Mometasone

Limits on what this shows

• Null findings: No suppression with nasal 100 mcg/day for 1 year [7], with MF DPI 100 to 200 mcg/day in children by plasma cortisol [8], or with 400 mcg twice daily DPI in adults at day 28 [11]. Fardon's authors state their data refute the claim that MF has negligible systemic effect compared with fluticasone [12].
• At-risk subgroups: High inhaled dose, long duration, co-use with strong CYP3A4 inhibitors, children (HPA suppression and growth effects are coupled), people also on other corticosteroids. Combination-product data [13] include formoterol; the cortisol effect is attributed to MF but was not separated.

Regulatory status

Labels list hypercorticism and adrenal suppression (sec 5.5 and 5.6) as possible, particularly at higher than recommended doses over prolonged periods or in susceptible people; no incidence given [1][3][4].

Population evidence

Fardon 2004 [12]: randomized crossover, 21 adults with persistent asthma, Twisthaler 400, 800, 1,600 mcg/day in weekly steps. Overnight urinary cortisol/creatinine geometric-mean fold suppression 1.39 (95% CI 1.04 to 1.88; p=0.02) at 800 mcg and 1.92 (1.26 to 2.93; p=0.001) at 1,600 mcg; 8 am plasma cortisol suppressed at the highest dose. Affrime 2000 [11]: three 28-day placebo-controlled studies in adults with asthma; 800 mcg twice daily by DPI cut cortisol AUC24 by 28.0 +/- 8.3% (prednisone 10 mg: 67.2 +/- 3.6%), 400 mcg twice daily matched placebo at day 28; MDI 800 mcg twice daily cut AUC24 by 24.0 +/- 3.1% (fluticasone 880 mcg twice daily: 51.7 +/- 3.8%). Label adult DPI study (n=16 per arm): day-29 post-cosyntropin cortisol 23.2 mcg/dL (440 mcg twice daily) and 20.8 (880 mcg twice daily) versus 25 placebo and 14.5 prednisone [3]. Children 6 to 11 (label): cortisol AUC0-12 difference versus placebo 3.4 (95% CI -14.0 to 20.7) at 110 mcg twice daily, -16.0 (-33.9 to 1.9) at 220 mcg, -17.9 (-35.8 to 0.0) at 440 mcg [3]. Mometasone/formoterol MDI (combination, n=66): 24-hour cortisol AUC ratio versus placebo 78% (90% CI 66 to 92%) at 400/10 mcg twice daily, 92% (78 to 110%) at 200/10 mcg [13]. Nasal: Schenkel 2000 cosyntropin tests at 26 and 52 weeks showed no HPA suppression in children given 100 mcg/day [7]; Ikeda 2019, 16 adults on 400 mcg/day for 6 months, plasma cortisol normal (single arm, no comparator) [15]; Skoner 2011, 187 children, cortisol changes similar to placebo at all MF doses [8].

Mechanism

Present: glucocorticoid-receptor mediated negative feedback after systemic absorption of a small fraction; exposure rises with dose and with strong CYP3A4 inhibitors (ketoconazole raised peak plasma mometasone above 200 pg/mL in 4 of 12) [3].

Class cohort test

Not class extrapolation. Mometasone was the studied drug in [3][7][8][11][12][15] and a component of the studied product in [13].

Why yellow

Hard Rule 2 cap: the evidence for a cortisol effect is strong (more than 2 independent Tier A sources) but cortisol is a hormone, not a nutrient, so it cannot be graded red or orange as a nutrient deficiency. It is carried as a mechanism clarification and monitoring prompt.

Counter-evidence held on record

Counter-evidence and confounding Cortisol suppression on assays does not equal clinical adrenal insufficiency; the labels give no incidence. Study populations were short-duration and mostly adults with asthma; sample sizes per arm were 12 to 21 in the dedicated HPA studies. Fluticasone produced larger suppression than MF in the head-to-head comparisons [11][12]. Framing caution This is a hormone effect and a monitoring prompt, not a nutrient deficiency. It does not imply any supplement. Do not present it as a vitamin or mineral finding.

Limits on what this shows

• Null findings: Nasal 100 mcg/day for 1 year [7]; inhaled 100 mcg once daily for 52 weeks [8]; short-term knemometry [9]. The Cochrane pooled estimate was not stratified to mometasone in the abstract read, so the pooled -0.48 cm/year is class-level for mometasone.
• At-risk subgroups: Children, especially at inhaled doses above the lowest labeled dose, those on other corticosteroids, and those with prolonged exposure.

Regulatory status

Nasonex OTC label: the growth rate of some children may be slower [2]. Rx labels list reduced growth velocity as a class effect; the Twisthaler label states mean reduction in growth velocity of approximately 1 cm per year (range 0.3 to 1.8) for the product class [3][4].

Population evidence

Skoner 2011 [8]: 52-week placebo-controlled trial, 187 children aged 4 to 9, MF DPI. Growth velocity difference versus placebo -0.10 +/- 0.31 cm/year (p=0.76) at 100 mcg once daily in the morning; -0.64 +/- 0.39 (p=0.10) at 100 mcg twice daily; -0.70 +/- 0.29 (p=0.02) at 200 mcg once daily in the morning. The Twisthaler label reports mean growth rates of 5.34, 5.93, 6.15 and 6.44 cm/year for the 110 mcg twice daily, 220 mcg morning, 110 mcg morning and placebo arms (n=44, 50, 48, 45) with differences versus placebo of -1.11 (95% CI -2.34 to 0.12), -0.51 (-1.69 to 0.67) and -0.30 (-1.48 to 0.89) [3]. Reconciliation attempted on 2026-10-08: the arm definitions match, because the published abstract (OpenAlex record of [8]) defines MF-DPI 100 mcg as the delivered dose with an actuated dose of 110 mcg, so the label 110 mcg arms are the paper 100 mcg arms and the label 220 mcg arm is the paper 200 mcg arm. The numeric differences do not match: the label differences versus placebo (-0.30, -0.51 and -1.11 cm/year) equal the raw gaps between the label arm means and the placebo mean of 6.44 cm/year (6.15, 5.93, 5.34), whereas the paper reports -0.10, -0.70 and -0.64 cm/year. The paper values are probably model-adjusted estimates, but this could not be confirmed because the full text is closed access (publisher page returned 403), so the gap is documented, not resolved. Neither set of figures changes the yellow Hard Rule 2 cap. Schenkel 2000 [7]: nasal MF 100 mcg once daily versus placebo for 1 year in 98 children aged 3 to 9 (82 completed: 42 MF, 40 placebo); height gain 6.95 cm versus 6.35 cm; growth rate about 0.018 cm/day, similar between groups; no CI or p-value in the records read. Agertoft/Pedersen 1999 [9]: crossover knemometry, 22 children aged 7 to 12, 2 weeks each; lower-leg growth 1.16 +/- 0.67 mm (MF 100 mcg), 0.95 +/- 0.79 (MF 200 mcg), 0.73 +/- 0.61 (budesonide 400 mcg), 0.69 +/- 0.70 (placebo); no short-term adverse effect. Cochrane 2014 [10]: 25 trials, 8,471 children, six ICS molecules including mometasone; year-1 growth velocity MD -0.48 cm/year (95% CI -0.65 to -0.30; 14 trials, 5,717 children) and height change MD -0.61 cm (-0.83 to -0.38); effect differed significantly between molecules (P<0.0001).

Mechanism

Present: systemic glucocorticoid exposure, which for mometasone is dose-dependent (see HPA entry). No micronutrient mechanism is claimed.

Class cohort test

Mometasone was in the cohort of [7][8][9]. For [10], mometasone was one of six molecules but its result was not reported separately; the pooled figure is labeled CLASS EXTRAPOLATION for mometasone, mometasone was in the cohort, and it is not used for the grade.

Why yellow

Hard Rule 2 cap. The evidence meets the strength of an orange or red outcome, but a growth outcome is not a nutrient deficiency and is not graded as one.

Counter-evidence held on record

Counter-evidence and confounding Asthma and allergic rhinitis themselves can slow growth; the trials are placebo-controlled, which addresses this. Trial durations were 2 weeks to 1 year; adult-height data for mometasone were not found (the Cochrane adult-height result is for budesonide). Label and paper numeric estimates for [8] differ (arm definitions reconcile, the cause of the numeric gap is unconfirmed); the ordering of the 200 mcg once-daily and 100 mcg twice-daily arms is reversed between the two. Framing caution This is a clinical outcome and a monitoring prompt for prescribers, not a nutrient deficiency. Do not suggest calcium, vitamin D or other supplements to treat it.

Limits on what this shows

• Null findings: Maspero 2013 [14] (1 year, supplemented, active comparator); Skoner 2011 bone markers [8]; label 440 mcg twice daily arm [3].
• At-risk subgroups: Adults on higher inhaled doses for 2 years or more, people with other BMD risk factors, people on additional corticosteroids. Not applicable to labeled nasal doses: no nasal BMD study was found.

Regulatory status

Twisthaler label sec 5.7: 2-year study, 220 mcg twice daily (103 patients), lumbar spine BMD change -0.015 (-1.43%) versus 0.002 (0.25%) placebo, described as a significant reduction; 440 mcg twice daily (87 patients) -0.018 (-1.57%) versus -0.006 (-0.43%) placebo, not statistically significant [3]. HFA label reports BMD data for the DPI only [4]. The summary does not make clear whether patient counts are per arm.

Population evidence

Maspero 2013 [14]: randomized, double-blind phase IV trial in adults with mild to moderate persistent asthma; MF 400 mcg once daily, MF 200 mcg once daily, montelukast 10 mg, fluticasone 250 mcg twice daily for 1 year, all participants on calcium and vitamin D supplements, baseline 25(OH)D at least 15 ng/mL. Lumbar spine BMD change +0.9% (MF 400), +0.7% (MF 200), +1.2% (montelukast), +1.1% (fluticasone); MF 400 versus montelukast -0.3% (95% CI -1.01 to 0.27), not significant. Femoral neck: MF 400 +0.4% versus fluticasone -0.4% (P=0.044). Sample size is not stated in the record read. Bone markers: Fardon 2004 [12] found serum osteocalcin significantly suppressed at the highest MF dose (1,600 mcg/day) in 21 adults over weekly dose steps; Skoner 2011 [8] measured serum osteocalcin and urinary N-telopeptide in 187 children and found no differences between groups.

Mechanism

Present for glucocorticoids in general: reduced osteoblast function (osteocalcin fall). No calcium or vitamin D measurement was made in any mometasone study read.

Class cohort test

Not class extrapolation: mometasone was studied in [3][8][12][14]. No nasal-route BMD data were retrieved, so the nasal route is not covered by this entry.

Why yellow

Hard Rule 2: BMD and osteocalcin are outcomes and markers, not measures of calcium or vitamin D status. Maspero's supplementation of all arms also prevents attributing any BMD result to calcium or vitamin D status.

Counter-evidence held on record

Counter-evidence and confounding Maspero 2013 compared against montelukast and fluticasone, not a no-treatment arm; supplementation may have blunted any loss; fall risk, age and smoking were not addressed in the abstract read. Label BMD patient counts are ambiguous. Framing caution This is a bone outcome entry. It does not show calcium or vitamin D deficiency and should not generate a supplement recommendation.

Limits on what this shows

• Null findings: No mometasone-specific 25(OH)D result was found. Maspero 2013 [14] required baseline 25(OH)D of at least 15 ng/mL and supplemented all arms, so it cannot test the question.
• At-risk subgroups: People on high inhaled doses or oral plus inhaled steroids, people with allergic disease (low vitamin D is reported in allergic rhinitis independent of the drug), older adults.

Regulatory status

Not mentioned in the mometasone labels retrieved [1][3][4].

Population evidence

ODS vitamin D fact sheet [18]: steroids such as prednisone can reduce calcium absorption and impair vitamin D metabolism; in NHANES 2001 to 2006 vitamin D deficiency was more than twice as common among people reporting oral steroid use (about 11% versus 5%, as relayed by the summarizing fetch; the primary NHANES paper was not opened). The cohort was oral steroid users; mometasone nasal or inhaled was not identified in the cohort. Guo 2023 [17]: RCT, 140 adults with moderate to severe allergic rhinitis, mometasone nasal spray in both arms and vitamin D added for 4 weeks in one arm (n=70 each); serum vitamin D was lower in patients with allergic rhinitis, with no numeric values in the record. This is the nutrient affecting the drug's clinical effect (Hard Rule 4), not the drug affecting the nutrient.

Mechanism

Present for systemic glucocorticoids. For mometasone the systemic fraction is under 1% by bioavailability but is pharmacologically active at higher inhaled doses [11][12], so the mechanism is plausible and unmeasured.

Class cohort test

CLASS EXTRAPOLATION. Studied class: oral steroid users (ODS and NHANES). Mometasone was not in the cohort. Capped at yellow.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication is presumed (Hard Rule 6): low vitamin D is reported in allergic rhinitis before treatment [17], and oral steroid users in NHANES have severe underlying disease. No baseline versus on-treatment 25(OH)D comparison exists for mometasone. Framing caution This is a monitoring prompt, not a deficiency claim for mometasone. The review makes no dosing recommendation for vitamin D (so no UL check is needed).

Limits on what this shows

• Null findings: None specific. No calcium measurement exists in the mometasone studies read.
• At-risk subgroups: As for vitamin D.

Regulatory status

Not mentioned in the mometasone labels retrieved [1][3][4].

Population evidence

ODS vitamin D fact sheet [18]: steroids such as prednisone can reduce calcium absorption (oral steroids). The ODS calcium fact sheet interactions section does not list corticosteroids [19]. No mometasone study read reported serum or urinary calcium. Maspero 2013 gave calcium and vitamin D to all arms [14].

Mechanism

Present for systemic glucocorticoids (reduced intestinal absorption, increased renal loss); unmeasured for mometasone at any route.

Class cohort test

CLASS EXTRAPOLATION. Studied class: systemic (oral) steroids as characterized by a reference sheet, with no named cohort. Mometasone was not in the cohort. Capped at yellow.

Counter-evidence held on record

Counter-evidence and confounding The calcium fact sheet lists other drug classes but not corticosteroids [19], so the NIH sources are inconsistent with each other. Reduced BMD (separate entry) is not evidence of calcium deficiency. Framing caution This is a monitoring prompt only. No calcium supplement is recommended here; none is needed to read this entry.

Limits on what this shows

• Null findings: Ikeda 2019 normal HbA1c [15]; Mizrachi 2012 no pooled nasal steroid change [27]; combination label infrequent clinically significant glucose changes [32]; oral rat dosing without glucose intolerance [23].
• At-risk subgroups: People with diabetes on higher inhaled doses, infants and small children with diabetes using larger off-label airway steroid doses, and people also on other corticosteroids.

Regulatory status

No hyperglycemia statement in the Twisthaler label text read in this repair [3]. The mometasone/formoterol combination label states that clinically significant changes in blood glucose or serum potassium were seen infrequently at recommended doses and attributes hypokalemia to the beta2-agonist [32].

Population evidence

Tier B, this drug: Zimath 2023 [23], rats of both sexes dosed daily for 7 days by intraperitoneal injection or oral gavage, with dexamethasone as positive control and mifepristone to test glucocorticoid receptor dependence: injected mometasone caused glucose intolerance in males (none in females) and dyslipidemia in both sexes; oral gavage caused neither; insulin sensitivity was attenuated and pancreatic beta-cell mass increased regardless of sex or route; effects were receptor-dependent and reversible. Doses and numeric values are not in the abstract. Human, mometasone: Ikeda 2019 [15], 16 adults on nasal mometasone 400 mcg/day for 6 months, HbA1c within normal ranges in all, no comparator. Ben-Dov 2023 [24], one 9-month-old with type 1 diabetes whose daily glucose rose by 40 to 50 points (units not stated) on dexamethasone-containing otic drops and normalized within 2 days after switching to mometasone 0.05% nasal spray; the rise was attributed to dexamethasone and the case is one patient. Class level, mometasone not confirmed in the cohort: Slatore 2009 [25], 1,698 US veterans, ICS dose expressed as triamcinolone equivalents (agents not named), no glucose association in people without diabetes and +1.82 mg/dL per 100 mcg ICS in people with self-reported diabetes (95% CI 0.49 to 3.15; P=.007); Faul 2009 [26], 10 completers, crossover, fluticasone 880 mcg/day versus montelukast in type 2 diabetes, HbA1c difference 0.25% (SD 0.29; P=.025), below the authors' 0.5% clinical threshold; Mizrachi 2012 [27], 1,768 people with diabetes on nasal steroid sprays, no change in HbA1c (n=245; P=.104) or fasting glucose (n=163; P=.101) at 3 months, with triamcinolone giving a larger glucose rise (P=.006) and mometasone not named in the abstract.

Mechanism

Present: glucocorticoid-receptor mediated insulin resistance, shown receptor-dependent in the rat study [23]. The route difference in rats is consistent with low systemic exposure by the oral route, but human exposure at labeled nasal and inhaled doses was not measured against glucose.

Class cohort test

Mometasone-specific support is Tier B only [23]. [25][26][27] are CLASS EXTRAPOLATION for mometasone: mometasone was not in the fluticasone trial [26], was not confirmed in [25] or [27]. [24] is a single case that points away from a mometasone glucose rise. Capped at yellow.

Why yellow

Tier B plus class-level Tier C support, and Hard Rule 2: hyperglycemia is a metabolic disturbance, not a nutrient. Rat dosing and route do not map to labeled human use.

Counter-evidence held on record

Counter-evidence and confounding Confounding by indication and disease severity affect [25]; the sample in [26] is 10 people; [27] and [25] cannot be attributed to mometasone. The PubMed MeSH list for [23] includes an inhalation term although the abstract describes injection and gavage, which may be an indexing error. Framing caution This is a glucose disturbance and a monitoring prompt for people with diabetes, not a nutrient finding. It does not imply any dietary or supplement change.

Limits on what this shows

• Why no grade: The dual condition in Step 7 is met: no Tier B or Tier C evidence was retrieved that supports even a yellow grade, and no circulating consumer claim for this category was found for mometasone in the repair audit (two consumer depletion charts opened, neither names mometasone or lists this category). Oropharyngeal candidiasis occurred in 4 to 6% of Twisthaler users versus 2% on placebo (195 of 3,007 patients overall) [3]; HFA 0.5 to 0.8% versus 0.5% placebo [4]; the EMC SmPC lists "disturbances of taste and smell" as frequency not known [35]; epistaxis rates are in the PK section [1]. These are adverse events; no appetite, swallowing or intake outcome was measured, so mechanism H (changed intake) is named but unmeasured, and no nutrient follows from it. Mometasone esophageal formulations improved dysphagia in eosinophilic esophagitis (opposite direction, different formulation and population, listing summaries only).

Channels tried

First review: PubMed mometasone AND (zinc OR magnesium OR dysgeusia OR dysphagia OR appetite OR dietary intake), 12 records, none showing a nutrient or intake effect in mometasone-treated airway patients. Repair: WebSearch "mometasone nasal spray dysgeusia OR anosmia OR taste OR appetite OR weight loss adverse effect food intake" (patient information pages and a hyposmia paper by title only); EMC SmPC opened [35]; Twisthaler label remainder read [3].

Gap type

Genuine gap.