Abstract
Introduction
Nasal congestion/obstruction (NC) contributes to the high disease burden in patients with severe chronic rhinosinusitis with nasal polyps (CRSwNP). Patient perception of NC may not accurately reflect nasal patency, while peak nasal inspiratory flow (PNIF) is an objective method with established thresholds for normal nasal airflow. This analysis evaluated the association between NC and PNIF and the impact of baseline PNIF on dupilumab efficacy in patients with severe CRSwNP.
Methods
This was a post hoc analysis of patients treated with placebo or dupilumab 300 mg every 2 weeks in the SINUS-24 (NCT02912468) and SINUS-52 (NCT02898454) phase III studies. Patients provided daily e-diary measures of PNIF (L/min) using PNIF meters, and NC by patient-reported evaluation of severity (scored 0–3). Other assessed outcomes were nasal polyp score (NPS), 22-item Sinonasal Outcome Test (SNOT-22), loss of smell (LoS), University of Pennsylvania Smell Identification Test (UPSIT), and Lund–Mackay computed tomography. Outcomes were assessed in two subgroups: baseline PNIF < 120 L/min and ≥ 120 L/min.
Results
Of 724 patients, 552 (76%) had PNIF < 120 L/min and 172 (24%) had PNIF ≥ 120 L/min at baseline. The PNIF < 120 L/min subgroup had higher mean scores for NPS and SNOT-22 and more smell impairment (LoS and UPSIT). PNIF weakly correlated with NC at baseline (Spearman coefficient − 0.348 [95% CI − 0.410, − 0.282], P < 0.0001). Correlations between change from baseline in PNIF and NC at week 24 were weak in the dupilumab group (− 0.390 [− 0.468, − 0.305], P < 0.0001) and moderate in the placebo group (− 0.497 [− 0.582, − 0.399], P < 0.0001).
Conclusion
These results confirm PNIF as a valuable method for assessing nasal obstruction in patients with severe CRSwNP. The degree of nasal flow impairment at baseline does not impact dupilumab’s efficacy.
A graphical abstract and video abstract are available for this article.
Supplementary Information
The online version contains supplementary material available at 10.1007/s12325-025-03378-2.
Keywords: CRSwNP, Dupilumab, Nasal airflow, Nasal congestion, Nasal polyps, PNIF, Smell
Plain Language Summary
Chronic rhinosinusitis with nasal polyps (CRSwNP) causes narrowing, and sometimes complete blockage, of the air passages in the nose, making it difficult to breathe. This can impact a person’s ability to smell, taste, sleep, and perform daily activities, which in turn negatively impacts their overall quality of life. Measures of nasal congestion and loss of smell rely on people’s self-perceptions, which can vary and may not reflect the actual level of congestion seen when cameras are inserted into the nose. This article looks at a measure of nasal airflow called peak nasal inspiratory flow (PNIF), a non-invasive method for directly measuring airflow through the nose, and how this compares with the patient-reported measures nasal congestion and loss of smell. Data from two studies (SINUS-24 and SINUS-52) assessing the effects of a drug called dupilumab in people with severe CRSwNP were used. Patients were grouped according to their PNIF scores at recruitment (a PNIF measure of less than 120 L per minute indicated poor nasal airflow). Results showed a relationship between low PNIF and severe nasal congestion and loss of smell, suggesting PNIF may be a useful and convenient method for directly assessing nasal airflow. The study also shows that dupilumab was effective for patients with severe CRSwNP regardless of nasal airflow quality at the beginning of the studies.
Video Abstract (MP4 157916 KB)
Graphical Abstract
Supplementary Information
The online version contains supplementary material available at 10.1007/s12325-025-03378-2.
Key Summary Points
| Nasal congestion contributes to the high disease burden in patients with severe chronic rhinosinusitis with nasal polyps (CRSwNP). |
| The patient-reported assessment of nasal congestion in CRSwNP can be subject to patient perception, making a reliable, objective, non-invasive measure of nasal airflow useful for more consistent assessment. |
| Peak nasal inspiratory flow (PNIF) was significantly correlated with nasal congestion and loss of smell scores, both at baseline and in changes from baseline to 24 weeks. |
| PNIF is a valuable, non-invasive method for assessing nasal obstruction in patients with severe CRSwNP. |
| The level of impairment of nasal airflow at baseline (< 120 L/min vs ≥ 120 L/min) did not impact the efficacy of dupilumab. |
Digital Features
This article is published with digital features, including a graphical abstract and a video abstract, to facilitate understanding of the article. To view digital features for this article, go to 10.6084/m9.figshare.30104854.
Introduction
Nasal congestion is one of the cardinal symptoms of chronic rhinosinusitis with nasal polyps (CRSwNP) and is recognized as contributing to the high burden of disease in patients with this condition [1, 2]. The severity of nasal congestion in clinical trials is often assessed using patient-reported measures such as the nasal congestion/obstruction (NC) score. However, patient perception of nasal congestion may not be a good indicator of obstruction [3, 4], which highlights the need for reliable, objective tools to measure this important symptom. Peak nasal inspiratory flow (PNIF) is a simple, reliable, and objective method [3, 4] to determine nasal patency, for which a threshold of ≥ 120 L/min has been established for normal nasal airflow [5–9]. PNIF has been shown to better correlate with nasal congestion and overall sinonasal symptoms than other objective methods of measuring obstruction, such as acoustic rhinometry or four-phase rhinomanometry [10].
CRSwNP is an inflammatory disease with multiple endotypes, primarily characterized by type 2 endotype in Europe and North America, and a rising prevalence of type 2 disease in other parts of the world, in which the cytokines interleukin (IL)-4 and IL-13 are key and central drivers [11–16]. Dupilumab, a fully human VelocImmune®-derived monoclonal antibody [17, 18], binds to IL-4Rα, the shared receptor component for IL-4 and IL-13, thereby inhibiting type 2 inflammatory responses [19].
In the phase III SINUS-24 (NCT02912468) and SINUS-52 (NCT02898454) studies, dupilumab significantly improved objective and patient-reported outcomes in patients with uncontrolled CRSwNP versus placebo [20]. Patients treated with dupilumab demonstrated improvement in nasal congestion based on the patient-reported NC score [20, 21].
The aim of the current analysis is to evaluate the association between PNIF, NC, and a range of objective and patient-reported outcomes in patients from the SINUS studies at baseline and following treatment.
Methods
Ethical Approval
The SINUS-24 and SINUS-52 studies were conducted according to the principles laid down in the Declaration of Helsinki. Institutional review boards and independent ethics committees reviewed and approved the protocols, informed consent forms, and patient information before study initiation. A full list is available in the supplementary materials.
Study Design and Patients
This was a post hoc analysis of the randomized, double-blind, placebo-controlled SINUS-24 and SINUS-52 studies, details of which were previously published [20]. Eligible patients had to be ≥ 18 years of age with bilateral nasal polyps and symptoms of chronic rhinosinusitis despite intranasal corticosteroid treatment, and have received systemic corticosteroids in the 2 years before randomization, or have undergone sinonasal surgery. At screening, patients had to have a minimum nasal polyp score (NPS) of 5 (range 0–8), with a score of ≥ 2 for each nostril. Patients also had to experience nasal congestion and at least one of the following: loss of smell and anterior or posterior nasal discharge.
Patients were randomized to subcutaneous (SC) administration of dupilumab 300 mg (1:1) or matching placebo every 2 weeks (q2w) for 24 weeks in SINUS-24, or to dupilumab 300 mg SC q2w for 52 weeks, matching placebo q2w for 52 weeks, or dupilumab 300 mg SC q2w for 24 weeks, then every 4 weeks for 28 weeks in SINUS-52. All patients received background therapy of 100 mg of mometasone furoate nasal spray (MFNS) in each nostril twice daily.
Trial conduct and documentation of the original SINUS-24 and SINUS-52 studies was overseen by the local institutional review board or ethics committee at each study center (see Supplementary Material Table S1). The study was conducted in accordance with the Helsinki Declaration of 1964. All patients provided written informed consent before participating in the trials.
Assessments
PNIF was recorded daily by the patients using PNIF meters supplied by the study investigator. Patients were to take three PNIF measurements (L/min) each morning before taking MFNS and record all three values in an e-diary. The highest value was used for evaluation. Baseline PNIF was the mean value over the 7 days before randomization, when four or more assessments were collected; if fewer than four assessments were collected over those 7 days, the mean of the four most recent assessments was taken. A PNIF response was defined as achieving the minimal clinically important difference (MCID) of 20 L/min [22].
Other outcomes assessed were changes from baseline to week 24 in NPS (range 0–8), NC score (0–3), 22-item Sinonasal Outcome Test (SNOT-22) total score (0–110), loss of smell (LoS) score (0–3), University of Pennsylvania Smell Identification Test (UPSIT) score (0–40), and Lund–Mackay computed tomography (LMK-CT) score (0–24). Symptom scores were either 7-day means when four or more assessments were collected, or the mean of the four most recent assessments.
Statistical Analyses
The analysis used pooled data from the intention-to-treat (ITT) populations of SINUS-24 and SINUS-52 in patients treated with placebo or dupilumab 300 mg q2w through to week 24. Outcomes were assessed for two subgroups: patients with baseline PNIF of < 120 L/min and patients with baseline PNIF of ≥ 120 L/min. Comparisons between dupilumab and placebo within each PNIF subgroup were analyzed using an analysis of covariance with the corresponding baseline value, treatment group, prior surgical history, asthma/non-steroidal anti-inflammatory-exacerbated respiratory disease (NSAID-ERD) status, region, and study indicator as covariates. Missing data were imputed using the worst observation carried forward. No between-subgroup statistical analyses were conducted. Associations between PNIF and NC, LoS, and UPSIT at baseline, and associations between changes in PNIF and NC, LoS, and UPSIT from baseline to week 24 for the placebo and dupilumab-treated groups, were analyzed using Spearman correlation.
Results
Baseline Characteristics
Of 724 patients in the pooled ITT population, 552 (76%) had impaired nasal inspiratory airflow (PNIF < 120 L/min) and 172 (24%) had PNIF ≥ 120 L/min at baseline. The PNIF < 120 L/min subgroup had a lower proportion of men than the PNIF ≥ 120 L/min subgroup (56% vs 75%) and higher mean scores for both NPS (6.2 vs 5.4, respectively) and SNOT-22 (53.3 vs 43.3, respectively); smell impairment (LoS and UPSIT mean scores) was also slightly worse in the PNIF < 120 L/min group. Other baseline characteristics were generally similar between the two groups overall (Table 1), and between the placebo and dupilumab groups across both subgroups (Supplementary Material Table S2).
Table 1.
Baseline characteristics for the two PNIF subgroups
| Baseline PNIF < 120 L/min (n = 552) | Baseline PNIF ≥ 120 L/min (n = 172) | |
|---|---|---|
| Age, years | 52.0 (12.9) | 49.4 (12.4) |
| Male, n (%) | 308 (55.8) | 129 (75.0) |
| Time since diagnosis, years | 10.9 (9.5) | 11.4 (9.3) |
| Prior sinonasal surgery, n (%) | 346 (62.7) | 113 (65.7) |
| PNIF, L/min | 62.5 (31.9) | 165.8 (42.9) |
| NPS | 6.2 (1.3) | 5.4 (1.0) |
| NC | 2.5 (0.6) | 2.2 (0.6) |
| UPSIT | 13.6 (7.9) | 15.1 (9.2) |
| LoS | 2.8 (0.5) | 2.6 (0.6) |
| SNOT-22 | 53.3 (20.3) | 43.3 (20.0) |
| LMK-CT | 18.6 (4.0) | 17.7 (4.3) |
Values are mean (SD) unless otherwise stated
LMK-CT Lund–Mackay computed tomography, LoS loss of smell, NC nasal congestion/obstruction, NPS nasal polyp score, PNIF peak nasal inspiratory flow, SD standard deviation, SNOT-22 22-item Sinonasal Outcome Test, UPSIT University of Pennsylvania Smell Identification Test
Association Between PNIF and NC, LoS, and UPSIT at Baseline
At baseline, there were significant but weak correlations between PNIF and NC (Spearman correlation coefficient − 0.348 [95% CI − 0.410, − 0.282]), P < 0.0001; LoS (− 0.191 [− 0.260, − 0.119]), P < 0.0001; and UPSIT (0.123 [0.049, 0.194]), P = 0.0011 (Fig. 1).
Fig. 1.
Associations at baseline between PNIF and NC (A), LoS (B), and UPSIT (C) (combined SINUS-24 and SINUS-52 ITT). PNIF, NC, LoS, and UPSIT values are the average of the prior 7 days’ patient e-diary recordings. If fewer than four measurements were collected within 7 days before randomization, the baseline was the average of the four most recent measurements before randomization. ITT intention-to-treat, LoS loss of smell, NC nasal congestion/obstruction, PNIF peak nasal inspiratory flow, UPSIT University of Pennsylvania Smell Identification Test
Association Between Changes from Baseline in PNIF and NC, LoS, and UPSIT
In the dupilumab treatment group, the changes from baseline in PNIF were weak but significantly correlated with the changes from baseline at week 24 and 52 in NC (− 0.390 [95% CI − 0.468, − 0.305], P < 0.0001) and (− 0.312 [95% CI − 0.424, − 0.201], P < 0.0001), respectively, LoS (− 0.250 [− 0.337, − 0.158], P < 0.0001), and UPSIT (0.180 [0.085, 0.272], P = 0.0002). In the placebo treatment group, PNIF also showed significant weak-to-moderate correlations with NC (− 0.497 [− 0.582, − 0.399], P < 0.0001) and LoS (− 0.336 [− 0.439, − 0.223], P < 0.0001), but not with UPSIT (0.078 [− 0.045, 0.199], P = 0.212) (Figs. 2, 3, 4). The direction of correlation was consistent for dupilumab and placebo arms: improvement in PNIF was associated with clinical improvements in NC, LoS, and UPSIT.
Fig. 2.
Associations between change in PNIF and NC from baseline to week 24 in patients treated with placebo (A) or dupilumab 300 mg q2w (B), and from baseline to week 52 in patients treated with placebo (C) or dupilumab 300 mg q2w (D). Calculated using PNIF and NC monthly average values. NC nasal congestion/obstruction, PNIF peak nasal inspiratory flow, q2w every 2 weeks
Fig. 3.
Associations between change in PNIF and LoS from baseline to week 24 in patients treated with placebo (A) or dupilumab 300 mg q2w (B). Calculated using PNIF and LoS monthly average values. LoS loss of smell, PNIF peak nasal inspiratory flow, q2w every 2 weeks
Fig. 4.
Associations between change in PNIF and UPSIT from baseline to week 24 in patients treated with placebo (A) or dupilumab 300 mg q2w (B). Calculated using PNIF and UPSIT monthly average values. PNIF peak nasal inspiratory flow, q2w every 2 weeks, UPSIT University of Pennsylvania Smell Identification Test
Change from Baseline in PNIF and Other CRSwNP Outcomes
Patients in the impaired and normal airflow groups both showed significant improvements in CRSwNP outcomes following dupilumab treatment versus placebo at week 24. Least squares mean differences (95% CI) in the PNIF < 120 L/min and ≥ 120 L/min subgroups, respectively, were PNIF 41.2 (33.8, 48.5) and 29.5 (15.9, 43.1); NPS − 1.86 (− 2.12, − 1.59) and − 2.01 (− 2.47, − 1.54); NC − 0.81 (− 0.96, − 0.67) and − 1.10 (− 1.32, − 0.89); LoS − 1.03 (− 1.18, − 0.89) and − 1.02 (− 1.30, − 0.75); SNOT-22 − 18.86 (− 21.97, − 15.75) and − 18.03 (− 23.18, − 12.88); UPSIT 10.03 (8.71, 11.35) and 11.41 (8.91, 13.91); and LMK-CT − 5.99 (− 6.63, − 5.36) and − 6.33 (− 7.43, − 5.23) (Supplementary Material Fig. S1). The proportion of patients achieving an MCID improvement of ≥ 20 L/min at week 24 was also significantly greater with dupilumab versus placebo in both subgroups: 78.4% versus 42.9% (odds ratio [95% CI] 4.68 [3.18, 6.88]) in the PNIF < 120 L/min subgroup and 62.7% versus 38.7% (2.61 [1.28, 5.30]) in the PNIF ≥ 120 L/min subgroup. The rate of systemic corticosteroid rescue treatment was 9.4% in the dupilumab group and 30.8% in the placebo group.
Discussion
The results of this analysis demonstrate that more than three-quarters of patients with severe CRSwNP from the combined SINUS study population had impaired nasal airflow at baseline, on the basis of a PNIF reading below the normal threshold of 120 L/min. The baseline characteristics of these patients showed a number of differences when compared with those of patients with nasal airflow above the normal threshold. Patients in the impaired nasal airflow subgroup had higher mean values for NPS and for SNOT-22. A greater nasal polyp burden may be expected to result in reduced nasal airflow, while higher SNOT-22 scores indicate more severely impacted health-related quality of life in these patients, which is consistent with previous findings that nasal obstruction is one of the most important CRSwNP symptoms affecting health-related quality of life [1, 2, 23]. LoS was evident across the SINUS population, regardless of baseline PNIF, although the subgroup with below normal nasal airflow had lower mean UPSIT scores and higher mean scores for LoS, indicating more smell impairment among these patients. Taken together, these findings suggest that routine measurement of nasal airflow using PNIF may be a simple and reliable tool that can provide complementary information alongside other measures for clinicians to identify patients with CRSwNP with higher disease burden. In support of this, previous studies have shown PNIF to be better correlated with patient-reported nasal obstruction and overall sinonasal symptoms than other objective methods of measuring obstruction, such as acoustic rhinometry and four-phase rhinomanometry [10, 24]. Among the patients in this analysis with impaired nasal airflow at baseline, nearly 80% experienced clinically meaningful improvements in PNIF with dupilumab treatment over 24 weeks. While the magnitude of improvement in PNIF was greater in the baseline < 120 L/min subgroup than in the ≥ 120 L/min subgroup, most patients in the latter group also experienced clinically meaningful PNIF improvements over 24 weeks. Moreover, in both subgroups, dupilumab treatment was associated with significant improvements in all the other assessed clinical measures. In contrast to the improvements in PNIF, improvements in NPS, LoS, NC, UPSIT, LMK-CT, and SNOT-22 were of similar magnitude between the < 120 and ≥ 120 L/min baseline PNIF subgroups. These findings suggest a substantial degree of independence between improvements in PNIF and improvements in other measures of CRSwNP. One possible mechanism contributing to this relative independence might be that PNIF is impacted more by inferior turbinate congestion than it is by polyps. The improvement of > 20 L/min in about 40% of placebo subjects suggests that the measurement is dynamic, and not explained by relatively fixed obstruction caused by nasal polyps. If reduced nasal polyp burden does not fully account for the improved nasal airflow with dupilumab, other potential mechanisms, such as reduction in inferior turbinate congestion, could explain some of the improvement in the placebo group with intranasal corticosteroids alone. However, rates of rescue with systemic corticosteroids were lower in the dupilumab group than the placebo group, suggesting most clinical improvements in SINUS-24 and SINUS-52 can be attributed to dupilumab treatment.
The significant but weak correlation between PNIF and NC, LoS, and UPSIT agrees with previous findings of weak correlation between PNIF and other subjective measures of NC, namely: nasal patency and visual analog scale for nasal obstruction [10, 25]. Similarly, change in PNIF was weakly but significantly correlated with change in NC and LoS following 24 weeks of dupilumab treatment, which is consistent with the observed relative independence of PNIF improvements from improvements in other CRSwNP disease parameters, including NC.
Conclusion
Assessment using PNIF meters has the potential to be a simple, reliable, objective, and useful method for evaluating disease burden in patients with CRSwNP. The degree of nasal flow impairment at baseline does not appear to impact the efficacy of dupilumab in patients with severe CRSwNP.
Supplementary Information
Below is the link to the electronic supplementary material.
Acknowledgements
Medical Writing/Editorial Assistance
Medical writing/editorial assistance provided by Jane Burch, PhD, of Adelphi Group, Macclesfield, UK, funded by Regeneron Pharmaceuticals Inc. and Sanofi, in accordance with the Good Publication Practice guidelines.
Author Contributions
Martin Desrosiers, Scott Nash, Andrew Lane, Stella E. Lee, Eugenio De Corso, Changming Xia, Mark Corbett, Amr Radwan, Paul J. Rowe, and Yamo Deniz made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising, or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
Funding
Research and Open Access fee sponsored by Regeneron Pharmaceuticals Inc. and Sanofi. ClinicalTrials.gov Identifiers: NCT02912468, NCT02898454. The authors would like to thank Harry Sacks (Regeneron Pharmaceuticals Inc.) and Juby Jacob-Nara (former employee of Sanofi) for providing insights and guidance.
Data Availability
The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.
Declarations
Conflict of Interest
Martin Desrosiers reports clinical trial funding from AstraZeneca, GSK, Probionase Therapies, and Sanofi, is a stock shareholder in Probionase Therapies, and is an advisory board member/consultant for Regeneron Pharmaceuticals Inc. Andrew Lane is an advisory board member for Regeneron Pharmaceuticals Inc. and Sanofi. Stella E. Lee is an advisory board member for and reports clinical trial finding from AstraZeneca, Genentech, GSK, Regeneron Pharmaceuticals Inc., and Sanofi, and reports publication support from AstraZeneca, GSK, Regeneron Pharmaceuticals Inc., and Sanofi. Eugenio De Corso is an advisory board member/consultant for and reports clinical trial funding and publication support from AstraZeneca, GSK, Novartis, and Sanofi. Scott Nash, Changming Xia, Amr Radwan, and Yamo Deniz are employees of Regeneron Pharmaceuticals Inc. and may hold stock and/or stock options in the company. Mark Corbett and Paul J. Rowe are employees of Sanofi and may hold stock and/or stock options in the company.
Ethical Approval
The SINUS-24 and SINUS-52 studies were conducted according to the principles laid down in the Declaration of Helsinki. Institutional review boards and independent ethics committees reviewed and approved the protocols, informed consent forms, and patient information before study initiation. A full list is available in the supplementary materials.
Footnotes
Prior Presentation: Some of the data in this manuscript were originally presented at the European Rhinologic Society congress, June 18–22, 2023, Sofia, Bulgaria.
This article was revised due to retrospective open access request.
Publisher's Note
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Change history
12/24/2025
A Correction to this paper has been published: 10.1007/s12325-025-03444-9
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.