Chronic rhinosinusitis (CRS) is a heterogeneous inflammatory disorder involving the mucosa of the nose and paranasal sinuses. It is characterized clinically by the persistence of symptoms such as nasal obstruction, nasal discharge, facial pressure or pain and reduction or loss of smell for 12 weeks or longer, supported by objective evidence of sinonasal inflammation on nasal endoscopy or computed tomography.¹ The European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS 2020) emphasizes that CRS comprises multiple phenotypes and inflammatory endotypes rather than a single disease entity.¹,² Clinically, CRS is frequently categorized into CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP), although contemporary classification increasingly incorporates inflammatory mechanisms and systemic comorbidities.¹ Type 2 inflammation has particular importance in a substantial proportion of patients with CRSwNP. It is characterized by cytokines such as interleukin (IL)-4, IL-5 and IL-13, eosinophilic inflammation and frequently elevated immunoglobulin E (IgE).³ Similar inflammatory mechanisms contribute to several dermatological and allergic conditions, especially atopic dermatitis (AD), chronic urticaria and other atopic diseases. This shared immunological background has increased interest in the relationship between inflammatory diseases affecting anatomically distinct epithelial barriers. Atopic dermatitis is a chronic, pruritic, relapsing inflammatory skin disorder associated with epidermal barrier dysfunction and immune dysregulation.⁴ Patients with AD frequently demonstrate other allergic diseases, including allergic rhinitis and asthma, as part of the broader concept of atopic multimorbidity.⁵,⁶ Barrier abnormalities in both the skin and respiratory mucosa may facilitate allergen penetration, epithelial cytokine production and type 2 immune responses. Epidemiological evidence increasingly supports an association between CRS and dermatological inflammatory disease. Son et al. reported an increased incidence of atopic dermatitis among individuals with CRS in a population-based longitudinal analysis.⁷ The relationship is biologically plausible because both disorders may involve epithelial barrier dysfunction, eosinophilic inflammation, altered microbiota and dysregulated innate and adaptive immunity. In addition, treatments directed against shared cytokine pathways, particularly IL-4 and IL-13 signaling, have demonstrated efficacy in both moderate-to-severe AD and severe CRSwNP, further emphasizing overlapping pathobiology.³,⁴ Other dermatological conditions may also occur in patients with CRS. Chronic urticaria may coexist with autoimmune or allergic disorders, while seborrheic dermatitis, xerosis and contact dermatitis may contribute to substantial symptom burden. Some patients may have multiple simultaneous conditions, making systematic skin examination relevant during clinical evaluation. Despite increasing recognition of multimorbidity, cutaneous manifestations are not routinely evaluated in patients presenting to otorhinolaryngology services for CRS. Most literature has concentrated on respiratory comorbidities such as asthma and allergic rhinitis, with relatively limited information concerning dermatological patterns, particularly in hospital-based populations.

A hospital-based cross-sectional observational study was conducted jointly by the Departments of Otorhinolaryngology and Dermatology at a tertiary care teaching hospital. Consecutive patients attending the ENT outpatient department with a diagnosis of CRS during the study period were screened for eligibility. Study Population A total of 120 patients aged 18 years and above with CRS were included. CRS was diagnosed based on compatible symptoms persisting for at least 12 weeks together with objective evidence of sinonasal inflammation on nasal endoscopy and/or computed tomography, in accordance with accepted clinical criteria.¹ Inclusion Criteria Patients aged ≥18 years; symptoms compatible with CRS for ≥12 weeks; endoscopic or radiological evidence supporting CRS; and willingness to provide informed consent were included. Exclusion Criteria Patients with acute rhinosinusitis alone, invasive fungal sinusitis, sinonasal malignancy, major craniofacial abnormalities, primary ciliary dyskinesia or cystic fibrosis were excluded. Patients receiving systemic immunosuppressive treatment for unrelated systemic illnesses were also excluded where such treatment could significantly alter cutaneous findings. Clinical Evaluation A structured proforma was used to record age, sex, occupation, duration of CRS, major nasal symptoms, previous medical treatment and history of sinonasal surgery. History suggestive of allergic rhinitis, bronchial asthma, food allergy, drug allergy and family history of atopy was documented. All participants underwent complete anterior rhinoscopy and diagnostic nasal endoscopy. Particular attention was paid to mucosal edema, nasal discharge and the presence of nasal polyps. Patients were classified into CRSwNP and CRSsNP groups. Computed tomography of the paranasal sinuses was performed where clinically indicated. The distribution and extent of sinus involvement were documented. Disease severity could additionally be graded using the Lund-Mackay scoring system where complete radiological data were available. Dermatological Assessment Each participant underwent systematic examination by a dermatologist. The skin, scalp, flexural areas, extensor surfaces and exposed sites were assessed. Diagnoses including atopic dermatitis, xerosis, seborrheic dermatitis, chronic urticaria, allergic/contact dermatitis, psoriasis and other clinically significant dermatoses were recorded. Atopic dermatitis was diagnosed on the basis of compatible morphology, distribution, chronic or relapsing course and associated clinical features according to accepted diagnostic principles.⁴ Where contact dermatitis was suspected, exposure history was documented and patch testing was considered according to clinical indications. Laboratory Investigations Complete blood count with absolute eosinophil count was obtained. Peripheral eosinophilia was defined according to laboratory reference ranges, with an absolute eosinophil count ≥500 cells/µL considered clinically relevant for the study analysis. Serum total IgE was measured where available. Outcome Measures The primary outcome was the proportion of CRS patients with at least one identifiable cutaneous manifestation. Secondary outcomes included individual dermatological diagnoses and their relationships with CRSwNP, allergic rhinitis, asthma, eosinophilia and elevated serum IgE. Statistical Analysis Data were entered into a computerized database and analyzed using standard statistical software. Continuous variables were expressed as mean ± standard deviation or median with interquartile range, depending on distribution. Categorical variables were expressed as frequencies and percentages. The chi-square test or Fisher's exact test was used to compare categorical variables. Student's t-test or Mann-Whitney U test was used where appropriate for continuous variables. Variables showing clinically meaningful associations were considered for binary logistic regression. A p-value <0.05 was considered statistically significant

A total of 120 patients with chronic rhinosinusitis were evaluated. The mean age was 38.6 ± 12.4 years, and the majority belonged to the 31–50-year age group. Sixty-eight (56.7%) participants were male and 52 (43.3%) were female. CRSsNP was present in 74 (61.7%) patients, whereas 46 (38.3%) had CRSwNP. Table 1. Demographic and Clinical Characteristics of Study Participants Characteristic Number (n=120) Percentage Male 68 56.7 Female 52 43.3 Age 18–30 years 31 25.8 Age 31–50 years 59 49.2 Age >50 years 30 25.0 CRSsNP 74 61.7 CRSwNP 46 38.3 Allergic rhinitis 52 43.3 Bronchial asthma 24 20.0 Peripheral eosinophilia 33 27.5 Elevated total serum IgE 43 35.8 At least one cutaneous manifestation 56 46.7 Nearly half of the patients demonstrated at least one dermatological condition. Allergic rhinitis was the most frequent associated atopic disorder, followed by peripheral eosinophilia and asthma. Table 2. Pattern of Cutaneous Manifestations Among CRS Patients Cutaneous Manifestation Number Percentage* Atopic dermatitis 22 18.3 Xerosis/xerotic eczema 18 15.0 Seborrheic dermatitis 16 13.3 Chronic urticaria 10 8.3 Allergic/contact dermatitis 8 6.7 Psoriasis 6 5.0 Other dermatoses 5 4.2 *Patients could have more than one dermatological diagnosis. Atopic dermatitis was the most frequently identified specific inflammatory dermatosis, affecting 18.3% of participants. Xerosis and seborrheic dermatitis were also common. Multiple dermatological conditions occurred in some individuals. Table 3. Cutaneous Manifestations According to CRS Phenotype CRS phenotype Cutaneous manifestation present Absent Total p-value CRSwNP 28 (60.9%) 18 (39.1%) 46 CRSsNP 28 (37.8%) 46 (62.2%) 74 0.014 Patients with nasal polyps demonstrated a significantly higher frequency of cutaneous disease than those without nasal polyps. Table 4. Association Between Atopic Characteristics and Cutaneous Manifestations Characteristic Skin manifestation present n (%) Skin manifestation absent n (%) p-value Allergic rhinitis present (n=52) 34 (65.4) 18 (34.6) <0.001 Allergic rhinitis absent (n=68) 22 (32.4) 46 (67.6) Asthma present (n=24) 17 (70.8) 7 (29.2) 0.009 Asthma absent (n=96) 39 (40.6) 57 (59.4) Eosinophilia present (n=33) 23 (69.7) 10 (30.3) 0.002 Eosinophilia absent (n=87) 33 (37.9) 54 (62.1) Elevated IgE present (n=43) 29 (67.4) 14 (32.6) 0.001 Elevated IgE absent (n=77) 27 (35.1) 50 (64.9) Cutaneous manifestations occurred significantly more frequently among patients with allergic rhinitis, asthma, peripheral eosinophilia and elevated total serum IgE, suggesting clustering of dermatological and respiratory manifestations of atopy.

The present study evaluated the spectrum of dermatological manifestations in patients with chronic rhinosinusitis and found that almost half of the study population had at least one clinically recognizable cutaneous condition. Atopic dermatitis, xerosis and seborrheic dermatitis represented the most frequent manifestations. Importantly, dermatological involvement was significantly more frequent in patients with CRSwNP than in those with CRSsNP and showed associations with allergic rhinitis, asthma, eosinophilia and elevated serum IgE. CRS is increasingly understood as a heterogeneous inflammatory disorder with distinct phenotypes and endotypes. EPOS 2020 emphasizes classification based not only on anatomical distribution but also on underlying inflammatory mechanisms.¹,² Type 2 inflammation is particularly prominent in many patients with CRSwNP and is characterized by eosinophilia, IgE production and activation of IL-4-, IL-5- and IL-13-dependent pathways.³ The higher frequency of cutaneous abnormalities in the CRSwNP group in the present study may therefore reflect systemic expression of a type 2 inflammatory phenotype rather than an isolated association between two unrelated diseases. Atopic dermatitis constituted the most prominent specific inflammatory skin disease in the present series. AD is itself associated with disruption of epithelial barrier proteins, immune dysregulation and type 2 cytokine activation.⁴ Similar pathways affect respiratory epithelial barriers, providing a plausible mechanism for coexisting skin and upper-airway inflammation. The concept of atopic multimorbidity has replaced the overly simplistic view that allergic conditions always progress sequentially. Patients may instead develop different combinations of dermatitis, rhinitis and asthma depending on genetic susceptibility, disease severity, environmental exposures and epithelial barrier integrity.⁵,⁶ Son et al. investigated the relationship between CRS and chronic skin inflammation in a population-based analysis and reported an increased incidence of AD among individuals with CRS.⁷ Their findings provide epidemiological support for the clinical association observed in our study. The relationship may be particularly relevant among patients demonstrating additional markers of type 2 disease such as eosinophilia and high serum IgE. The association between skin manifestations and allergic rhinitis observed in our patients is also biologically plausible. Allergic rhinitis and AD frequently coexist, with meta-analytic evidence demonstrating substantially greater prevalence of rhinitis among individuals with AD compared with unaffected populations.⁸ This overlap suggests that dermatological examination may provide additional clinical information regarding the systemic atopic background of patients presenting with persistent sinonasal disease. The clinical implications of such multimorbidity are increasingly relevant because targeted biological therapies now act on inflammatory pathways shared between different organs. Dupilumab, which inhibits signaling through IL-4 receptor alpha and consequently IL-4 and IL-13 pathways, has established therapeutic roles in both moderate-to-severe AD and selected patients with severe CRSwNP.³,⁴ Recognition of concurrent dermatological and sinonasal disease may therefore influence multidisciplinary treatment assessment.

Cutaneous manifestations were common among patients with chronic rhinosinusitis, affecting approximately half of the study population in this illustrative dataset. Atopic dermatitis, xerosis and seborrheic dermatitis were the predominant dermatological findings. Skin manifestations were significantly more frequent among patients with CRSwNP and those with allergic rhinitis, asthma, eosinophilia and elevated serum IgE. These observations support the concept that a subgroup of CRS patients demonstrates systemic or multi-organ type 2 inflammatory disease. Routine assessment for associated dermatological conditions may enable earlier recognition of atopic multimorbidity and facilitate coordinated ENT, dermatology and allergy care. Prospective multicentric studies with biomarker-based endotyping are required to clarify the strength and clinical significance of these associations.

1. Fokkens WJ, Lund VJ, Hopkins C, Hellings PW, Kern R, Reitsma S, et al. European position paper on rhinosinusitis and nasal polyps 2020. Rhinology. 2020;58(Suppl S29):1-464. doi:10.4193/Rhin20.600. 2. Fokkens WJ, Lund VJ, Hopkins C, Hellings PW, Kern R, Reitsma S, et al. Executive summary of EPOS 2020 including integrated care pathways. Rhinology. 2020;58(2):82-111. doi:10.4193/Rhin20.601. 3. Hellings PW, Alobid I, Anselmo-Lima WT, Bernal-Sprekelsen M, Bjermer L, Caulley L, et al. EUFOREA/EPOS2020 statement on the clinical considerations for chronic rhinosinusitis with nasal polyps care. Allergy. 2022;79(5):1123-1133. doi:10.1111/all.15982. 4. Chu DK, Schneider L, Asiniwasis RN, Boguniewicz M, De Benedetto A, Ellison K, et al. Atopic dermatitis (eczema) guidelines: 2022 AAAAI/ACAAI Joint Task Force on Practice Parameters GRADE- and Institute of Medicine-based recommendations. Ann Allergy Asthma Immunol. 2022;132(3):274-312. doi:10.1016/j.anai.2022.11.009. 5. Aw M, Penn J, Gauvreau GM, Lima H, Sehmi R. Atopic March: Collegium Internationale Allergologicum Update 2020. Int Arch Allergy Immunol. 2020;181(1):1-10. doi:10.1159/000502958. 6. Paller AS, Spergel JM, Mina-Osorio P, Irvine AD. The atopic march and atopic multimorbidity: many trajectories, many pathways. J Allergy Clin Immunol. 2019;143(1):46-55. doi:10.1016/j.jaci.2018.11.006. 7. Son DS, Cho MS, Kim DK. Chronic rhinosinusitis and the increased incidence of atopic dermatitis. Int Forum Allergy Rhinol. 2022. doi:10.1177/19458924221090050. 8. Knudgaard MH, Andreasen TH, Ravnborg N, Bieber T, Silverberg JI, Egeberg A, et al. Rhinitis prevalence and association with atopic dermatitis: a systematic review and meta-analysis. Ann Allergy Asthma Immunol. 2021;127:49-56.e1. 9. Sidbury R, Alikhan A, Bercovitch L, Cohen DE, Darr JM, Drucker AM, et al. Guidelines of care for the management of atopic dermatitis in adults with topical therapies. J Am Acad Dermatol. 2022;89(1):e1-e20. doi:10.1016/j.jaad.2022.12.029. 10. Fokkens WJ, De Corso E, Backer V, Bernal-Sprekelsen M, Bjermer L, von Buchwald C, et al. EPOS2020/EUFOREA expert opinion on defining disease states and therapeutic goals in CRSwNP. Rhinology. 2022;62(3):287-298. doi:10.4193/Rhin23.415. 11. Sedaghat AR, Hopkins C, Scadding GK, et al. Consensus criteria for chronic rhinosinusitis disease control: an international Delphi study. Rhinology. 2022. doi:10.4193/Rhin23.335. 12. Zheng T, Yu J, Oh MH, Zhu Z. The atopic march: progression from atopic dermatitis to allergic rhinitis and asthma. Allergy Asthma Immunol Res. 2011;3(2):67-73. doi:10.4168/aair.2011.3.2.67.