The Differentiating Effects of Co-Morbid Psoriasis and Atopic Dermatitis on Chronic Rhinosinusitis Immunopathology and Clinical Presentation

Updated: Apr 15

VJM Spring Edition 2026

https://doi.org/10.18130/x69y-ap02

Authors: Aaron D. Smith, BS¹, Catherine E. Lyons, BS BA¹, James T. Patrie, MS², Larry Borish, MD*1

Author Affiliation:

¹Division of Allergy and Immunology, University of Virginia Health System, Charlottesville, VA 22908

²Department of Public Health Sciences, University of Virginia School of Medicine, Charlottesville, VA 22908

Abstract

Introduction

Psoriasis is a papulosquamous condition characterized by type 1 (T1) inflammation, while atopic dermatitis (AD) cutaneous disease is defined as a type 2 (T2) process. Since both psoriasis and atopic dermatitis are predictive for higher rates of CRS, our objective was to determine whether CRS with concurrent psoriasis or atopic dermatitis would share its T1 or T2 pathogenic signature, respectively. In comparison to T1 CRS, a T2 process can be predicted by presence of more extensive sinus disease via Lund-MacKay score (LMS), reduced sense of smell, and greater concurrence of purulent drainage and pain/pressure.

Methods

CRS patients with psoriasis or AD were compared to those with CRS alone. Subjective outcomes were assessed using the Sino-Nasal Outcome Test (SNOT-22), and objective findings were measured via Lund-MacKay CT scores, Lund-Kennedy endoscopy scores, and inflammatory markers. Statistical comparisons were performed using chi-square and non-parametric methods. Results

Forty-two patients were analyzed (14 CRS alone, 14 psoriasis, 14 AD) with comparable demographics. Co-morbid AD exhibited a T2-skewed profile, with higher eosinophil counts (P = 0.043), greater nasal polyp prevalence (P = 0.008), and the highest SNOT-22 scores (P = 0.006), especially in productivity and concentration (P < 0.01). Despite similar imaging findings, AD showed disproportionate symptom severity. Psoriasis-associated CRS presented an intermediate, non-T2 phenotype between AD and CRS alone.

Conclusions

CRS with AD reflects a T2 inflammatory with greater symptom severity and eosinophilia. In contrast, psoriasis-associated CRS presents with a non-T2 pattern with distinct clinical features, supporting divergent inflammatory mechanisms.

Introduction

Psoriasis and atopic dermatitis (AD) are chronic inflammatory skin diseases characterized by distinct immunologic endotypes. Psoriasis is driven predominantly by type 1 and type 3 (T1/T3) cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-17, and IL-23, whereas AD reflects type 2 (T2) inflammation, mediated by IL-4, IL-5, and IL-13 ^1–3. Chronic rhinosinusitis (CRS), defined as persistent inflammation of the nasal mucosa and paranasal sinuses lasting at least 12 weeks, is heterogeneous and can be categorized into T1/T3- or T2-skewed endotypes ⁴. The T1/T3 CRS phenotype typically presents with preserved olfaction, purulent drainage, and reduced eosinophilia, while T2 CRS is associated with nasal polyps, asthma, elevated IgE, and eosinophilic infiltration. ⁵

Both psoriasis and AD have been linked to increased CRS prevalence, suggesting shared or parallel inflammatory mechanisms ^6,7. However, whether co-morbid psoriasis or AD predicts CRS features consistent with T1/T3 versus T2 inflammation has not been systematically examined. Recent frameworks emphasize immunologic endotyping to refine disease classification and guide mechanism-based treatment approaches ⁸.

Emerging evidence highlights complex bidirectional relationships between cutaneous and airway inflammation. Patients with CRS have an elevated risk of developing AD and psoriasis, however CRS patients with psoriasis appear to lack distinct T1-driven sinus pathology ^7,9. Shared mechanisms such as immunoglobulin E (IgE) activation, epithelial barrier dysfunction, and Staphylococcus aureus colonization further unite nasal and cutaneous disease processes ¹⁰. Additionally, recently recognized subtypes like central compartment atopic disease exemplify localized allergic CRS with prominent eosinophilia ¹¹.

Given these overlapping yet divergent inflammatory pathways, this study aims to delineate whether CRS coexisting with psoriasis or AD demonstrates distinct clinical and immunologic profiles reflective of their respective cutaneous phenotypes. Clarifying these associations may improve endotype-based diagnosis and therapeutic decision-making in patients with co-morbid airway and skin disease.

Methods

We compared phenotypic and inflammatory markers of CRS among three cohorts: CRS alone, CRS with co-morbid psoriasis, and CRS with co-morbid AD. Electronic medical records were retrospectively reviewed for patients diagnosed with CRS by an otolaryngologist and psoriasis or AD by a dermatologist between 2013 and 2023. Clinical assessments were obtained prior to initiation of any systemic monoclonal antibody or immunosuppressant therapy. Patients actively receiving systemic immune-modulating treatments for either skin or sinus disease were excluded; only those managed with topical therapies (e.g., nasal saline irrigation, topical corticosteroids, emollients, or topical calcineurin inhibitors) were included to minimize confounding effects of systemic therapy.

Patient reported measurements utilized the Sino-Nasal-Outcome Test (SNOT-22).¹² Objective measurements included Lund-Mackay Score (LMS) derived from a screening sinus CT scan, Lund-Kennedy Score (LKS) from the initial endoscopic examination, and the T2 inflammatory markers IgE, absolute eosinophil count, and presence of nasal polyps. SNOT-22 composite scores were compared between cohorts via negative binomial regression, while the SNOT-22 questions were summarized individually as either the trait being present or absent. Trait frequencies were compared between patient groups via non-parametric logistics regression.

Results

Forty-two patients were analyzed, including 14 with CRS alone, 14 with CRS and psoriasis, and 14 with CRS and AD. Baseline demographics were similar across groups (Table I). Co-morbid AD demonstrated a T2-skewed profile, with higher absolute eosinophil counts (median 610 cells/µL vs 240 in psoriasis and 330 in CRS alone; P = 0.043) and more frequent nasal polyps (85.7% vs 50.0% and 28.6%; P = 0.008). Total IgE trended higher in AD but did not reach significance. AD also exhibited the highest SNOT-22 total scores (median 61.0 vs 57.0 and 39.5; P = 0.006), with significant impairments in productivity and concentration (P < 0.01) (Table I)

Despite increased symptom burden, imaging findings did not differ significantly. Median Lund-MacKay and Lund-Kennedy scores were comparable across groups, suggesting similar anatomic disease extent. Psoriasis-associated CRS demonstrated an intermediate, non-T2 phenotype, with fewer nasal polyps, lower eosinophilia, and milder symptom severity relative to AD.

Summarized, Co-morbid AD was linked to enhanced T2 inflammatory activity and greater subjective morbidity despite stable objective findings, whereas psoriasis-associated CRS reflected a non-T2 inflammatory pattern consistent with T1/T3-dominant immune mechanisms.

Discussion

Our data provides evidence that co-morbid psoriasis and AD exert distinct influences on the clinical and inflammatory presentation of CRS. While both conditions are associated with an elevated prevalence of CRS, our findings indicate that only AD meaningfully modifies the CRS phenotype toward a T2-dominant pattern, whereas psoriasis appears to exert minimal impact on sinus inflammation.

Patients with CRS and AD exhibited higher absolute eosinophil counts, markedly greater nasal polyp prevalence, and the most severe symptom burden on SNOT-22, consistent with a systemic T2-skewed presentation ^2,5. These findings align with prior reports suggesting that AD is linked to heightened CRS morbidity and a greater likelihood of eosinophilic disease ^9,11. In contrast, co-morbid psoriasis did not significantly alter objective or subjective CRS metrics. Eosinophil counts, IgE levels, and nasal polyp prevalence were comparable to those in CRS alone, suggesting that the T1/T3 inflammatory axis characteristic of psoriasis does not extend to the sinonasal mucosa. These results reinforce earlier observations that psoriasis-associated CRS lacks distinct histologic or immunopathologic signatures and should therefore be considered an overlapping but mechanistically independent process ⁷. CRS pathogenesis in patients with inflammatory skin disease may not be uniform.

The strong T2 association seen in CRS with AD underscores the utilization for endotype-specific therapeutic approaches, including biologics targeting IL-4/IL-13 pathways, while the absence of such influence in psoriasis suggests that management should remain disease-specific and independent across organ systems. Furthermore, the observed symptom–imaging discordance in the AD cohort highlights the importance of incorporating patient-reported outcomes into treatment evaluation and clinical decision-making.

Statements

Statement of Ethics

Please address the following aspects in your Statement of Ethics.

Study approval statement: This study protocol was reviewed and approved by the University of Virginia IRB, approval number 21482.

Consent to participate statement: Study was granted exemption from requiring written informed consent by the University of Virginia IRB, approval number 21482.

Conflict of Interest Statement

LB reports investigator-initiated research grants from Regeneron (all funds are awarded to the University of Virginia). LB serves on advisory boards for GSK, Sanofi/Genzyme, Regeneron, and Astra Zeneca. All other authors have no conflicts of interest to declare.

Funding Sources

This study was not supported by any sponsor or funder.

Author Contributions

Aaron D. Smith: Conceptualization; writing – original draft; methodology; validation; writing- review and editing; data curation; resources; formal analysis; supervision. Catherine E. Lyons: Writing – original draft; writing – review and editing; validation. James T. Patrie: Methodology; investigation; validation; software; formal analysis; data curation; supervision; visualization. Larry Borish: Conceptualization; investigation; writing – original draft; methodology; validation; writing – review and editing; data curation; supervision; resources; project administration.

Data Availability Statement

All data generated or analyzed during this study are included in this article. Further enquiries can be directed to the corresponding author.

References

1. Griffiths CEM, Armstrong AW, Gudjonsson JE, Barker JNWN. Psoriasis. Lancet. 2021;397(10281):1301-1315. doi:10.1016/S0140-6736(20)32549-6

2. Guttman-Yassky E, Renert-Yuval Y, Brunner PM. Atopic dermatitis. The Lancet. 2025;405(10478):583-596. doi:10.1016/S0140-6736(24)02519-4

3. Renert-Yuval Y, Thyssen JP, Bissonnette R, et al. Biomarkers in atopic dermatitis-a review on behalf of the International Eczema Council. J Allergy Clin Immunol. 2021;147(4):1174-1190.e1. doi:10.1016/J.JACI.2021.01.013

4. Bachert C, Akdis CA. Phenotypes and Emerging Endotypes of Chronic Rhinosinusitis. J Allergy Clin Immunol Pract. 2016;4(4):621-628. doi:10.1016/J.JAIP.2016.05.004

5. Stevens WW, Peters AT, Tan BK, et al. Associations Between Inflammatory Endotypes and Clinical Presentations in Chronic Rhinosinusitis. J Allergy Clin Immunol Pract. 2019;7(8):2812-2820.e3. doi:10.1016/J.JAIP.2019.05.009

6. Chandra RK, Lin D, Tan B, et al. Chronic rhinosinusitis in the setting of other chronic inflammatory diseases. Am J Otolaryngol. 2010;32(5):388. doi:10.1016/J.AMJOTO.2010.07.013

7. Smith AD, Lyons CE, Patrie JT, Borish L. The Effect of Co-Morbid Psoriasis Diagnosis on Chronic Rhinosinusitis Immunopathology. Int Arch Allergy Immunol. 2024;185(12). doi:10.1159/000539918,

8. Xie X, Xuan L, Zhao Y, Wang X, Zhang L. Diverse Endotypes of Chronic Rhinosinusitis and Clinical Implications. Clin Rev Allergy Immunol. 2023;65(3):420-432. doi:10.1007/S12016-023-08976-Y

9. Son DS, Cho MS, Kim DK. Chronic Rhinosinusitis and the Increased Incidence of Atopic Dermatitis. Am J Rhinol Allergy. 2022;36(5):574-582. doi:10.1177/19458924221090050

10. Olze H, Zuberbier T. Comorbidities between nose and skin allergy. Curr Opin Allergy Clin Immunol. 2011;11(5):457-463. doi:10.1097/ACI.0B013E32834A9764

11. Vizcarra-Melgar J, Moreno-Luna R, Martín-Jiménez D, et al. Phenotypic Features of Central Compartment Atopic Disease Compared with Other Types of Chronic Rhinosinusitis: A Systematic Review. Curr Allergy Asthma Rep. 2025;25(1):43. doi:10.1007/S11882-025-01225-6

12. Kennedy JL, Hubbard MA, Huyett P, Patrie JT, Borish L, Payne SC. Sino-nasal outcome test (SNOT-22): a predictor of postsurgical improvement in patients with chronic sinusitis. Ann Allergy Asthma Immunol. 2013;111(4):246-251.e2. doi:10.1016/J.ANAI.2013.06.033

Table 1: Summary of objective and subjective measurements in studied CRS cohorts,

Parameter	CRS Alone (n=14)	Psoriasis (n=14)	Dermatitis (n=14)	p-value
Age (±SD) at presentation	59.6 (18.8)	59.0 (13.9)	53.2 (9.9)	0.617
Female gender; n (%)	4 (28.6)	9 (66.7)	7 (53.8)	0.369
Presence of NPs; n (%)	4 (28.6)	7 (50.0)	12 (92.3)	0.008*
AEC cells/µl; median [IQR]	330 [140, 410]	240 [73, 468]	610 [358, 1003]	0.043*
IgE kU/L; median [IQR]	176.0 [38.8, 365.8]	51.8 [5.0, 221.7]	217.0 [138.7, 1601.5]	0.505
Atopic Patients; n (%)	0 (0)	7 (50)	14 (100)	--
SNOT-22 Total Score; median [IQR]	39.5 [30.0, 49.5]	57.0 [40.8, 64.3]	61.0 [52.0, 74,0]	0.006*
Components of SNOT-22; median [IQR]
Q4, Nasal Obstruction	3.0 [2.0, 4.0]	3.0 [0.5, 4.0]	4.0 [3.0, 4.0]	0.538
Q5, Loss of Smell or Taste	3.0 [1.5, 4.3]	2.5 [2.0, 3.0]	1.0 [1.0, 3.0]	0.398
Q7, Post-Nasal Discharge	2.5 [1.8, 3.0]	1.5 [1.0, 3.5]	3.0 [2.0, 4.0]	0.276
Q8, Thick Nasal Discharge	3.5 [1.8, 4.0]	2.0 [1.0, 3.8]	3.0 [2.0, 4.0]	0.690
Q12, Facial Pain/Pressure	2.0 [1.0, 3.0]	2.0 [1.0, 3.8]	3.0 [3.0, 4.0]	0.202
Q15, Lack of a Good Night’s Sleep	3.5 [0. 4.0]	4.0 [3.3, 4.0]	4.0 [4.0, 4.0]	0.309
Q16, Wake Up Tired	3.0 [0, 4.0]	4.0 [3.3, 4.8]	4.0 [3.0, 5.0]	0.192
Q18, Reduced Productivity	1.0 [0 ,3.0]	3.5 [3.0, 4.8]	4.0 [3.0, 4.0]	0.001*
Q19, Reduced Concentration	1.0 [0.0, 2.0]	3.5 [2.3, 4.0]	3.0 [3.0, 4.0]	0.006*
Lund-McKay Score; median [IQR]	10.0 [9.0, 11.5]	3.5 [2.0, 8.8]	5.5 [4.0, 12.0]	0.166
Lund-Kennedy Score; median [IQR]	1.5 [0.8, 2.5]	4.0 [2.0, 8.0]	2.0 [0.0, 2.0]	0.613

Abbreviations: AEC= Absolute Eosinophil Count, CRSsNP= Chronic Rhinosinusitis without Nasal Polyps, CRSwNP= Chronic Rhinosinusitis with Nasal Polyps, IgE= Immunoglobulin E, NP= Nasal Polyps, SD= Standard Deviation, SNOT-22= Sino-Nasal Outcome Test.

*Significant