The effects of Helicobacter pylori eradication therapy on salivary pepsin concentration in patients with laryngopharyngeal reflux.

OBJECTIVE: To investigate the effect of Helicobacter pylori (HP) eradication therapy on salivary pepsin concentration in laryngopharyngeal reflux (LPR) patients with HP infection. MATERIALS AND METHODS: A total of 477 patients with suspected LPR were enrolled from June 2020 to September 2021. Reflux symptom index, reflux finding score, the positive rates and disintegrations per minute values of HP infection detected by 14C urea breath test and salivary pepsin concentrations analyzed using enzyme-linked immunosorbent assay were compared in LPR patients and non-LPR patients with or without HP infection. HP-positive patients were treated with HP eradication therapy while HP-negative patients with PPI therapy. RESULTS: The scores of nagging cough (0.88 vs. 0.50, P = 0.035), erythema or hyperemia (1.93 vs. 1.78, P = 0.035) and vocal fold edema (1.04 vs. 0.85, P = 0.025) were higher in the LPR (+) Hp (+) subgroup than in LPR (+) Hp (-) subgroup. The concentrations of salivary pepsin in the Hp (+) subgroup were higher than in the Hp (-) subgroup either in LPR patients (75.24 ng/ml vs. 61.39 ng/ml, P = 0.005) or the non-LPR patients (78.42 ng/ml vs. 48.96 ng/ml, P = 0.024). Compared to baseline (before treatment), scores of nagging cough (0.35 vs. 0.84, P = 0.019) and erythema or hyperemia (1.50 vs. 1.83, P = 0.039) and the concentrations of salivary pepsin (44.35 ng/ml vs. 74.15 ng/ml, P = 0.017) in LPR patients with HP infection decreased after HP treatment; yet, this was not observed for the LPR patients without HP infection treated with PPI only (P > 0.05). CONCLUSION: HP infection may aggravate the symptoms and signs of LPR patients, partly by increasing their salivary pepsin concentration.

[Study on the oxidative injury of the vascular endothelial cell affected by PM2.5].

OBJECTIVE: To study the mechanism of cardiovascular disease affected by PM2.5. METHODS: ECV304 cells were exposed to PM2.5 of different concentration (50, 200 and 400 microg/ml), after 24h, the viability of cells by MTT, SOD and GSH contents in cells and apoptosis of cells determined by flow cytometer were measured. RESULTS: Viability of ECV304 cells declined and mortality of ECV304 cells increased gradually with increase of concentration, GSH contents in cells (mg/g prot) were 20.643 +/- 2.167, 16.774 +/- 2.911 (P < 0.05), 15.658 +/- 3.471 (P < 0.01), and SOD contents in cells (U/mg prot) were 5.878 +/- 0.401, 5.140 +/- 0.448 (P < 0.01), 4.817 +/- 0.451 (P < 0.01) when the concentration of PM2.5 was 50, 200 and 400 microg/ml. CONCLUSION: PM2.5 can cause vascular endothelial cells to die by way of oxidative injury, then induce cardiovascular disease.