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1                                              LABA step-up was significantly more likely to provide th
2 ICS mean daily = 0.78, 0.76-0.79, p < 0.001; LABA = 0.83, 0.82-0.85, p < 0.001; other add-on = 0.86,
3 ICS mean daily = 0.80, 0.74-0.87, p < 0.001; LABA = 1.01, 0.92-1.11, p = 0.87, other add-on = 1.00, 0
4 tiotropium monotherapy initiators and 19 530 LABA-ICS initiators, the mean (SD) age was 75.1 (6.7) ye
5        97.1% used ICS (dose 2000 BDP), 93.6% LABA in association with ICS, 53.3% LTRAs, 64.1% anti-Ig
6 dults with asthma treated with ICS, adding a LABA did not improve time to asthma exacerbation compare
7 vides mechanistic insight as to how adding a LABA to an inhaled corticosteroid may improve clinical o
8 of therapy, which included the addition of a LABA (salmeterol) to an inhaled glucocorticoid (fluticas
9                                 The use of a LABA but not an LTRA as an "add-on controller" is associ
10  were established as follows: (1) users of a LABA plus low-dose ICS combination or users of a medium-
11  the other subcohort included 198 users of a LABA plus medium-dose ICS and 156 users of a high-dose I
12 sers of a medium-dose ICS and (2) users of a LABA plus medium-dose ICS combination or users of a high
13 had a superior response to the addition of a LABA.
14 alformations in asthmatic women exposed to a LABA plus ICS combination and those exposed to ICS monot
15 ne subcohort there were 643 women who used a LABA plus low-dose ICS and 305 who used a medium-dose IC
16 lformations was 1.1 (95% CI, 0.6-1.9) when a LABA plus low-dose ICS was used compared with a medium-d
17 um-dose ICS and 1.2 (95% CI, 0.5-2.7) when a LABA plus medium-dose ICS was used compared with a high-
18 orticosteroid alone or in combination with a LABA alters protein and gene expression pathways associa
19 sk of major malformations was similar with a LABA plus ICS combination and ICS monotherapy at higher
20                 The role of treatment with a LABA-LAMA regimen in these patients is unclear.
21 enotype-guided treatment consisted of adding LABA for children with ADRB2 Gly16/Gly16, whilst childre
22 roate (FF) and long-acting beta(2) -agonist (LABA) vilanterol (VI) on early and late asthmatic respon
23 -up therapy) or long-acting beta(2)-agonist (LABA step-up therapy).
24 at incorporated long-acting beta(2)-agonist (LABA) inhalers were included.
25 nclude adding a long-acting beta(2)-agonist (LABA) or increasing the ICS dose.
26 e effect of ICS/long-acting beta(2)-agonist (LABA) treatment on both lung function measures of hyperi
27  for the use of long-acting beta(2)-agonist (LABA)/long-acting muscarinic antagonist (LAMA) combinati
28 )/long-acting beta (2)-adrenoceptor agonist (LABA) combination therapy should be a first-in-line trea
29 ICS)/long-acting B (2)-adrenoceptor agonist (LABA) combination therapy should be a first-in-line trea
30 l, a long-acting B (2)-adrenoceptor agonist (LABA), enhanced the expression of inflammatory genes, an
31 a long-acting beta (2)-adrenoceptor agonist (LABA), enhanced the expression of inflammatory genes, an
32 ng a long-acting beta2-adrenoceptor agonist (LABA)/ICS combination therapy, we tested the hypothesis
33 utic doses of long acting beta(2)AR agonist (LABA; clenbuterol; CLEN) and/or GR agonist (dexamethason
34 nts associated with longacting beta agonist (LABA) use have caused the US Food and Drug Administratio
35 osteroid (ICS) and long-acting beta-agonist (LABA) administered in a randomized crossover fashion.
36 16 amino acid) and long-acting beta-agonist (LABA) exposure for asthma exacerbations in children.
37 recommend either a long-acting beta-agonist (LABA) plus an inhaled glucocorticoid or a long-acting mu
38 from addition of a long-acting beta-agonist (LABA) than from increased glucocorticoids; however, thes
39                    Long-acting beta-agonist (LABA) therapy improves symptoms in patients whose asthma
40 ticosteroid (ICS)/long-acting beta2-agonist (LABA) therapy in patients with chronic obstructive pulmo
41 -acting beta(2)-adrenergic receptor agonist (LABA) is well documented.
42 g-acting beta2 -adrenergic receptor agonist (LABA) on GCM in the bronchial epithelium are unknown.
43 =600 mug/day], and long-acting beta-agonist [LABA] use [yes/no]).
44 dd-on medication (long-acting beta2-agonist [LABA], leukotriene receptor antagonist [LTRA], theophyll
45 ren treated with long-acting B(2) -agonists (LABA).
46 d long-acting beta2-adrenoreceptor agonists (LABA), are the mainstay of pharmacological treatment of
47 d montelukast and long-acting beta-agonists (LABA).
48                  Long-acting beta2-agonists (LABA) and leukotriene receptor antagonists (LTRA) are tw
49                  Long-acting beta2-agonists (LABA) in combination with inhaled corticosteroids (ICS)
50                  Long-acting beta2-agonists (LABA) were shown to inhibit LPS-induced bronchial inflam
51 oids (ICS) and long-acting beta(2)-agonists (LABAs) are frequently exposed to oral corticosteroids an
52 oids (ICS) and long-acting beta(2)-agonists (LABAs) are recommended in patients with asthma that is n
53 adding inhaled long-acting beta(2)-agonists (LABAs) to corticosteroids in asthma.
54 ns of long-acting beta2-adrenergic agonists (LABAs) and long-acting muscarinic antagonists (LAMAs) pr
55  by long-acting beta2-adrenoceptor agonists (LABAs) and may contribute to the clinical superiority of
56 , long-acting beta(2)-adrenoceptor agonists (LABAs) given twice daily cause the same degree of bronch
57  long-acting beta (2)-adrenoceptor agonists (LABAs) salmeterol, indacaterol, and formoterol.
58 osteroids (ICS) and long-acting B2-agonists (LABAs) for moderate to severe asthma remain unclear.
59 luded 2 trials of long-acting beta-agonists (LABAs) (n = 3174), 1 RCT of LABAs and inhaled corticoste
60 ppropriate use of long-acting beta-agonists (LABAs) for the treatment of asthma has been widely debat
61 rround the use of long-acting beta-agonists (LABAs) for the treatment of asthma, even in combination
62 acy and safety of long-acting beta-agonists (LABAs) have been questioned.
63                   Long-acting beta-agonists (LABAs) have been shown to increase the risk of asthma-re
64 nists (LAMAs) and long-acting beta-agonists (LABAs) over inhalers containing inhaled corticosteroids
65 o the addition of long-acting beta-agonists (LABAs) to ICSs.
66 cocorticoids plus long-acting beta-agonists (LABAs) to receive subcutaneous itepekimab (at a dose of
67 rapy with/without long-acting beta-agonists (LABAs).
68 atment response to longacting beta-agonists (LABAs).
69 cocorticoids plus long-acting beta-agonists (LABAs).
70 ucocorticoids and long-acting beta-agonists (LABAs).
71 led therapy with long-acting beta2 agonists (LABAs) and corticosteroids is beneficial in treating ast
72  associated with long-acting beta2-agonists (LABAs) have led to many US Food and Drug Administration
73 g-acting beta2-adrenergic receptor agonists (LABAs).
74 substitute the combination of an LTRA and an LABA for the combination of inhaled corticosteroid and a
75 combination of inhaled corticosteroid and an LABA.
76             In subjects treated with ICS and LABA (n = 832, age: 3-21 years), Arg16/Gln27 versus Gly1
77 adequately controlled with high-dose ICS and LABA therapy.
78 ay be a synergistic benefit between LAMA and LABA as a consequence of receptor cross-talk, which in t
79 es were observed between the montelukast and LABA patients when analyzing the risk of specific neurop
80 ta(2)-adrenergic receptor agonists (SABA and LABA, respectively) relieve asthma symptoms, use of eith
81 inflammatory cytokines, corticosteroids, and LABAs affect ASM structure and function, with particular
82  levels who used inhaled glucocorticoids and LABAs, dupilumab therapy, as compared with placebo, was
83 spite the use of inhaled glucocorticoids and LABAs, the addition of tiotropium significantly increase
84 o were receiving inhaled glucocorticoids and LABAs, we compared the effect on lung function and exace
85 ontaining inhaled corticosteroids (ICSs) and LABAs.
86 agonists /long-acting muscarinic antagonist, LABA/LAMA) represented the least common medication regim
87                           Among the approved LABA, indacaterol has a 24 h duration of action, whereas
88                                   In asthma, LABAs enhance glucocorticoid receptor (GR) nuclear trans
89 oflumilast, including its ability to augment LABA-induced gene expression changes, may contribute to
90                             However, because LABAs are given twice daily but tiotropium bromide is re
91              There was no difference between LABA + ICS vs tiotropium + ICS in time to first exacerba
92 erlie the complementary interactions between LABAs and corticosteroids, although the precise signal t
93 d long-acting B2 adrenergic bronchodilators (LABA).
94 ong-acting beta2 adrenergic bronchodilators (LABA).
95 ations may be disproportionately affected by LABA risks.
96 gulation and associated tolerance induced by LABA.
97   The elements of asthma control achieved by LABAs (improved lung function) and leukotriene receptor
98 the superior clinical effects of combination LABA/corticosteroid treatment compared with either as mo
99                 Newly prescribed combination LABAs and inhaled corticosteroids or LABAs alone.
100 g beta2-agonist plus inhaled corticosteroid (LABA-ICS) who were 66 years or older with COPD and witho
101                               New once-daily LABA, including vilanterol, olodaterol, milveterol, carm
102 ce-daily tiotropium (n = 532) or twice-daily LABAs (n = 538,) and were followed up for up to 18 month
103 g of a long-acting beta-agonist twice daily (LABA step-up), or 100 microg of fluticasone twice daily
104 h an increased risk of exacerbations despite LABA treatment.
105 l leukotriene inflammation can differentiate LABA step-up responses from responses to LTRA or ICS ste
106      Patients were instructed to discontinue LABAs at week 4 and to taper and discontinue inhaled glu
107 Effect on Exacerbations in Patients on Dual [LABA/ICS] Therapy) trial (NCT01443845), participants age
108 ns are associated with adverse events during LABA therapy and should be evaluated in large clinical t
109 ave uncontrolled, persistent symptoms during LABA treatment (p=0.008-0.04).
110             Stepping down medication, either LABAs or ICSs, could save annually around pound 17,000,0
111 with a differential FEV(1) response favoring LABA over ICS step-up therapy, whereas higher urinary le
112 hs (change in score from baseline, -0.68 for LABA + ICS vs -0.72 for tiotropium + ICS; between-group
113  in change in FEV1 at 12 months (0.003 L for LABA + ICS vs -0.018 L for tiotropium + ICS; between-gro
114 inhaler of budesonide (ICS) with formoterol (LABA) was effective to reduce these symptoms.
115 trolled Patients on Medium Strength of ICS + LABA [TRIMARAN] and Triple in Asthma High Strength Versu
116  superiority of inhaled corticosteroid (ICS)/LABA combinations in asthma and chronic obstructive pulm
117 e therapy with inhaled corticosteroids (ICS)/LABA/LAMA over dual therapy with LABA/LAMA in patients w
118                                          ICS+LABA therapy seems to be more effective than ICS+LTRA th
119 icantly modified the effect of high-dose ICS+LABA therapy on lung function.
120  significantly attenuate the efficacy of ICS+LABA therapy on lung function in Black children.
121 w median NO(2) exposures while receiving ICS+LABA therapy had a reduction of 5.86 (95% CI 1.16, 10.56
122 rtion of days covered, was higher in the ICS+LABA group compared with the ICS+LTRA group.
123 l setting subjects were more adherent to ICS+LABA therapy than ICS+LTRA therapy.
124 nd costs associated with ICS+LTRA versus ICS+LABA as step-up therapies for asthma.
125 s old) receiving ICS+LTRA therapy versus ICS+LABA therapy after a period of monotherapy with an ICS.
126 corticosteroid-long-acting beta-agonist (ICS-LABA) combination inhalers.
127 orticosteroid long-acting beta2-agonist (ICS-LABA) medications (change, 0.06 [95% CI, 0.01 to 0.10] f
128 umeclidinium-vilanterol) and combination ICS-LABA inhalers (budesonide-formoterol, fluticasone-salmet
129 atients with uncontrolled asthma despite ICS-LABA treatment and conclude that SITT is a safe and effe
130 icant decreases in the use of fixed-dose ICS-LABA agents in children (-0.98 percentage points) and ad
131 significant absolute decrease in PDC for ICS-LABA compared with controls (-4.8%; 95% CI, -7.7% to -1.
132 ecreases in annual 30-day fills only for ICS-LABA medications (absolute change, -0.04; 95% CI, -0.07
133 ars; 69 530 [50.4%] female) (107 004 new ICS-LABA users and 30 829 new LAMA-LABA users), 30 216 match
134 rence to controller medications, notably ICS-LABA medications used by patients with more severe asthm
135 scription for a combination LAMA-LABA or ICS-LABA inhaler between January 1, 2014, and December 31, 2
136 ncreased proportion of days covered with ICS-LABA (6.0% [0.7% to 11.3%] of days; 15.6% increase).
137 improved clinical outcomes compared with ICS-LABA therapy, suggesting that LAMA-LABA therapy should b
138                            Compared with ICS-LABA use, LAMA-LABA use was associated with an 8% reduct
139 ibitors, and ICS long-acting B-agonists [ICS-LABAs]).
140 ound 1-4 days' wages, ICSs 2-7 days, and ICS-LABAs at least 6 days.
141  for SABAs, 2.6-340 for ICSs, and 24 for ICS-LABAs in the single study reporting this.
142 hese combination inhalers (LAMA-LABAs vs ICS-LABAs) have been conflicting and raised concerns of gene
143                                          ICS/LABA treatment significantly increased abundance of desm
144 combined with long-acting beta2-agonist (ICS/LABA) are standard treatments for asthma.
145 CS) or with long-acting beta(2)-agonist (ICS/LABA) or placebo.
146 icosteroid and long-acting beta-agonist (ICS/LABA).
147 ICS alone, a PDE4 inhibitor alone, or an ICS/LABA combination therapy.
148 rapy alone, and 54% were treated with an ICS/LABA combination.
149  trial was conducted to evaluate ICS and ICS/LABA against placebo.
150  assess the relationship between ICS and ICS/LABA combination therapy and severe asthma exacerbations
151 ndividuals using ICS treatment alone and ICS/LABA combination therapy suggested that the overall prot
152                                  ICS and ICS/LABA exposure was estimated from pharmacy data for patie
153 Week 24 for triple therapy (n = 911) and ICS/LABA therapy (n = 899), mean changes from baseline in FE
154                                  ICS and ICS/LABA use was estimated for each day of follow-up to crea
155             This signature, decreased by ICS/LABA treatment was enriched for genes associated with in
156 zed clinical trial suggest that combined ICS/LABA treatment is beneficial for prematurity-associated
157 5 mug; ELLIPTA inhaler) with twice-daily ICS/LABA therapy (budesonide/formoterol 400 mug/12 mug; Turb
158 related quality of life with twice-daily ICS/LABA therapy in patients with COPD.
159 atients with uncontrolled asthma despite ICS/LABA treatment.
160 ered a 1-month run-in period on low-dose ICS/LABA budesonide/formoterol (BUD/F) 200/6 one inhalation
161 ion rate with triple therapy versus dual ICS/LABA therapy (35% reduction; 95% CI, 14-51; P = 0.002).
162 tective effect was as good or better for ICS/LABA combination therapy when compared with ICS treatmen
163                            After 3-month ICS/LABA treatment, residual volume (RV)/total lung capacity
164 scomfort with the middle or high dose of ICS/LABA combination agents under well technique (32 of BUD/
165 e is no evidence either ICS plus Tulo or ICS/LABA combination is better for elder patient.
166  was defined as poor adherence to ICS or ICS/LABA inhaler of 75% or less.
167 trolled asthma patients receiving ICS or ICS/LABA were assessed for physical and psychiatric problems
168 washout prior to randomization to ICS or ICS/LABA.
169 ear (stable condition under the previous ICS/LABA).
170 andomization ICS), 19 children receiving ICS/LABA (including 4 with prerandomization ICS), and 14 chi
171                               Short-term ICS/LABA treatment improves RV/TLC% predicted in severe COPD
172 , 7.3% to 21.0%; P = .002) higher in the ICS/LABA group compared with the placebo group.
173    Recently, three novel triple therapy (ICS/LABA/LAMA) formulations in a single-inhaler device (SITT
174 ents with COPD receiving triple therapy (ICS/LABA/LAMA) if the patient has had no exacerbations in th
175 nd Triple in Asthma High Strength Versus ICS/LABA HS and Tiotropium [TRIGGER]) recruited patients fro
176                           Treatment with ICS/LABA fixed-dose combination therapy appeared to perform
177 gle-inhaler triple therapy compared with ICS/LABA therapy in patients with advanced COPD.
178                                          ICS/LABAs were switched to FP/FM-pMDI and slow and deep inha
179 in hospital admission rates were recorded in LABA-treated non-Hispanic white patients with the rare I
180                   Combined use of an inhaled LABA with tiotropium bromide should provide important th
181 ce in vivo of an interaction between inhaled LABA and corticosteroid on GR nuclear translocation in h
182                             Combination LAMA-LABA inhalers (aclidinium-formoterol, glycopyrronium-for
183 ed a new prescription for a combination LAMA-LABA or ICS-LABA inhaler between January 1, 2014, and De
184 7 004 new ICS-LABA users and 30 829 new LAMA-LABA users), 30 216 matched pairs were identified for th
185                   In this cohort study, LAMA-LABA therapy was associated with improved clinical outco
186  with ICS-LABA therapy, suggesting that LAMA-LABA therapy should be preferred for patients with COPD.
187             Compared with ICS-LABA use, LAMA-LABA use was associated with an 8% reduction in the rate
188 s comparing these combination inhalers (LAMA-LABAs vs ICS-LABAs) have been conflicting and raised con
189                                         LAMA/LABA fixed dose combinations (FDCs) provide the convenie
190 me children lack response to the addition of LABA.
191 lly responsible for the increased benefit of LABA/LAMA combinations over single long-acting bronchodi
192 iated the effect of a given concentration of LABA was gene-dependent.
193 hance, sensitize, and prolong the effects of LABA/ICS combination therapies.
194 ults support the possibility that effects of LABA/LAMA combinations on hyperinflation, mucociliary cl
195 e findings do not support the superiority of LABA + ICS compared with tiotropium + ICS for black pati
196 e, continued favorable changes in the use of LABA agents were observed after the 2010 FDA regulatory
197 ies might have contributed to reduced use of LABA agents, as intended; however, their effect, indepen
198 ect of these regulatory activities on use of LABA-containing agents or other asthma medications.
199 score matching, there were 8712 new users of LABA-inhaled corticosteroid combination therapy and 3160
200 ased the potency and doubled the efficacy of LABAs.
201 g beta-agonists (LABAs) (n = 3174), 1 RCT of LABAs and inhaled corticosteroids (ICS) (n = 1097), 5 RC
202  dose escalation and comparable with that of LABAs.
203 OPD hospitalization compared with new use of LABAs alone (difference in composite outcome at 5 years,
204                                   New use of LABAs and inhaled corticosteroids was associated with a
205 pitalizations [27.8%]) and 2129 new users of LABAs alone (1179 deaths [37.3%]; 950 COPD hospitalizati
206 id combination therapy and 3160 new users of LABAs alone who were followed up for median times of 2.7
207 outcome was observed among 5594 new users of LABAs and inhaled corticosteroids (3174 deaths [36.4%];
208 s over single long-acting bronchodilators or LABA/inhaled corticosteroids in decreasing exacerbation.
209 t be exacerbated in people receiving LABA or LABA plus glucocorticoids.
210 requency than either their monocomponents or LABA/inhaled corticosteroid combinations in patients at
211 ination LABAs and inhaled corticosteroids or LABAs alone.
212 ferential FEV(1) response favoring LTRA over LABA step-up therapy.
213 c antagonist (LAMA) combination therapy over LABA or LAMA monotherapy in patients with COPD and dyspn
214 ients with asthma uncontrolled with ICS plus LABA or ICS alone.
215 tor antagonists (LTRA; n = 338), or ICS plus LABA plus LTRA (n = 686).
216                           LAMA plus ICS plus LABA provided modest improvements in bronchodilation and
217                    The after/before ICS plus LABA treatment ratio of B2AR number was 1.0 for alendron
218  randomization and after 8 weeks of ICS plus LABA treatment.
219  for patients receiving high-dosage ICS plus LABA with baseline blood eosinophils 300 cells per muL o
220  plus long-acting beta(2)-agonists (ICS plus LABA) and a history of two or more exacerbations in the
221 ids and long-acting beta2-agonists (ICS plus LABA) in the previous year.
222 ich are uncontrolled by high-dosage ICS plus LABA, and provide support for benralizumab to be an addi
223 common than presumed in concomitant ICS plus LABA-treated asthmatic patients.
224 to first severe exacerbation versus ICS plus LABA.
225 MA in combination with ICS alone or ICS plus LABA.
226 cerbations in patients treated with ICS plus LABA.
227 ated with inhaled corticosteroids (ICS) plus LABA.
228 tor antagonist (LTRAs; n = 354) or ICSs plus LABAs plus LTRAs (n = 569).
229 ted with inhaled corticosteroids (ICSs) plus LABAs but not for treatment with ICSs alone (n = 1758) o
230 he use of ADRB2 polymorphisms for predicting LABA treatment response is still limited and further pro
231 anticholinergic medication, newly prescribed LABA and inhaled corticosteroid combination therapy, com
232 tion therapy, compared with newly prescribed LABAs alone, was associated with a significantly lower r
233                         After randomization, LABA was discontinued at week 4, and inhaled glucocortic
234 th rare ADRB2 variants in patients receiving LABA therapy.
235                           Patients receiving LABA with a rare ADRB2 variant had increased asthma-rela
236 cts might be exacerbated in people receiving LABA or LABA plus glucocorticoids.
237 ty score-matched patients who were receiving LABA-based therapies were included.
238 hite and African American patients receiving LABAs with these rare variants had increased exacerbatio
239  to determine whether alendronate can reduce LABA-associated LOBP in inhaled corticosteroid (ICS)-tre
240 d not find evidence that alendronate reduces LABA-associated LOBP, which relates to the occurrence of
241  formoterol and budesonide as representative LABA and ICS, respectively.
242         Although preclinical studies suggest LABAs and LAMAs have antiinflammatory effects, such effe
243 ed to evaluate the risk of administering the LABA salmeterol in combination with an inhaled glucocort
244 ers and 2.41 per 100 patient-years among the LABA users.
245  combination of the LTRA montelukast and the LABA salmeterol could provide an effective therapeutic s
246 tation of GRE-dependent transcription by the LABA formoterol.
247 signed to receive, by inhalation, either the LABA indacaterol (110 mug) plus the LAMA glycopyrronium
248 e montelukast patients and 566 events in the LABA patients were identified.
249 periority comparison) or the addition of the LABA salmeterol (secondary noninferiority comparison).
250 al prospectively evaluated the safety of the LABA salmeterol, added to fluticasone propionate, in a f
251 MA glycopyrronium (50 mug) once daily or the LABA salmeterol (50 mug) plus the inhaled glucocorticoid
252  roflumilast N-oxide) each sensitized to the LABA, formoterol.
253 patients were stepped down by dropping their LABAs or another add-on or by halving their ICS dose (ha
254                                        Thus, LABAs modulate glucocorticoid action, and comparable tra
255  at baseline) predicted a better response to LABA step-up (P=0.009).
256                              The response to LABA step-up therapy was most likely to be the best resp
257    White race predicted a better response to LABA step-up, whereas black patients were least likely t
258 be needed to predict individual responses to LABA step-up therapy.
259 2 variants modulate therapeutic responses to LABA therapy and contribute to rare, severe adverse even
260 tive biomarkers is crucial for understanding LABA safety.
261 matitis: OR 3.76 [2.14-6.61]), and drug use (LABA + ICS: 1.86 [1.27-2.74], antileukotrienes 4.83 [1.6
262 %]); 26 462 used montelukast and 47 829 used LABA.
263  The proportions of asthmatic patients using LABA-containing products, inhaled corticosteroids (ICSs)
264 curring after initiation of dupilumab versus LABA-containing therapies was measured.
265 rences in the effects of tiotropium + ICS vs LABA + ICS (hazard ratio for time to first exacerbation,
266 atment initiation, tiotropium monotherapy vs LABA-ICS initiation was associated with a small increase
267 ia associated with tiotropium monotherapy vs LABA-ICS was of questionable clinical importance, partic
268 ociated with fewer asthma exacerbations when LABAs and inhaled glucocorticoids were withdrawn, with i
269 elevance, especially in target tissues where LABAs behave as partial agonists.
270 um monotherapy initiators were compared with LABA-ICS initiators.
271  the rare, life-threatening events seen with LABA use.
272 roids (ICS)/LABA/LAMA over dual therapy with LABA/LAMA in patients with COPD and dyspnea or exercise
273 erious asthma-related events associated with LABAs.
274 comitant use of inhaled glucocorticoids with LABAs mitigates those risks.
275  glucocorticosteroid therapy with or without LABAs.

 
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