Rethinking Chronic Rhinosinusitis and Pediatric Asthma: Aspirin Alternatives and Social Determinants

In chronic rhinosinusitis with nasal polyps (CRSwNP), standard care centers on intranasal corticosteroids, saline irrigation, short courses of systemic steroids when needed, and endoscopic sinus surgery (ESS) in selected cases. Aspirin desensitization is a targeted option for patients with NSAID‑exacerbated respiratory disease (AERD), not a general cornerstone for CRSwNP. Against that backdrop, new data are prompting reassessment of where aspirin desensitization fits—and how evolving therapies should be sequenced—while social determinants continue to shape asthma risk in children, linking the biology and the lived context of chronic inflammatory disease.

A recent Finnish report drew attention to mixed outcomes with aspirin desensitization in patients with AERD, highlighting uncertainty around improvements in polyp burden, symptom control, and steroid‑sparing effects. Current specialty guidelines describe aspirin desensitization as a selective strategy for AERD rather than routine CRSwNP care, and they emphasize careful patient selection and outcome tracking to determine benefit.

When CRSwNP remains severe and uncontrolled despite optimized intranasal therapy—and often after ESS—biologics such as dupilumab, omalizumab, and mepolizumab can be considered. Across trials, these agents have been shown to reduce polyp size, improve nasal obstruction and smell, and decrease reliance on systemic steroids and revision surgery, including in patients with AERD. Selecting among surgery, repeat surgery, and biologics is best approached through shared decision‑making that weighs symptom burden, comorbid asthma, access, and patient preference.

In AERD, COX‑1 inhibition amplifies dysregulated arachidonic‑acid metabolism and leukotriene overproduction, while Type 2 inflammation is a shared pathway across CRSwNP and asthma. Biology is only part of the story, though: environmental exposures, housing quality, and access to specialty care and advanced therapies can widen outcome gaps, especially for children.

Community health worker programs can narrow these gaps by addressing triggers at home and barriers to care; for example, the Community Asthma Initiative reported substantial reductions in emergency department visits and hospitalizations alongside improved symptom control after home-based education and environmental remediation support. Such results illustrate how public health interventions translate biology into better outcomes.

Treatment planning therefore benefits from a stepwise, guideline‑aligned approach. Start with intranasal corticosteroids and saline irrigation, use short courses of systemic steroids judiciously for exacerbations, and consider ESS when disease remains refractory or when obstructive polyps impair ventilation and drainage. For patients with AERD, aspirin desensitization may be discussed as a targeted option, with clear expectations and monitoring; for those with persistent, severe disease after optimized local therapy and often after ESS, biologics are reasonable to consider.

Because many patients with CRSwNP also carry comorbid asthma, aligning sinus and airway strategies can improve overall control. The shared Type 2 endotype supports coordinated use of intranasal steroids, inhaled therapies for asthma, and, when appropriate, biologics that address both conditions. Practical barriers—insurance coverage, clinic proximity, and caregiver capacity—can modulate access to these options and should be anticipated in care plans.

Diagnostics play a role in tailoring care. Objective measures (nasal endoscopy findings, polyp grading, smell testing) help stage severity, while history can uncover AERD clues such as respiratory reactions to COX‑1–inhibiting NSAIDs. Where available, multidisciplinary clinics that include allergy/immunology and otolaryngology can streamline evaluation and align timing of ESS, desensitization, and biologic initiation.

Follow‑up and outcome tracking are essential. Symptom scores, polyp grading, need for systemic steroids, and time to revision surgery provide a pragmatic framework for judging benefit from ESS, desensitization, or biologics. For pediatric patients and families facing environmental triggers, linkage to community resources can complement clinic‑based care.

Finally, population‑level efforts matter. School‑based asthma education, housing remediation partnerships, and CHW programs extend beyond the clinic to reduce exposure burdens and improve adherence. These initiatives can be particularly impactful where Type 2 biology intersects with socioeconomic constraints.

Key Takeaways:

• Aspirin desensitization is a selective therapy for AERD, not a cornerstone of CRSwNP care; first‑line management remains intranasal corticosteroids, saline irrigation, short systemic steroids as needed, and ESS when indicated.
• Therapeutic sequencing is key: consider ESS for refractory obstruction, then weigh biologics (dupilumab, omalizumab, mepolizumab) for severe, uncontrolled disease—including AERD—using shared decision‑making grounded in symptom burden, steroid‑sparing needs, and patient preferences.
• Shared Type 2 inflammation links CRSwNP and asthma, but outcomes are also shaped by social determinants; programs like the Community Asthma Initiative show how addressing home triggers and access barriers can reduce ED visits and hospitalizations.
• Structured follow‑up with objective and patient‑reported outcomes helps determine benefit and guides adjustments across ESS, desensitization, and biologics.