Vitamin D Deficiency in Chronic Rhinosinusitis with Nasal Polyps

Introduction: Vitamin D plays an important role in sinonasal immune homeostasis, suppressing IL-36γ production and inhibiting the proliferation of nasal polyp-derived fibroblasts. While deficiency is mechanically linked to polyp severity, its impact on postoperative trajectory remains undefined. This study utilizes real-world data to determine if preoperative Vitamin D deficiency predicts surgical failure or increased acute healthcare burden following functional endoscopic sinus surgery (FESS).

Methods: A retrospective cohort study was conducted using the TriNetX Global Health Research Network. Adult patients with CRSwNP undergoing FESS were stratified by diagnosed preoperative Vitamin D deficiency (ICD-10 E55). Patients with Cystic Fibrosis were excluded. Propensity score matching (PSM) was performed for age, sex, race, obesity, smoking status, asthma, type 2 diabetes, and previous sinus surgery. Outcomes assessed surgical revision, emergency department utilization, acute sinusitis diagnoses, rescue medication dependence (systemic steroids, antibiotics), and escalation to biologic therapy.

Results: Vitamin D deficiency was associated with a statistically significant increase in the rate of revision sinus surgery within 3 years (8.10% vs 7.31%; p=0.009). Furthermore, deficient patients demonstrated an increase in ED visits within 1 year (18.71% vs 9.78%; p< 0.0001) and a markedly higher risk of postoperative acute sinusitis within 1 year (19.86% vs 10.97%; p< 0.0001). Deficiency also predicted an increase in rescue medication utilization, including antibiotics (40.41% vs 25.99%), systemic steroids (35.61% vs 22.72%), and escalation to biologic therapy (7.51% vs 5.42%; p< 0.0001 for all comparisons).

Conclusions: Vitamin D deficiency acts as a predictor of therapeutic failure in CRSwNP. Deficient patients are less likely to achieve surgical cure and suffer from a burden of acute care utilization. Preoperative Vitamin D optimization may be a critical strategy to restore IL-36γ-mediated homeostasis and reduce the healthcare burden of CRSwNP.