Bronchial asthma is a chronic inflammatory disorder of the airways characterised by reversible airflow obstruction, bronchial hyperresponsiveness, and a spectrum of respiratory symptoms including wheezing, breathlessness, and chest tightness [1]. It affects approximately 300 million individuals worldwide, imposing a substantial burden on healthcare systems and on patients’ quality of life [2]. In India, the estimated prevalence ranges between 3% and 10%, with higher rates in urban areas attributed to pollution and allergen exposure [3]. Although the pathophysiology of asthma centres on the lower respiratory tract, accumulating evidence supports a complex interplay between the upper and lower airways, often termed the “united airway hypothesis” [4]. This framework proposes that inflammatory processes in the upper respiratory tract, particularly the paranasal sinuses, may exacerbate or contribute to the severity of lower airway disease.

The paranasal sinuses — the frontal, ethmoid, maxillary, and sphenoid sinuses — are air-filled cavities that communicate with the nasal cavity through their ostia and participate in humidification and filtration of inspired air. They are also prone to inflammation, infection, and obstruction, collectively referred to as sinusitis [5]. Chronic rhinosinusitis (CRS), a persistent inflammation of the sinonasal mucosa, is increasingly recognised as a comorbidity of asthma, with reported prevalence rates of 20–60% in asthmatic populations compared with 5–15% in the general population [6]. The pathophysiological link between CRS and asthma is thought to involve shared inflammatory pathways, including type 2 immune responses mediated by interleukins (IL-4, IL-5, IL-13), eosinophilic infiltration, and mucosal remodelling [7]. Sinus inflammation may additionally trigger asthma exacerbations through mechanisms such as postnasal drip, systemic cytokine release, and neural reflex pathways [4].

The concept that nasal and bronchial disease coexist is well established; up to 80–90% of asthmatics report rhinitis symptoms, and inflammation in one region influences the other through local and systemic pathways [8]. Chronic sinus disease in severe asthma has been shown to relate to sputum eosinophilia, reinforcing the notion of a shared eosinophilic endotype that spans the respiratory tract [9]. These observations position asthma and paranasal sinus pathology as interconnected components of a single airway rather than isolated conditions.

Computed tomography (CT) has emerged as the reference standard for evaluating paranasal sinus pathology because of its superior spatial resolution and clear delineation of bony structures, mucosal thickening, and ostiomeatal complex obstruction [10]. Its sensitivity for detecting mucosal abnormalities substantially exceeds that of plain radiography and nasal endoscopy [13]. The Lund-Mackay scoring system provides a reproducible, standardised means of quantifying sinus opacification on CT, making it an indispensable metric in research and clinical practice [11]. A refinement of this system — the Modified Lund-Mackay (Zinreich) score, which grades each sinus from 0 to 5 according to the degree of opacification and the ostiomeatal complex from 0 to 2 — is considered a better representative of disease burden [12].

Despite the diagnostic utility of CT, the cross-sectional prevalence and severity of paranasal sinus abnormalities in asthma, as assessed by CT, have not been adequately characterised across diverse populations, and most studies have examined allergic rhinitis or CRS as isolated entities rather than at their intersection with asthma [6]. Geographical, environmental, and ethnic factors may modulate sinonasal inflammation and its impact on asthma, necessitating region-specific investigation. Objective imaging can non-invasively quantify the extent of sinus involvement, identify anatomical predispositions, and correlate imaging findings with clinical parameters, thereby informing risk stratification and therapeutic decisions [9]. Against this background, the present cross-sectional study was undertaken with two objectives: (i) to evaluate the incidence of changes on CT of the paranasal sinuses in patients with bronchial asthma, and (ii) to assess the degree and severity of rhinosinusitis radiologically. We hypothesised that patients with bronchial asthma would exhibit a high burden of paranasal sinus abnormalities and that the severity of sinus disease would correlate with poorer asthma outcomes.

Study design and setting This was a hospital-based cross-sectional study conducted in the Department of Radio-diagnosis at Bangalore Medical College and Research Institute (BMCRI), Bengaluru, over an 18-month period from May 2023 to October 2024. Patients diagnosed with bronchial asthma who attended the outpatient and inpatient departments of Otorhinolaryngology and Pulmonary Medicine were referred for CT of the paranasal sinuses, and all imaging was performed at a single centre to ensure uniformity of equipment, protocol, and reporting expertise. The design captured a snapshot of paranasal sinus abnormalities at a single point in time without longitudinal follow-up. Participants Adults older than 18 years with a confirmed diagnosis of bronchial asthma based on clinical examination and the Global Initiative for Asthma (GINA) 2022 criteria, who were willing to provide written informed consent, were eligible for inclusion [1]. Patients were excluded if they had an episode of rhinosinusitis within the preceding 4 weeks, a diagnosis of pneumonia at enrolment, a requirement for mechanical ventilation, a nasogastric tube in situ, pregnancy, or were unwilling to provide informed and written consent. Sample size The sample size was calculated using the formula for estimating a single proportion, n = (Z² × p × (1 − p)) / d². Based on the study by Zamarron et al., in which mucosal thickening was observed in 70.5% of 161 adults with severe asthma, the expected proportion (p) was set at 0.705 [14]. With a Z-score of 1.96 corresponding to a 95% confidence level and an absolute precision (d) of 0.105, the calculation yielded a required sample size of approximately 72 subjects. Seventy-two participants were therefore enrolled. Imaging technique and protocol After written informed consent was obtained and Institutional Ethics Committee clearance secured, a detailed clinical history of bronchial asthma was recorded for each participant, including symptoms of episodic wheezing, shortness of breath, cough, and chest tightness, together with duration of asthma, frequency of acute exacerbations in the preceding 6 months, and current treatment status. Eligible patients underwent CT of the paranasal sinuses using a 128-slice CT scanner (Philips Ingenuity 128 Elite) with the patient supine. The scan extended from the hard palate to the superior margin of the frontal sinuses in a caudocranial direction with a slice thickness of 1 mm, and each acquisition lasted approximately 10 seconds. Imaging parameters were a field of view of 350 mm, 100 kV, and 300 mAs, with coronal and sagittal multiplanar reconstructions (Figure 1). CT images were assessed using the Modified Lund-Mackay scoring system, in which the percentage opacification of each paranasal sinus caused by mucosal thickening is graded from 0 to 5 (0 = 0%; 1 = <25%; 2 = 26–50%; 3 = 51–75%; 4 = 76–99%; 5 = 100%) and the ostiomeatal complex from 0 to 2 (0 = normal, 1 = partially obstructed, 2 = completely obstructed), scored separately for each side to give a maximum total of 54 [11,12]. Additional structures — the nasal septum, ethmoid air cells, turbinates, orbits, and visualised brain parenchyma — were examined to provide a comprehensive radiological profile, with specific attention to mucosal thickening and polyposis. Figure 1. Representative coronal non-contrast CT of the paranasal sinuses (bone window) demonstrating the standard coronal reconstruction used in this study. The maxillary and ethmoid sinuses are well aerated and the ostiomeatal complexes are patent, with an incidental leftward deviation of the nasal septum. Statistical analysis Data were entered into Microsoft Excel and summarised using descriptive statistics, with continuous variables expressed as mean ± standard deviation (SD). Categorical associations were assessed using the Chi-square test or Fisher’s exact test, differences in mean scores across age groups using analysis of variance (ANOVA), and relationships between the Modified Lund-Mackay score and continuous clinical parameters using correlation analysis. A p-value less than 0.05 was considered statistically significant. Results are presented in accordance with STROBE recommendations for observational studies.

Table 1. Baseline demographic and clinical characteristics of study participants (n=72).

Seventy-two patients with bronchial asthma were enrolled. The mean age was 35.15 ± 6.94 years (range 24–56 years), and nearly half of the participants (47.22%, n=34) were aged 31–40 years, indicating a predominantly young and middle-aged cohort. Males accounted for 56.94% (n=41) and females for 43.06% (n=31), a male-to-female ratio of approximately 1.32:1. The mean duration of asthma was 13.18 ± 5.35 years (range 2–30 years), and participants experienced a mean of 3.58 ± 2.89 acute exacerbations in the preceding 6 months. Only 37.50% (n=27) of patients were currently on treatment for bronchial asthma, while 62.50% (n=45) were not (Table 1).

Table 2. Overall incidence and severity distribution of CT paranasal sinus changes (n=72).

Abnormal CT findings in the paranasal sinuses were present in 70 of 72 patients (97.22%), with only 2.78% (n=2) showing normal scans. The mean total Modified Lund-Mackay score was 25.38 ± 12.88 (range 0–51). Based on severity categories, moderate changes (score 21–40) were the predominant pattern, seen in 59.72% (n=43) of patients, while 27.78% (n=20) had mild changes (score 1–20), 9.72% (n=7) had severe changes (score >40), and 2.78% (n=2) had normal findings (Table 2, Figure 7).

Sinus-specific analysis showed that the right maxillary sinus was most frequently involved (90.28%, n=65), followed by the right frontal sinus and left maxillary sinus (both 88.89%, n=64). The highest mean severity scores were recorded in the right anterior ethmoid sinus (2.64 ± 1.59) and the right posterior ethmoid sinus (2.57 ± 1.50), whereas the left compartment of the sphenoid sinus showed the lowest involvement rate (69.44%, n=50) and the lowest mean score (1.60 ± 1.44). A slightly higher involvement of right-sided sinuses compared with left-sided sinuses was observed, with the ethmoid sinuses demonstrating the most severe opacification (Table 3, Figures 2–4 and 8).

Figure 2. Axial non-contrast CT (bone window) at the level of the frontal sinuses showing bilateral frontal sinus mucosal thickening and opacification (bilateral frontal sinusitis).

Figure 3. Coronal non-contrast CT (bone window) showing bilateral maxillary and ethmoid sinus mucosal disease (bilateral maxillary and ethmoid sinusitis) with hypertrophy of the left inferior turbinate.

Figure 4. Axial non-contrast CT (bone window) in two representative patients (A, B) showing bilateral ethmoid sinus mucosal opacification (bilateral ethmoid sinusitis).

Associated anatomical variations were common. Nasal septal deviation was the most frequent (65.28%, n=47), followed by inferior turbinate hypertrophy (59.72%, n=43) and concha bullosa (12.50%, n=9). Regarding mucosal and bony changes, nasal mucosal thickening was present in 48.61% (n=35) of participants, bony changes (sclerosis, excluding polyposis) in 31.94% (n=23), and polyposis in 23.61% (n=17) (Table 4, Figures 5 and 9).

Figure 5. Coronal non-contrast CT (bone window) showing a pneumatised left middle turbinate (concha bullosa), an anatomical variant of the ostiomeatal region.

Correlation and subgroup analyses are summarised in Table 5. There was a weak, non-significant positive correlation between the duration of asthma and the Modified Lund-Mackay score (r=0.109, p=0.938), whereas a strong, statistically significant positive correlation was found between the frequency of acute exacerbations and the Modified Lund-Mackay score (r=0.813, p=0.042; Figure 11). Patients on treatment had a higher mean Modified Lund-Mackay score (30.37 ± 11.99) than those not on treatment (22.38 ± 12.45), but this difference was not statistically significant (p=0.746). Male participants had a slightly higher mean score (26.17 ± 14.40) than females (24.32 ± 10.43), a difference that was not significant (p=0.963). A statistically significant difference in mean scores was observed across age groups (p=0.002; Figure 10), with patients older than 50 years having the highest mean score (28.33 ± 12.04), followed by those aged 18–30 years (27.00 ± 13.68).

Patients with polyposis (23.61%, n=17) experienced significantly more acute exacerbations (6.29 ± 2.47) than those without polyposis (2.75 ± 2.47), and this difference was statistically significant (p=0.042) (Table 6, Figure 6).

Figure 6. Non-contrast CT of the paranasal sinuses showing sinonasal polyposis. (A) Coronal image (bone window) with bilateral ethmoid polyposis; (B) axial image (bone window) with bilateral ethmoid and right sphenoid polyposis.

Taken together, the results demonstrate a high prevalence of paranasal sinus abnormalities in bronchial asthma, a predominance of moderate-severity changes, and a significant association between the severity of sinus involvement — and the presence of nasal polyposis — and the frequency of asthma exacerbations.

Figure 7. Distribution of paranasal sinus disease severity on CT, graded by the total Modified Lund-Mackay score (Normal, 0; Mild, 1–20; Moderate, 21–40; Severe, >40). Moderate changes predominated, seen in 59.72% of the 72 patients (data from Table 2).

Table 3. Sinus-specific involvement on CT (n=72).

Figure 8. Sinus-specific involvement rates on CT, showing the proportion of the 72 patients with abnormalities in each paranasal sinus compartment and the ostiomeatal complex. The right maxillary sinus was most frequently involved (90.28%) and the left compartment of the sphenoid sinus least (69.44%) (data from Table 3).

Table 4. Associated anatomical variations and mucosal/bony changes (n=72).

Table 5. Modified Lund-Mackay score: correlation with clinical parameters and subgroup comparisons.

*Statistically significant (p<0.05). Age-group comparison by ANOVA.

Figure 9. Frequency of associated anatomical variations and mucosal/bony changes among the 72 patients. Nasal septal deviation (65.28%) and inferior turbinate hypertrophy (59.72%) were the commonest findings (data from Table 4).

Figure 10. Mean total Modified Lund-Mackay score by age group. Scores differed significantly across age groups (ANOVA p=0.002), with the highest mean score in patients older than 50 years (data from Table 5).

Figure 11. Correlation of the total Modified Lund-Mackay score with clinical parameters. The score correlated strongly with the frequency of acute exacerbations (r=0.813, p=0.042) but not with the duration of asthma (r=0.109, p=0.938) (data from Table 5).

Table 6. Relationship between polyposis and frequency of acute exacerbations (n=72).

*Statistically significant (p<0.05).

This cross-sectional study evaluated the incidence and severity of CT changes in the paranasal sinuses of 72 patients with bronchial asthma. Paranasal sinus abnormalities were present in 97.22% of patients, most demonstrating moderate-severity changes on the Modified Lund-Mackay scoring system, and the severity of sinus involvement correlated significantly with the frequency of asthma exacerbations. These findings lend strong support to the “united airway disease” concept, which regards the upper and lower airways as an integrated functional unit in which inflammatory processes affect both regions concurrently [15]. The remarkably high prevalence of sinus abnormalities in our cohort is consistent with, and at the upper end of, previous reports. Bresciani et al. found radiological evidence of rhinosinusitis in 85% of asthmatic patients, and Ural et al. reported paranasal sinus abnormalities in 90.3% of adult asthmatics [16,17]. Our figure of 97.22% exceeds earlier estimates such as the approximately 75% of patients with moderate-to-severe asthma reported by Slavin et al. [18]. This difference may reflect variations in patient populations, asthma severity, and assessment methods; recruitment from specialised pulmonology and otorhinolaryngology services may have selected patients with more pronounced upper and lower airway involvement. The mean Modified Lund-Mackay score of 25.38 indicates moderate sinus involvement and is comparable to the mean score of 23.6 documented by Yaşar et al. in asthmatic patients with chronic rhinosinusitis [19]. The pattern of sinus involvement, with the right maxillary sinus most commonly affected and the ethmoid sinuses showing the highest severity scores, differs somewhat from studies such as that of Kim et al., who found the ethmoid sinuses to be most frequently involved [20]. The predominance of maxillary involvement may relate to the larger volume and more complex drainage of these sinuses, predisposing them to mucus retention. The slight right-sided predominance we observed has been noted previously by Ashraf and Bhattacharyya, who attributed such asymmetry to minor developmental differences in sinus anatomy or nasal-cycle physiology [21]. The severity distribution in our study, with moderate-to-severe involvement in the majority, is comparable to the 57% reported by Dietz de Loos et al. in asthmatic patients with chronic rhinosinusitis, and ten Brinke et al. similarly observed moderate-to-severe sinus disease in a substantial proportion of patients with difficult-to-treat asthma [22,9]. A key finding was the strong positive correlation (r=0.813, p=0.042) between the Modified Lund-Mackay score and the frequency of acute exacerbations, indicating that more severe sinus involvement is associated with poorer asthma control. This association has been documented previously, albeit with weaker correlations; Dixon et al. reported a moderate correlation (r=0.54) between sinus CT scores and exacerbation frequency [23]. The mechanisms likely include postnasal drip triggering lower airway inflammation, neural reflexes between the upper and lower airways, and systemic propagation of inflammatory mediators [24]. Sinonasal microbial dysbiosis has also been implicated, with specific microbial signatures correlating with eosinophilic inflammation and asthma severity [25]. In contrast, we found only a weak, non-significant correlation between asthma duration and sinus involvement (r=0.109, p=0.938), consistent with Lee et al., suggesting that sinus disease relates more to the inflammatory phenotype and current disease activity than to chronicity — an observation that aligns with the recognition of asthma as a heterogeneous syndrome with distinct endotypes [26,27]. Patients receiving treatment had higher mean scores than untreated patients (30.37 vs 22.38), although the difference was not significant (p=0.746). This contrasts with Matsuno et al., who reported significantly lower sinus CT scores in asthmatics on inhaled corticosteroids [28]. The discrepancy may reflect the cross-sectional design, confounding by indication (patients with more severe disease being more likely to receive treatment), and heterogeneity of therapy. The relationship between treatment and sinus disease is further complicated by biological therapies: anti-IL-5 (mepolizumab) and anti-IgE (omalizumab) agents improve both nasal polyps and asthma control in patients with comorbid disease, reinforcing a shared, therapeutically targetable inflammatory pathway [29,30]. No patient in our cohort was receiving biologics. We observed a statistically significant difference in Modified Lund-Mackay scores across age groups (p=0.002), with the highest scores in patients older than 50 years and a second peak in those aged 18–30 years. This bimodal distribution differs from the steadily increasing prevalence of chronic rhinosinusitis with age in the general population [31]. The relatively high scores in younger adults may reflect early-onset, atopy-associated asthma phenotypes that are more strongly linked to upper airway inflammation; Jarvis et al. found higher rates of concomitant rhinitis in younger adults with asthma, and Ponte et al. reported a stronger association of early-onset asthma with severe chronic rhinosinusitis [32,33]. Higher scores in older patients may represent cumulative inflammatory burden and structural remodelling. We found no significant gender difference in sinus scores (males 26.17 vs females 24.32; p=0.963), in keeping with Han et al., who reported no significant difference between male and female asthmatic patients, even though asthma is generally more prevalent and severe in women [34,35]. Anatomical variations were common in our cohort. Nasal septal deviation (65.28%) and inferior turbinate hypertrophy (59.72%) occurred at rates consistent with the 59.6% and 62% reported by Sedaghat et al. and Berger et al., respectively [36,37]. Such variations may contribute to upper airway obstruction and altered sinus ventilation; correction of significant septal deviation has been reported to improve asthma symptoms [38], although other authors have found no significant association between anatomical variations and asthma severity [39]. The prevalence of polyposis in our study (23.61%) exceeds that typically reported in the general asthmatic population (7–15%) but is comparable to rates in more severe asthma, such as the 25.5% reported by Pearlman et al. in difficult-to-control asthma [40,41]. Bony changes (sclerosis) without polyposis in nearly one-third of patients indicate longstanding inflammation with tissue remodelling, similar to the osteitic changes described by DeMarcantonio et al. in asthmatic patients with chronic rhinosinusitis [42]. A particularly notable finding was that patients with polyposis experienced significantly more acute exacerbations than those without (6.29 vs 2.75; p=0.042). This strong association echoes previous research: Stevens et al. reported a 1.8-fold higher risk of exacerbations requiring emergency care in asthmatics with nasal polyps, and Tanaka et al. found nasal polyps to be independently associated with frequent exacerbations [43,44]. The link likely involves shared type 2 inflammation with eosinophilia, elevated IgE, and upregulation of IL-4, IL-5, and IL-13, together with nasal obstruction and mouth breathing that expose the lower airways to unconditioned air and allergens. Molecular phenotyping has identified similar endotypes in nasal polyps and severe asthma, explaining their frequent coexistence [45]. Importantly, endoscopic sinus surgery in asthmatic patients with chronic rhinosinusitis and nasal polyps has been shown to reduce asthma exacerbations substantially [46], and biologics targeting type 2 inflammation, such as dupilumab, are efficacious in both conditions [47,48]. The strengths of this study include the use of a standardised, reproducible imaging modality and the Modified Lund-Mackay scoring system applied uniformly on a single 128-slice scanner, and the systematic correlation of quantitative radiological findings with clinically relevant parameters. The principal limitation is the cross-sectional design, which precludes inference of causality and does not allow evaluation of temporal changes in sinus involvement with disease progression or treatment. The absence of a non-asthmatic control group limits direct comparison of prevalence and severity with the general population, and the sample size, although adequate for the primary objectives, may have limited statistical power for subgroup analyses. Detailed inflammatory phenotyping and microbiome data, which could clarify the mechanistic links between upper and lower airway disease, were not available. Recruitment from specialised services may also have introduced a degree of selection bias toward patients with more pronounced airway involvement.

Paranasal sinus abnormalities were nearly universal (97.22%) in this cohort of patients with bronchial asthma, with moderate-severity changes predominating and the right maxillary sinus most commonly affected. The severity of sinus involvement correlated strongly and significantly with the frequency of asthma exacerbations, and patients with nasal polyposis experienced significantly more exacerbations than those without. Sinus severity varied significantly with age but not with gender, treatment status, or asthma duration. These findings support the concept of united airway disease and indicate that CT evaluation of the paranasal sinuses may be valuable in the comprehensive assessment of patients with bronchial asthma, particularly those with frequent exacerbations or suspected upper airway involvement. Prospective, longitudinal studies with control groups and detailed inflammatory phenotyping are warranted to establish causal relationships and to determine whether targeted treatment of sinus disease improves asthma outcomes.

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