International Forum of Allergy & Rhinology最新文献

Background: Temperature-controlled radiofrequency (TCRF) ablation of the posterior nasal nerve has been shown to improve chronic rhinitis (CR) symptoms and quality of life (QoL). This study assesses the durability of TCRF's effectiveness and safety 3 years post-procedure in patients with perennial allergic CR and nonallergic CR.

Methodology: This prospective, multicenter, single-blinded, randomized controlled trial included a sham control arm and long-term follow-up. Analysis combined patients from the active treatment and control crossover arms. Outcomes include reflective total nasal symptom score (rTNSS), postnasal drip (PND), and cough scores, as well as QoL measured by the Mini Rhinoconjunctivitis Quality-of-Life Questionnaire (MiniRQLQ).

Results: Of 104 patients who underwent TCRF, 59 participated in the 3-year follow-up. The baseline mean rTNSS was 8.2 (95% confidence interval [95% CI, 7.9-8.6]), reduced to 3.5 (95% CI, 2.9-4.1) at 3 years, a 57.3% reduction and mean change of -4.7 (95% CI, -5.3 to -4.1; p < 0.0001). Most patients (79.7%) were responders. Cough scores decreased from a mean baseline of 1.5 (95% CI, 1.3-1.7) to 0.7 (95% CI, 0.5-0.9; mean change, -0.8; p < 0.0001). PND symptoms were also reduced from 2.5 (95% CI, 2.4 - 2.7) to 1.4 (95% CI, 1.2-1.7; mean change, -1.1; p < 0.0001). No severe adverse events were reported throughout the study, and no adverse events were reported between 24 months and 36 months of follow-up.

Conclusion: TCRF ablation of the posterior nasal nerve provided sustained safety and improvement in CR symptoms, cough, postnasal drip, and patient-reported QoL at 3 years, supporting its long-term safety and efficacy in CR.

Background: Combination pharmacotherapies are often selected for moderate-to-severe allergic rhinitis (AR), particularly when monotherapies do not control symptoms effectively. However, few studies have compared the efficacy and safety of different combination regimens. Therefore, we performed this study to investigate the clinical benefits of different combination strategies for moderate-to-severe AR.

Methods: Electronic databases were searched (inception-May 31, 2024) for randomized controlled trials involving combination therapies for treating moderate-to-severe AR. The medication classes included intranasal corticosteroids (INCS), intranasal antihistamines (INAH), oral antihistamines (OAH), and oral leukotriene receptor antagonists (LTRA). A network meta-analysis with a random-effects model was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines.

Results: Forty-eight eligible studies with 17,188 participants were included. In this meta-analysis, INAH and INCS, OAH and INCS, and INCS were the most effective in improving Total Nasal Symptom Score, and INAH and INCS, INAH, and INCS most effectively enhanced the total ocular symptom score. INCS and LTRA, OAH and INCS, and INAH and INCS showed the greatest benefit in improving the Rhinitis Quality of Life Questionnaire. Although INCS and INAH and INAH increased the risk of overall adverse events, specific adverse events predominantly included a bitter taste.

Conclusion: Combination therapies demonstrated superior efficacy compared to monotherapies overall. The INAH and INCS combination provided the greatest advantage in symptom improvement. The combination of OAH and INCS could be a viable alternative treatment option if the bitter taste is unacceptable. Our findings provide novel insights into optimizing personalized combination therapies.

Background: Mast cells (MCs) are involved in type 2 inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP), which depends on interleukin (IL)-33 stimulation. MiR-221 is reported to be an important regulator of MCs, and miR-221-3p can be expressed in CRSwNP. However, the role of miR-221-3p in CRSwNP is unclear.

Methods: Ethmoid tissues from control subjects (n = 12) and polyps from patients with CRSwNP (n = 40) were collected. The expression of miR-221-3p and cytokines was detected by real-time quantitative polymerase chain reaction (qPCR). The activation of P65 and ERK was determined by western blotting. The localization of miR-221-3p was detected via in situ hybridization combined with immunofluorescence (IF), and its target was identified via a luciferase reporter system. Human MCs were incubated with IL-33 or stem cell factor. MicroRNA mimics/inhibitor and lentiviral plasmids were used to determine the role of miR-221-3p in MCs.

Results: We observed increased expression of miR-221-3p in CRSwNP, and localized its expression in MCs. The expression of miR-221-3p was negatively correlated with that of IL-4, IL-5, and IL-13 in CRSwNP. MiR-221-3p can be induced by IL-33 in MCs and plays a negative regulatory role in cytokine expression and signaling pathways in IL-33-induced MC activation. As the direct target of miR-221-3p, the receptor KIT was negatively correlated with miR-221-3p and decreased in CRSwNP. In MCs, KIT is essential for an effective response to IL-33 stimulation. We here demonstrated that miR-221-3p regulates cytokine expression by targeting KIT in IL-33-activated MCs.

Conclusions: MiR-221-3p inhibits MC-dependent type 2 inflammatory conditions, rendering it a negative regulator of CRSwNP.