Eosinophils are key effector cells in allergic inflammation, playing a crucial role in both innate and adaptive immune responses. In allergic rhinitis and asthma, eosinophils infiltrate the nasal mucosa and bronchial epithelium, leading to mucosal oedema, increased mucus production, and airway hyperresponsiveness. In CRSwNP, eosinophil accumulation within the sinonasal mucosa is associated with polyp formation and chronic inflammation 6, 7. The persistence of eosinophils within tissues is mediated by survival-promoting cytokines, resulting in prolonged inflammatory responses even in the absence of ongoing allergen exposure. Understanding the mechanisms underlying eosinophilic infiltration and persistence is critical for elucidating the relationship between serum and tissue eosinophilia 8, 9.

Peripheral blood eosinophil count is frequently utilized as a biomarker for eosinophilic diseases. Elevated serum eosinophil levels have been reported in patients with allergic rhinitis, asthma, and CRSwNP, often correlating with disease severity and treatment response. A higher eosinophil count in the blood may reflect systemic Th2 inflammation and increased eosinophil trafficking to target tissues. However, serum eosinophilia alone may not always accurately represent local tissue inflammation. Some patients with severe tissue eosinophilia may exhibit normal or only mildly elevated peripheral eosinophil counts 10, 11.

Allergic rhinitis which is an Ig E- mediated allergic reaction and cause of inflammatory reaction after allergen exposure is the most common disease in patients.

Histopathological examination of affected tissues / barrier provides valuable insights into the extent of eosinophilic inflammation in allergic diseases. In allergic rhinitis, eosinophils infiltrate the nasal mucosa, contributing to epithelial damage and mucosal hyperplasia. In CRSwNP, eosinophilic inflammation is a defining histopathological feature, with studies demonstrating a correlation between tissue eosinophil density and disease recurrence 7, 9.

Despite the clear role of tissue eosinophilia in disease pathogenesis, its relationship with serum eosinophilia remains variable.

Understanding the relationship between serum and tissue eosinophilia has significant clinical implications for the diagnosis, prognosis, and management of allergic diseases 12, if a strong correlation exists, serum eosinophil count could serve as a non-invasive biomarker for disease severity and treatment response, reducing the need for invasive biopsies. However, if discordance is frequently observed, reliance on serum eosinophilia alone may be insufficient for guiding clinical decision-making 13.

Biologic therapies targeting eosinophils, such as anti-IL-5 monoclonal antibodies (mepolizumab, reslizumab, benralizumab), have revolutionized the treatment of eosinophilic diseases 14, 15. These therapies selectively reduce eosinophil levels in circulation and tissues, improving clinical outcomes in patients with severe eosinophilic asthma and CRSwNP. Investigating the relationship between serum and tissue eosinophilia could provide insights into treatment response variability and help identify patients who may benefit most from targeted eosinophil-depleting strategies 16.

Interview based techniques were used to ensure eligibility criteria and then to obtain a detailed history of study participants. Data obtained secondarily from medical records department and laboratory / department of pathology were also used in the present study. They are as follows:

Data was entered in Microsoft Excel and was analysed using trial version of SPSS-22. Median and inter-quartile range (IQR) were used to represent measures of central tendency as the continuous variables were not normally distributed. Proportions were used to summarise and understand the distribution of data. Appropriate graphical representations are used for easy understanding.

To understand the association between blood parameters of eosinophils and tissue eosinophils, chi-square test was used. To compare the difference between the medians across various grades of tissue eosinophilia, Mann-Whittney U test and Kruskal-Wallis test were used. Additionally, Spearman’s rho correlation co-efficient was computed to determine the relationship between serum IgE levels and AEC. All the above tests of significance were considered as statistically significant if p value was less than 0.5.

Data collection was initiated only after the process of obtaining ethical clearance from Institutional ethics committee. All the four principles of medical ethics were abided to, as per the researcher’s best knowledge. Individual’ data was not shared at any level throughout the process of data dissemination.

In the present study, peak prevalence was seen in children <10 years (28.1%), next peak in adolescents (19.1% aged 10–19 years) and only 10% aged >50 years. This paediatric predominance is seen in many other studies where lymphoid tissue hypertrophy especially adenoid hypertrophy peaks at the age of 6 years and atrophies after the age of 12 years 17, 18, 19. Another study by Rout et al., reported 21% of adult nasal obstructions from adenoid hypertrophy, primarily in 16–25-year-olds (60%) 20. This suggests adult-onset hypertrophy may involve distinct triggers (e.g., pollution, chronic infection). With respect to gender, male predominance seen at 67% in the present study. Study conducted by Rout et al. found 70% of male predominance 21. Other studies also show similar findings suggesting environmental / gender-specific risk factors amplify male susceptibility 17. Also, male predominance warrants research into androgen-driven lymphoid proliferation or exposure biases 22. With respect to demographics, other studies 17, 18, 19, 20 linked adult hypertrophy to pollution / occupation (e.g., roadside workers, construction site workers etc.), which may affect all demographics uniformly. These aspects could be explored in future studies. This demographic alignment with pediatric-focused studies validates the present study’s cohort’s representativeness, while adult disparities underscore the condition’s evolving epidemiology. The uniform age / sex distribution across allergic / non-allergic subgroups suggests environmental or systemic drivers (e.g., IL-6/CRP elevation) may transcend traditional atopic pathways.

In the present study, high serum IgE levels were observed in 51.0% of allergic individuals compared to 27.5% of non-allergic individuals. A study by Agha et al. found significantly elevated serum IgE levels in patients with allergic disorders (e.g., asthma, allergic rhinitis, urticaria) compared to healthy controls (P < 0.001). The mean IgE levels were higher in allergic individuals across all age groups, consistent with our findings 23. Similarly, a longitudinal study reported that persistent serum IgE levels ≥200 kU/L were strongly associated with allergic rhinitis, asthma, and eczema during childhood 24. This difference was statistically significant, reinforcing the role of serum IgE as a biomarker for allergic conditions. Overlap between allergic and non-allergic groups limits the standalone diagnostic utility of these markers.

In the present study, high AEC was observed in 67.3% of allergic individuals compared to 35.0% of non-allergic individuals. Elevated AEC is commonly linked to allergic conditions such as asthma and rhinitis. A study on eosinophilia found that allergic patients frequently exhibit peripheral eosinophilia due to IL-5-mediated recruitment and activation of eosinophils 24, 25. This difference was statistically significant, highlighting the role of eosinophilia as a marker of Th2-mediated inflammation.

Overall, the combination of serum IgE and AEC improves diagnostic accuracy for allergic diseases compared to either marker alone.

In the present study, a significantly higher proportion of allergic individuals exhibited high (overall: 51% i.e. more than half; high: 36.7% and moderate: 14.3%) tissue eosinophilia compared to non-allergic individuals. This statistically significant difference underscores the role of eosinophils as a hallmark of Th2-mediated inflammation in allergic conditions. Another study aligns with the findings of the present study; it was a study on children undergoing adenotonsillectomy which found significantly higher tissue eosinophil counts in atopic patients compared to non-atopic patients 26. Research activities on CRSwNP patients reported elevated tissue eosinophilia in allergic individuals, correlating with type 2 cytokines like IL-5 and eotaxins. These cytokines drive eosinophil recruitment and activation, consistent with the higher levels observed in your allergic group 27.

In the present study, the observation that 31.9% of individuals with high AEC exhibited high tissue eosinophilia compared to 19.0% of those with normal AEC suggests a possible correlation between systemic eosinophilia and localized tissue inflammation. High tissue eosinophilia was seen in 36.1% of individuals with high serum IgE, compared to 18.9% in those with normal serum IgE levels. Studies have shown that elevated AEC often correlates with increased tissue eosinophilia in allergic conditions such as asthma and rhinitis. For instance, a study found that patients with asthma had significantly higher tissue eosinophil counts when their AEC was elevated, suggesting that systemic eosinophilia reflects ongoing local inflammation 28. Conversely, some studies report cases where patients exhibit high tissue eosinophilia despite normal AEC levels, indicating that local factors (e.g., cytokine milieu) can drive eosinophilic infiltration independent of systemic counts 28, 29.

The findings in present study highlight the complexity of eosinophilic responses, where local tissue environments can modulate eosinophil activity regardless of systemic levels. This aligns with research indicating that local production of chemokines (e.g., eotaxins) can attract eosinophils to tissues even when peripheral counts are normal. Similarly, the presence of high serum IgE does not always guarantee high tissue eosinophilia; some patients may have elevated IgE levels without significant eosinophilic infiltration due to factors such as desensitization or variations in individual immune responses.

The observed trends highlight the importance of considering both AEC and serum IgE levels when evaluating patients for allergic conditions or eosinophilic disorders. However, clinicians should be cautious about relying solely on these markers for diagnosis or treatment decisions due to their variability. Understanding the relationship between these markers can guide personalized treatment strategies for patients with allergic diseases or conditions characterized by eosinophilic inflammation. For example, patients exhibiting high tissue eosinophilia despite normal systemic markers might benefit from localized therapies targeting the inflammatory process.

Given the complexity observed in the relationships among AEC, serum IgE, and tissue eosinophilia, it is crucial for clinicians to conduct comprehensive evaluations that include clinical history, physical examination, and possibly additional testing (e.g., allergen-specific tests) to accurately assess the underlying pathologies.

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