Fluticasone

Limits on what this shows

• Null findings: Contoli [24]: increase in potentially pathogenic bacteria load did not reach significance; viral detection did not differ; sputum inflammatory cell counts did not differ; exacerbations 22 (fluticasone plus salmeterol) vs 28 (salmeterol), none requiring hospitalization; pneumonia not an outcome. Singanayagam [25]: total bacterial load and diversity did not differ between ICS users and non-users. MUSIC [47][48]: no change in alpha diversity, no FS250 effect, adverse events similar, primary oropharyngeal endpoint null. INCOGNITO (Keir, randomized, 80 patients with moderate to severe COPD, 6 months, tiotropium/olodaterol with ICS withdrawal n=38 vs fluticasone furoate/vilanterol continuation n=42) [49]: sputum bacterial load difference -0.03 log units (95% CI -0.15 to 0.09; p=0.61), a null for fluticasone furoate; after withdrawal Streptococcus rose and Haemophilus fell in relative terms; conference abstract, metagenomics on a 54-patient subset. The furoate and propionate products are different salts and doses, so the null does not cancel the propionate findings, but it is contradicting randomized data for the fluticasone family.
• At-risk subgroups: COPD with low blood or sputum eosinophils; age over 65 (label pneumonia rates) [3]; people with prior pneumonia. Not shown for asthma or for intranasal use.

Regulatory status

Advair Diskus label (fluticasone propionate with salmeterol): pneumonia in COPD 7% (250/50) vs 3% (salmeterol) in 1-year trials and 16% (500/50) vs 9% (placebo) in a 3-year trial, higher in patients over 65 [3]. Oropharyngeal candidiasis is a labeled event for the propionate and furoate products (Arnuity 100 mcg adults and adolescents: 3% vs 0% placebo) [1][2]. The labels do not mention the microbiome.

Population evidence

Contoli 2017 [24]: prospective randomized open-label blinded-endpoint trial, 60 patients (30 per arm), steroid-naive moderate COPD (FEV1 50 to 80% predicted), fluticasone propionate 500 mcg plus salmeterol 50 mcg twice daily vs salmeterol 50 mcg twice daily, 12 months. Total sputum bacterial load rose with fluticasone plus salmeterol (p=0.005) and was unchanged with salmeterol alone. Post hoc split of the fluticasone arm: blood eosinophils under 2% +2.47 +/- 0.44 log10 CFU/mL; 2% or above +0.91 +/- 0.37 (not significant). S. pneumoniae and H. influenzae relative abundance rose (p under 0.05), limited to blood eosinophils under 2%. Singanayagam 2019 [25]: sputum from 23 COPD patients, 10 ICS users (5 fluticasone propionate, 4 budesonide, 1 beclomethasone); ICS users had higher Streptococcus relative abundance and qPCR copies (p under 0.05), with total load (p=0.1) and diversity not different. Yip 2022 [26] (DISARM RCT, 12 weeks, salmeterol/fluticasone 250 mcg twice daily n=18 with paired data): host gene expression correlated with change in bronchial alpha diversity only in the salmeterol/fluticasone arm; correlational, no stated mean shift in taxa. Second independent randomized trial, added 2026-10-08, Richardson MUSIC [47][48]: multicentre, severe COPD (FEV1 under 50% predicted and/or 2 or more exacerbations a year), 4-week ICS washout (122 entered, 61 withdrew before randomisation, 45 of them after an exacerbation), 61 randomized to budesonide/formoterol 400/12, fluticasone propionate/salmeterol 500/50 (FS500), fluticasone propionate/salmeterol 250/50 (FS250) or aclidinium/formoterol (no ICS), twice daily for 3 months; per-arm n not on the pages read. Key secondary outcome, sputum bacterial load at month 3, FS500 minus budesonide/formoterol: 0.87 log units (95% CI 0.29 to 1.44; p=0.0037) in the 2023 congress abstract [48]; the 2025 journal abstract states the same direction (significantly higher with FS500, not with FS250) without effect sizes [47]. Alpha diversity (Shannon) and sputum inflammatory markers did not differ. The 2023 abstract states budesonide/formoterol did not raise load versus the non-ICS arm, so the contrast is fluticasone-specific against another ICS, not against non-use. Primary endpoint (oropharyngeal load, budesonide/formoterol vs FS500) was not significant, so the rise was lower-airway only.

Mechanism

Present and named: fluticasone propionate suppressed airway cathelicidin (hCAP18/LL-37) in mice and in human epithelial cells including primary COPD cells; fluticasone had no effect on bacterial load in cathelicidin-knockout mice and exogenous LL-37 reversed the Streptococcus increase; cathepsin D was implicated [25]. In vitro, fluticasone also increased growth of Gram-negative airway pathogens [29].

Boundary

COPD only; fluticasone propionate 500 mcg plus salmeterol twice daily (not the 250 mcg dose in MUSIC); steroid-naive moderate COPD for 12 months with the rise confined to blood eosinophils under 2% (post hoc, 30 patients per arm, GSK-funded unrestricted grant) [24], or severe COPD for 3 months after washout, lower airway only, against budesonide/formoterol [47][48]; not shown for fluticasone furoate [49], asthma or intranasal use.

Counter-evidence held on record

Counter-evidence and confounding Open-label design with blinded endpoints; 41 selected pathogens analyzed, not the full airway ecology; sputum sampling incomplete (73 to 80% had all visits); GSK employees among authors [24]. ICS users in the cross-sectional cohort were older (median 74 vs 68 years) and the ICS drugs were mixed, so confounding by indication is not excluded [25]. Not red, though close: MUSIC [47][48] is a second independent propionate randomized trial with the load directly measured, in a consistent direction, with the cathelicidin mechanism named [25]. It is held at orange because its comparator is an active ICS arm (it does not test fluticasone against non-use), the effect size comes from a 2023 conference abstract while the 2025 paper was read at abstract level only, the effect is limited to the 500 mcg dose, 61 patients were randomized after 50% dropped out during washout, the fluticasone furoate randomized trial found no difference [49], no clinical outcome is tied to the load, and bacterial load is neither a nutrient nor the gut-microbiome category. The bronchial-brush RCT analysis reports host gene correlations only [26], and the fluticasone treatment study in asthma (Durack 2017) reported only that specific taxa changed, without direction or size in the abstract read [27]. Framing caution This is an infection-risk context for prescribers and a microbiome shift in the lung. It is not a probiotic, supplement or dietary indication, it does not describe the gut, and it is not a reason to stop the drug. Mouth rinsing after each inhaled dose is label advice for candidiasis [1].

Limits on what this shows

• Null findings: TORCH hip and spine BMD not different from placebo [7]; Maltais hip noninferiority met [8]; ISOLDE fractures 2.4% of 372 fluticasone vs 4.6% of 370 placebo and TORCH fractures about 5.4% vs 5.1% (secondhand via a narrative review, no CIs) [10]; pediatric studies null [11][12]. An early budesonide BMD trial in COPD [44] and letters on the ISOLDE trial [45] were opened and contain no fluticasone BMD data, so neither is used. In 6-month data from 16 completers (8 on fluticasone 400 mcg/day), bone formation and resorption markers did not change [13].
• At-risk subgroups: Older adults, postmenopausal women, smokers, people with prior oral corticosteroid courses, long-term high-dose users, poor nutrition (label) [1][2].

Regulatory status

Flovent HFA: BMD decreases seen with long-term ICS; a 2-year trial in 160 subjects showed no statistically significant lumbar BMD change; risk factors include poor nutrition, advanced age, tobacco use and postmenopausal status [1]. Arnuity lists the same risk factors including "poor nutrition" [2]. Advair Diskus: assess BMD before starting in COPD and periodically; a 2-year asthma trial showed no significant BMD change; a 3-year COPD trial was inconclusive, with 7 non-traumatic fractures in 5 subjects on the combination vs 1 in 1 subject on salmeterol [3].

Population evidence

Thorax 2011 meta-analysis [9]: 16 RCTs (14 fluticasone, 2 budesonide), 17,513 participants, fracture Peto OR 1.27 (95% CI 1.01 to 1.58, I2 0%); 7 observational studies, about 69,000 participants, pooled OR 1.21 (1.12 to 1.32); per 500 mcg beclomethasone-equivalent increment OR 1.09 (1.06 to 1.12). No drug-stratified estimate appears in the abstract read, and a second independent record of the same abstract (University of East Anglia repository) [56] repeats the same figures and the same absence of a fluticasone-versus-budesonide split. A 2025 meta-analysis of nine observational studies in COPD (six case-control, three cohort; Huang, Front Med) [57] lists fluticasone propionate only inside mixed ICS groups (for example Pujades-Rodriguez any-fracture OR 1.12, 95% CI 0.97 to 1.29, 5,833 participants; European pooled OR 1.12, 95% CI 1.01 to 1.24, I2 0%) and reports no fluticasone-only estimate; the page read has internally inconsistent tables, so no figure from it is attributed to fluticasone. TORCH BMD substudy [7]: 658 patients, 3 years, fluticasone propionate 500 mcg twice daily vs placebo; hip BMD change -2.9% (fluticasone) vs -3.1% (placebo) and lumbar spine -0.3% vs 0%, no significant difference (arm assignment as extracted from the abstract by a summarizer); only 43% completed all testing. Maltais 2020 [8]: 283 randomized, 3 years, fluticasone furoate/vilanterol 100/25 vs vilanterol 25; annual total hip change -0.27% vs +0.18%, difference -0.46% per year (95% CI -0.97 to 0.06), noninferior at the -1% margin; lumbar spine difference -0.51% per year (95% CI -1.11 to 0.10); fracture rates similar. Children: Ozkaya 2012 [11], 230 children on fluticasone for 5 or more years (mean about 200 mcg/day) vs 170 untreated, no difference in osteocalcin, cortisol or lumbar BMD; Griffiths 2004 [12], 49 children on fluticasone 1,000 mcg/day for 6 months or more vs 32 controls, bone turnover markers not different, and lumbar BMD more than 1 SD low in 13 of 37 (35.1%) but 6 of 37 (16.2%, not significant) after bone-age correction.

Mechanism

Glucocorticoid receptor-mediated systemic effect at higher exposure; HPA suppression is documented on the label [1][3]. No calcium or vitamin D handling mechanism was shown in any source read, and neither nutrient was measured in the BMD trials.

Counter-evidence held on record

Counter-evidence and confounding Confounding is large: COPD severity, smoking, age, falls, immobility and oral steroid bursts all affect bone and fracture. The two strongest BMD trials are null or within a noninferiority margin, and one trial shows fewer fractures on fluticasone. Short-term marker data in nine healthy volunteers at 750 and 1,500 mcg/day showed a paradoxical rise in the PICP:ICTP ratio (27.4 to 42.6) with no significant ICTP change on fluticasone, which does not support increased resorption [15]. Full-text Thorax 2011 drug subgroups could not be reached (PMC bot-verification on the 2023 meta-analysis page, Europe PMC 429), so a drug-stratified fracture estimate remains unretrieved. Framing caution Fracture and low BMD are outcomes, not calcium or vitamin D deficiency. Do not recommend calcium or vitamin D supplementation from this entry; bone health review follows the label and standard of care.

Limits on what this shows

• Null findings: Fluticasone furoate 50 mcg: no significant growth effect [2]. Pediatric bone marker and BMD data are null at the doses studied [11][12].
• At-risk subgroups: Prepubertal children, higher doses, concurrent intranasal and inhaled corticosteroids (not studied in the sources read).

Regulatory status

Flovent HFA: may reduce growth velocity; controlled trials show a mean reduction of about 1 cm/year (range 0.3 to 1.8) for the ICS class; in a 52-week Flovent ROTADISK trial mean growth velocity was 6.32 (placebo), 6.07 (50 mcg) and 5.66 cm/year (100 mcg) [1]. Arnuity: 457 prepubertal children, 1 year, 5.90 (50 mcg) vs 6.06 cm/year (placebo), difference -0.16 cm/year (95% CI -0.46 to 0.14) [2]. The nasal spray label text read did not address growth [4].

Population evidence

Cochrane summary [18]: 25 trials, 8,471 children, one-year growth velocity mean difference -0.48 cm/year (95% CI -0.65 to -0.30; 14 trials, 5,717 children); height change -0.61 cm (-0.83 to -0.38). Subgroup difference among six molecules P under 0.0001; the summary article reports no pooled fluticasone-specific estimate [18]. Dose-comparison overview [19]: three industry trials (fluticasone, ciclesonide, mometasone), 728 school-aged children over 52 weeks, higher dose about 0.20 cm/year lower growth velocity; no drug-specific estimate shown.

Mechanism

Glucocorticoid receptor-mediated systemic effect, supported by label HPA-axis findings. No nutrient intake or nutrient absorption mechanism was shown in any source read.

Counter-evidence held on record

Counter-evidence and confounding Uncontrolled asthma itself slows growth. The class effect is molecule-dependent [18], so the class pooled estimate is not a fluticasone estimate. Two label figures (ROTADISK and the furoate trial) are the only drug-specific fluticasone numbers retrieved. Framing caution Growth is an outcome, not a nutrient. Do not imply that dietary change or supplements correct it; the label advises routine stadiometry and the lowest effective dose [1][2].

Limits on what this shows

• Null findings: Faul: change vs baseline not significant and the authors judged the difference not clinically significant [22]. Label trials showed no clinically relevant glucose changes [3]. Saif-Ur Rahman [50]: fluticasone users did not differ from non-steroid asthmatics on fasting, 2-hour or HbA1c values. O'Byrne 2012 [51], retrospective analysis of double-blind trials: budesonide primary datasets (asthma, hazard ratio 0.98, 95% CI 0.38 to 2.50; COPD, 0.99, 0.67 to 1.46) showed no excess new diabetes or hyperglycaemia events; fluticasone (n=2,773) appears only in a 60-trial secondary asthma dataset with the 0.19% event rate not split by drug, so it is class-level counter-evidence. Dendukuri 2002 [52], nested case-control in 21,645 Quebec residents aged 66 or older: any inhaled corticosteroid (fluticasone one of five agents, no fluticasone-specific estimate) adjusted rate ratio for antidiabetic prescription 0.9 (0.8 to 1.1), crude 1.4 (1.2 to 1.5), explained by oral steroid use. A 2024 pilot of 48 children on mixed ICS (fluticasone count not given) found no HbA1c change over 6 months and no difference between ICS types [54].
• At-risk subgroups: People with diabetes or prediabetes, higher doses, concurrent oral corticosteroid courses.

Regulatory status

Flovent HFA: hyperglycemia appears only in the postmarketing list [1]. Advair Diskus: the hypokalemia and hyperglycemia warning (sec 5.18) concerns the beta-agonist component; no clinically relevant glucose changes in the asthma and COPD trials [3].

Population evidence

Faul 2009 [22]: randomized double-blind placebo-controlled crossover, 12 randomized and 10 completed, adults with type 2 diabetes and asthma or COPD, fluticasone propionate 440 mcg twice daily vs oral montelukast 10 mg, 6 weeks per arm; HbA1c difference fluticasone vs montelukast 0.25 percentage points (P under 0.025); fluticasone vs baseline +0.11 (not significant). Suissa 2010 [23]: 388,584 new users of respiratory drugs in Quebec, 30,167 developed diabetes; current ICS use rate ratio 1.34 (95% CI 1.29 to 1.39); highest dose (fluticasone-equivalent 1,000 mcg/day or more) 1.64 (1.52 to 1.76); progression to insulin 1.54 (1.18 to 2.02) at the highest dose. A second independent record of the abstract (PubMed, PMID 20870201) [53] gives the same figures and adds overall current-use progression to insulin RR 1.34 (95% CI 1.17 to 1.53) and names fluticasone only as the dose reference (1,000 mcg/day or more); an OpenAlex lookup of the record returned no abstract and no full text (closed access) and the journal page returned 403, so no molecule-level estimate was retrievable. Fluticasone-specific data from the 2026-10-08 update: Saif-Ur Rahman 2021 [50], cross-sectional, 70 normoglycaemic adults with asthma in Bangladesh, 35 on inhaled fluticasone for at least 3 months (dose not stated) vs 35 on no steroid: fasting glucose 5.27 +/- 0.48 vs 5.17 +/- 0.59 mmol/L (p=0.25), 2-hour OGTT glucose 6.04 +/- 1.21 vs 5.69 +/- 1.09 (p=0.20), HbA1c 5.57 +/- 0.41 vs 5.47 +/- 0.40% (p=0.75), no correlation with duration of use (r under 0.02 for all three).

Mechanism

Systemic glucocorticoid effect on glucose handling is the presumed pathway; it was not tested in the sources read, and the mechanism is not named in them.

Class cohort test

CLASS EXTRAPOLATION for [23]: ICS pooled; fluticasone appears only as the unit for dose equivalence, so a fluticasone-specific estimate is not available from the text read. Fluticasone propionate was in the Faul cohort [22] (n=10) and in the Saif-Ur Rahman cohort [50] (n=35). Re-confirmed on 2026-10-08 from two independent records (PubMed abstract [53] and a news summary of the paper) that fluticasone is only the dose unit in Suissa.

Counter-evidence held on record

Counter-evidence and confounding Tiny crossover trial; the cohort adjusted for respiratory severity, but residual confounding by indication and oral steroid bursts remains likely. The two fluticasone-specific normoglycaemic or diabetic studies disagree in direction (Faul +0.25 points vs montelukast; Saif-Ur Rahman null), so a graded excess finding for fluticasone itself is not supported. Direction is an excess or disturbance effect, not a deficiency. Framing caution This is a monitoring prompt for people with diabetes on higher doses, not a nutrient claim. It does not support changing diet or adding supplements.

Limits on what this shows

• Null findings: Vitamin D was not measured before and after fluticasone in any source read; Kunisaki measured it only at baseline [17].
• At-risk subgroups: Severe COPD and pediatric asthma populations have high baseline insufficiency independent of the drug [16][17].

Regulatory status

Not mentioned in any fluticasone label text read [1][2][3][4].

Population evidence

Searing 2010 [16]: 100 children with asthma, median 25(OH)D 31 ng/mL, 47% under 30 and 17% under 20; inverse correlations with inhaled steroid use (P=.0475), oral steroid use (P=.02) and total steroid dose (P=.001); inhaled steroid agent not named in the abstract. Kunisaki 2011 [17]: 60 former smokers with severe COPD after a 4-week ICS-free period, baseline 25(OH)D 23.3 +/- 9.3 ng/mL, 35% insufficient and 40% deficient; then fluticasone propionate 500 mcg twice daily for 4 weeks; baseline 25(OH)D did not predict FEV1 change.

Mechanism

Not shown for fluticasone. Systemic corticosteroid effects on vitamin D handling are not demonstrated in any source read.

Class cohort test

CLASS EXTRAPOLATION for [16]: ICS pooled with oral steroids, fluticasone not named, so it is Tier C. Kunisaki [17] had fluticasone in the cohort but tests whether vitamin D status modifies the drug response (nutrient-to-drug direction, Hard Rule 4) and found none; it does not test depletion.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication is presumed: severe COPD and asthma severity, indoor time, smoking and oral steroid use all lower 25(OH)D. The baseline prevalence in [17] predates the fluticasone course, which argues the deficiency belongs to the population, not the drug (Hard Rule 6). Framing caution A monitoring prompt only. Do not recommend vitamin D supplementation from this entry.

Limits on what this shows

• Null findings: Al-Khayat inhaled beclomethasone group null across all minerals measured [21]. Pediatric bone studies did not report magnesium [11][12].
• At-risk subgroups: Children with frequent oral steroid bursts; patients on diuretics or other magnesium-lowering drugs.

Regulatory status

Not mentioned in the fluticasone label text read [1][2][3][4].

Population evidence

Fatouh 2009 [20]: 89 children aged 5 to 15 with chronic asthma plus about 27 healthy controls; fluticasone propionate inhaled, with short oral methylprednisolone courses during exacerbations; serum magnesium significantly lower in steroid-treated asthmatics than in controls or untreated asthmatics, negatively correlated with frequency of oral steroid use, and reported to recover after steroid cessation. No numeric values appear on the page read; full text is paywalled. Al-Khayat 2010 [21] (full text opened 2026-10-08; the abstract did not name the agents): 69 asthmatic adults, 31 on inhaled beclomethasone dipropionate and 38 on oral prednisolone for about one year, vs 35 controls; total magnesium 0.752 +/- 0.081 (controls), 0.719 +/- 0.064 (inhaled beclomethasone) and 0.565 +/- 0.058 mmol/L (oral prednisolone); ionized magnesium 0.473, 0.454 and 0.353 mmol/L; the inhaled group did not differ from controls, the oral group was lower (p under 0.001). Duhok 2017 case-control [55]: 100 asthmatic children with acute attacks vs 100 controls, serum magnesium 1.91 +/- 0.33 vs 2.03 +/- 0.33 mg/dL (p=0.01), lower with asthma itself and inversely related to severity (p=0.05); steroid users vs non-users not significantly different (p=0.7), steroid agent not named. The Fatouh full text and numeric values remain unretrieved (Inderscience page shows the abstract only; two retrieval attempts).

Mechanism

Systemic glucocorticoid-related renal magnesium loss is the usual proposal for oral steroids; it was not shown for fluticasone, whose renal clearance is negligible [1].

Class cohort test

Fatouh has fluticasone propionate in the cohort [20] but cannot separate it from methylprednisolone. Al-Khayat [21] studied inhaled beclomethasone dipropionate and oral prednisolone, no fluticasone user, so it is Tier C for fluticasone (class member beclomethasone) and is used only as counter-evidence; Duhok [55] did not name the steroid and is used only to show that asthma itself lowers magnesium.

Counter-evidence held on record

Counter-evidence and confounding The oral methylprednisolone bursts are a direct competing explanation, the magnesium correlation was with oral steroid frequency, not inhaled dose, and the Duhok data show asthma severity alone is associated with lower magnesium [55]. The Tier D claim list that names fluticasone for magnesium is a 1999 handbook reprint with no cited study [40]. Framing caution Not a fluticasone deficiency claim. Do not recommend magnesium supplementation from this entry.

Limits on what this shows

• Null findings: No clinically relevant potassium change in the fluticasone/salmeterol trials [3]; no change in the inhaled group in [21].
• At-risk subgroups: Patients on loop or thiazide diuretics, high-dose beta-agonists or oral steroid bursts.

Regulatory status

Advair Diskus sec 5.18: "Beta-adrenergic agonist medicines may produce significant hypokalemia in some patients"; usually transient; no clinically relevant potassium or glucose changes in the asthma and COPD trials [3]. Flovent HFA and Arnuity text read did not mention hypokalemia [1][2].

Population evidence

Al-Khayat 2010 [21]: oral prednisolone group (n=38, about one year) had significantly lower potassium vs controls (3.305 +/- 0.089 vs 4.117 +/- 0.439 mmol/L, p under 0.001); the inhaled beclomethasone dipropionate group (n=31) had no significant change (3.961 +/- 0.432 mmol/L). Fluticasone propionate was in the Advair trials [3] but the label gives no potassium numbers.

Mechanism

Mineralocorticoid-type renal potassium wasting is the oral-steroid proposal; it is not shown for fluticasone, with renal clearance under 0.02% of total [1]. The beta-agonist shifts potassium into cells.

Class cohort test

CLASS EXTRAPOLATION: the supporting data are oral prednisolone [21]; fluticasone was not in that oral cohort (the inhaled arm used beclomethasone). A Tier D list names budesonide and flunisolide, not fluticasone, for potassium [39].

Counter-evidence held on record

Counter-evidence and confounding Fluticasone-specific laboratory findings run against the claim, and the label-documented hypokalemia belongs to the beta-agonist. Retained as yellow, not white, because systemic glucocorticoid effects at high exposure (HPA suppression) are documented and a potassium effect is not mechanistically excluded. Framing caution Do not recommend potassium supplementation. The label says the beta-agonist potassium decrease usually does not require supplementation [3].

Limits on what this shows

• Why no grade: Dual condition met: the labeled events (candidiasis, nausea at a rate near placebo, postmarketing taste change) are symptoms, not an intake or nutrient finding, no Tier B or C source connects them to reduced intake in fluticasone users, and no circulating consumer claim was found to rebut. Gap, not safety. Taste and smell change is a symptom and is not filed as a deficiency (Hard Rule 2).

What was searched

Original pass (2026-10-07), WebSearch: "inhaled corticosteroid oral candidiasis dysgeusia dietary intake nutrition weight loss elderly COPD fluticasone". Opened: Dekhuijzen 2016 [46], a matched observational cohort of UK COPD patients, which reports thrush odds ratios (fixed-dose ICS/LABA vs bronchodilator alone adjusted OR 2.18, 95% CI 1.84 to 2.59; fluticasone/salmeterol pMDI vs DPI OR 0.67; high vs low fluticasone/salmeterol dose OR 1.97, 1.22 to 3.17) and no dietary or nutritional outcome. Repair pass (2026-10-08): (a) label text searched for appetite, weight loss, taste and dysgeusia terms: Flovent HFA, Arnuity and Advair labels contain none beyond "poor nutrition" as a bone risk factor and Flovent postmarketing weight gain with Cushingoid features [1][2][3]; the fluticasone propionate nasal label page lists nausea or vomiting at 4.8% (100 mcg) and 2.6% (200 mcg) versus 2% placebo, and postmarketing "alteration or loss of sense of taste and/or smell" without frequency [63]; (b) WebSearch: "intranasal fluticasone dysgeusia OR taste disturbance OR smell loss adverse event frequency fluticasone nasal spray trial dysgeusia" and "inhaled corticosteroid oral candidiasis dysphagia odynophagia esophageal candidiasis food intake nutritional status elderly fluticasone". Results were label mirrors, a COVID-era anosmia trial listing, and eosinophilic esophagitis patents; none measured food or nutrient intake. A pilot paper on eating immediately after inhalation to reduce local adverse events (PMID 23166541) returned a bot-verification page and was not read.

Channel outcomes

Label and web channels worked; PubMed single-record page for the pilot paper was blocked; a systematic review page on long-term ICS adverse effects in COPD returned Access Denied in the original pass. Mixed: clean zero on label and web channels plus two blocked records.