The scores on patient-based questionnaires such as the SNOT-20, SF-36, and VAS correlate with each other. The CT stage correlated weakly but significantly with the scores in the patient-based questionnaires only in the CRSwNP subgroup. The presence of nasal polyps was not associated with poor QoL in CRS patients.

Pepsin in saliva has moderate value in the diagnosis of LPR. The cutoff value used could affect the diagnostic value. Therefore, further investigations are required to find the optimal method to detect salivary pepsin in diagnosing LPR.

Objectives We aimed to confirm the presence of pepsinA in the nasal secretions and tissues of chronic rhinosinusitis (CRS) patients and reveal the relationship between CRS and laryngopharyngeal reflux (LPR). Study Design Cross-sectional study. Setting The study was conducted at the Department of Oto-Rhino-Laryngology, West China Hospital, Sichuan University. Subjects and Methods A total of 32 CRS patients with or without nasal polyps (CRSwNP and CRSsNP, respectively) and 10 normal controls were enrolled in our study. We investigated the expression of pepsinA in the nasal tissues, secretions, and blood plasma from the subjects by immunohistochemical staining, Western blot, or ELISA. Additionally, the expressions of MUC4, MUC5AC, MUC5B, MUC8, and pepsinogenA in nasal tissue were evaluated by quantitative real-time polymerase chain reaction. Results Immunohistochemistry and Western blot revealed that the pepsinA expression levels in the turbinate mucosa in CRSwNP/CRSsNP patients, which were largely restricted to the epithelial layer or glandular mucous cells in nasal tissues, were significantly higher than those in controls and in the polyp tissues of CRSwNP patients ( P < .05). In addition, the concentration of pepsinA in nasal secretions was significantly increased in the CRSwNP (147.85 ± 53.69 ng/mL, P < .001) and CRSsNP (134.12 ± 36.23 ng/mL, P < .001) groups as compared with the controls (68.69 ± 19.28 ng/mL). Although MUC5AC, MUC5B, and MUC8 expression differed among the groups, no correlation between pepsinA and mucin genes was found. Conclusion The results of this study provided evidence of an association between LPR and CRS, although no correlation was found to exist between LPR and mucin genes in CRS patients.

These results suggest that LPR may play a role in the development of CRS through pepsin A reflux, and increased HSP70 expression may be associated with the pathogenic mechanism of mucosal injury in CRS.

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The present study aimed to evaluate the relationship between OSA and adenotonsillar size in children of different weight status. A total of 451 patients aged 2–13 years with suspected OSA were retrospectively enrolled in the study. Correlations between the apnea-hypopnea index (AHI) and adenotonsillar size in different weight status were investigated. The adenoidal/nasopharyngeal (A/N) ratio of underweight children was significantly higher than that of normal-weight children ( P = 0.027). Both adenoid and tonsil size were positively correlated with logAHI in children of normal weight (r = 0.210, P = 0.001; and r = 0.212, P = 0.001) but uncorrelated in the other groups. Gender (OR = 1.49, 95% CI: 1.01–2.20, P = 0.043), obese (OR = 1.93, 95% CI: 1.10–3.40, P = 0.012), A/N ratio (OR = 1.55, 95% CI: 1.28–1.88, P < 0.001) and tonsil size (OR = 1.36, 95% CI: 1.18–1.57, P < 0.001) were all associated with the severity of OSA. Adenotonsillar hypertrophy contributed to OSA in normal-weight children. In children of abnormal weight, instead of treatment for adenotonsillar hypertrophy, appropriate treatments for other factors are required.

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