OBJECTIVE:To investigate therapeutic efficacy and safety of clarithromycin intensive therapy on patients with chronic rhinosinusitis and its effects on serum inflammatory cytokines.METHODS:A total of 186 patients with chronic rhinosinusitis were randomly divided into control group 1 (62 cases),control group 2 (62 cases) and observation group (62 cases).Control group 1 was given Amoxicillin and clavulanate potassium tablet (7∶ 1) 0.457 g,3 times a day.Control group 2 was given Clarithromycin dispersible tablet 0.25 g orally,once a day.Observation group was given Clarithromycin dispersible tablet 0.5 g orally on the first week,twice a day,0.25 g at the second week,twice a day.Both groups were treated for 2 weeks.Clinical efficacies of 3 groups were observed.Clinical symptom score,TNF-α,IL-6 and hs-CRP before and after treatment as well as the occurrence of ADR were observed.RESULTS:Total response rate was in descending order:observation group (93.55％) ＞control group 2 (80.65％) ＞control group 1 (65.51％),with statistical significance (P＜0.05).Before treatment,there was no statistical significance in clinical symptom score,the levels of TNF-α,IL-6 and hs-CRP among 3 groups (P＞0.05).After treatment,clinical symptom score,the levels of TNF-αt,IL-6 and hs-CRP were significantly lower than before treatment;those indexes of 3 groups were in ascending order:observation group＜control group 2＜control group 1,with statistical significance (P＜0.05).The incidence of ADR in observation group and control groups were significantly lower than control group 1,with statistical significance (P＜0.05).There was no statistical significance between observation group and control group 2 (P＞0.05).CONCLUSIONS:Clarithromycin intensive therapy shows significant therapeutic efficacy for chronic rhinosinusitis,improves clinical symptoms of patients and reduces the level of serum inflammatory factor without increasing the occurrence of ADR.

Objective To study the effect of high mobility group box B1(HMGB1)gene knockout on alleviating a-cute lung injury and inhibiting toll-like receptor 4(TLR4)/nuclear factor-KB(NF-κB)pathway of sepsis mice.Methods Wild-type(WT)mice were divided into WT-Sham group and WT-model group,and HMGB1 knockout(KO)mice were divided into KO-sham group and KO-model group.Sepsis ALI model was established by cecal ligation and perforation in WT-model group and KO-model group.Sham operation was performed in WT-Sham group and KO-Sham group.24 h after modeling,the partial pressure of arterial oxygen(PaO2)was detected,oxy-genation index(OI)was calculated,pathological changes of lung tissue were detected and lung injury score was calculated,the concentrations of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1 β),interleukin-6(IL-6),reactive oxygen species(ROS),malondialdehyde(MDA),superoxide dismutase(SOD),in serum and lung tissues and the expression of HMGB1,TLR4 and nuclear NF-κB in lung tissues were detected.Results The PaO2,OI and the concentration of SOD in serum and lung tissue of WT-model group were lower than those of WT-Sham group,the lung injury scores,the concentrations of TNF-α,IL-1 β,IL-6,ROS and MDA in serum and lung tissue,and the expression levels of HMGB1,TLR4 and nuclear NF-κB in lung tissue were higher than those in WT-Sham group(P＜0.05).HMGB1 was not expressed in lung tissue of KO-model group,and the concentrations of PaO2,OI and the concentration of SOD in serum and lung tissue of KO-model group were higher than those of WT-model group,the lung injury scores,the concentrations of TNF-α,IL-1β,IL-6,ROS and MDA in serum and lung tissue,and the expression levels of TLR4 and nuclear NF-κB in lung tissue were lower than those of the WT-model group(P＜0.05).Conclusion HMGB1 gene knockout alleviates acute lung injury of sepsis mice,the re-lated molecular mechanism may be the inhibition of TLR4/NF-κB pathway mediated inflammation and oxidative stress.