Azithromycin In Patients With Chronic Sinusitis And Nasal Polyps Surgical Cavity Of Mucosal Epithelium And Mucosa Nf-kbp65 In Il-8 Expression

Objective To observe the effect of azithromycin on the nasal mucosalepithelialization of chronic sinusitis after endoscopic sinus surgery.Methods From December 2004 to December 2005, 59 patients withchronic sinusitis and/or nasal polyps were treated with endoscopic surgery.one month after operation, they were divided into 2 groups, and 37 patientswere treated with cephamycin as a control group, and 22 with Azithromycinas a experimental group. The course and the number of epithelialization werecounted.Results within 6 months, epithelialization happened in 22-126 days(average 51.143±27.655 days) in control group, and in 11～88(average33.046±18.874) in experimental group, the difference was statisticallysignificant(t=2.624, P=0.006). epithelialiazation happenen in 28 cases in thecontrol group and 22 cases in experimental group, and the difference wasalso statistically significant (χ~2=4.573 p=0.033).Conclusions (1)Azithromycin is effective in accelerating theepithelialization of nasal mucosa after endoscopic sinus surgery combinedwith local glucocorticoid. (2)The effect of azithromycin combined with local glucocorticoid on epithelialization Is better than cephamycin combined withlocal glucocorticoid. Objective To observe the effect of azithromycin on the expression ofNF-KBp65 and IL-8 in nasal mucosa of chronic sinusitis and nasal polypsafter endoscopic sinus surgery.Methods 45 patients with chronic sinusitis and/or nasal polyps whowere treated with endoscopic surgery 2 weeks ago were divided into 3groups, 15 patients treated with local glucocorticoid as a control group, 15patients were added with cephalosporin(500mg, once a day) as anothercontrol group, others were added with Azithromycin(500mg, once a day) as aexperimental group. The PV-6000 immunohistochemical method wereapplied to explore the expression of NF-KBp65 and IL-8 in nasal mucosabefore and after 3 weeks medical therapy while counting the quantity ofpositive cells.Results Chronic inflammation was observed in the nasal mucosa afterendoscopic sinus surgery by HE staining. There were many inflammatorycells such as neutrophil cell and eosinophil cell under the mucosal epithelium,The neutrophil cell is the key cell. The expression of NF-KBp65 waspositive in cytoplasm and some nuclear of the mucosal epithelia and the inflammatory cells in nasal mucosa. The expression of IL-8 was positive incytoplasm of the mucosal epithelia and the inflammatory cells in nasalmucosa. The expression of NF-KBp65 and IL-8 was significantly reduced inthe mucosal epithelia and inflammatory cells of nasal mucosa after 3 weeksmedical treatment compared with that of pre-treated in the 3 groups(p＜0.05).The difference of the expression of NF-KBp65 and IL-8 in the mucosalepithelia and inflammatory cells of nasal mucosa was statistically significantin the azithromycin group compared with the cephalosporin group and thecontrol group after treatment(p＜0.05). There were no statistical significanceof the expression of NF-KBp65 and IL-8 in the mucosal epithelia andinflammatory cells of nasal mucosa between the cephalosporin group and thecontrol group after treatment(p＞0.05).Conclusions (1) Chronic inflammation is the key representation in thenasal mucosa of chronic sinusitis and/or nasal polyps after endoscopic sinussurgery. (2) Inhibiting the expression of NF-KBp65 and IL-8 in mucosalepithelia and inflammatory cells in nasal mucosa may be one of themechanisms of azithromycin on chronic sinusitis and/or nasal polyps afterendoscopic sinus surgery. (3) Azithromycin combined with localglucocorticoid is better than glucocorticoid to inhibit the expression ofNF-KBp65 and IL-8 in mucosal epithelia and inflammatory cells in nasalmucosa of chronic sinusitis and/or nasal polyps after endoscopic sinus surgery. It is a effective method to cure the chronic inflammation of nasalmucosa in nasal cavity after endoscopic sinus surgery with azithromycinhcombined with glucocorticoid.