall score at 27 weeks ) . RESULTS In total , 164 patients ( omalizumab , n=115 ; control , n=49 ) were receiving high-dose ICS plus a LABA .  Annual asthma exacerbation rate was significantly reduced by 59 % in the omalizumab group vs. control ( 1.26 vs. 3.06 ; P<0.001 ) . ADRI rate was significantly reduced by 40 % in the omalizumab group compared with control ( 5.61 vs. 9.40 ; P<0.05 ) . Significant improvements were also seen in % predicted FEV(1 ) ( 71 % vs. 60 % ; P<0.001 ) , change from baseline in asthma symptom scores ( -6.7 vs. 0.5 ; P<0.05 ) and Mini-AQLQ overall score ( 1.32 vs. 0.17 ; P<0.001 ) . In omalizumab-treated patients , 71/102 ( 70 % ) were judged to have responded to therapy . In these Mini-AQLQ-assessed responders , exacerbation rate was reduced by 64 % vs. control ( 1.12 vs. 3.06 ; P<0.001 ) , ADRI rate was reduced by 50 % vs. control ( 4.71 vs. 9.40 ; P<0.01 ) . Percent predicted FEV(1 ) ( 73 % vs. 60 % ; P<0.001 ) , change from baseline in asthma symptom scores ( -8.1 vs. 0.5 ; P<0.001 ) and Mini-AQLQ overall score ( 1.81 vs. 0.17 ; P<0.001 ) were also further significantly improved vs. control . CONCLUSIONS Adding omalizumab to BSC is efficacious in patients with inadequately controlled severe persistent allergic asthma despite high-dose ICS plus a LABA ( EU label population ) , with further efficacy observed in patients judged to have responded to therapy which may more accurately illustrate the actual benefit of omalizumab therapy in clinical practice . The naturalistic setting of this study confirms the benefits observed in double-blind r and omized clinical trials Background : Omalizumab may inhibit allergic inflammation and could contribute to decreasing airway remodeling in patients with asthma . Objective : The aim of this study was to assess the effects of omalizumab on airway wall thickness using computed tomography ( CT ) . Methods : Thirty patients with severe persistent asthma were r and omized to conventional therapy with ( n = 14 ) or without omalizumab ( n = 16 ) for 16 weeks . The following airway dimensions were assessed by a vali date d CT technique : airway wall area corrected for body surface area ( WA/BSA ) , percentage wall area ( WA% ) , wall thickness (T)/√BSA , and luminal area (Ai)/BSA at the right apical 
    Output:
    
Omalizumab was associated with significant improvements in quality of life and the Global Evaluation of Treatment Effectiveness .
Omalizumab also allowed patients to completely withdraw from inhaled corticosteroid therapy and did not increase the overall incidence of adverse events .
Our data indicated that omalizumab use for at least 52 weeks in patients with persistent uncontrolled allergic asthma was accompanied by an acceptable safety profile , but it lacked effect on the asthma exacerbations .
Use of omalizumab was associated with a higher cost than conventional therapy , but these increases may be cost-effective if the medication is used in patients with severe allergic asthma