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目的观察超短波治疗支原体肺炎的疗效及其对血清细胞因子的影响。方法将80例支原体肺炎患儿随机分为治疗组和对照组,每组40例。对照组给予单纯药物治疗,治疗组在药物治疗的基础上加用超短波治疗。2组患者均在治疗前、后记录其临床症状及体征,并检测血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-6 (IL-6)和白细胞介素-8(IL-8)水平。结果对照组40例中,治愈25例,基本治愈6例,有效9例;治疗组40例中,治愈34例,基本治愈5例,有效1例,2组差异有统计学意义(P<0.05),治疗组疗效优于对照组。治疗组住院天数明显比对照组短,差异有统计学意义(P<0.01)。2组治疗后细胞因子水平(TNF-α、IL-6和IL-8)均较治疗前明显降低,差异有统计学意义(P<0.01);且治疗组降低更为明显,与对照组比较,差异有统计学意义(P<0.05或P<0.01)。结论超短波治疗小儿支原体肺炎可加速肺部炎症的吸收,缩短疗程,治疗机制可能与其影响细胞因子的分泌,从而调节机体对炎症的免疫反应有关。
Objective To observe the curative effect of ultrashort wave therapy on mycoplasma pneumonia and its effect on serum cytokines. Methods 80 cases of children with mycoplasma pneumonia were randomly divided into treatment group and control group, 40 cases in each group. The control group was given simple drug treatment, and the treatment group was treated with ultrashort wave based on the drug treatment. The clinical symptoms and signs of both groups were recorded before and after treatment. The levels of TNF-α, IL-6 and IL- 8) level. Results Of 40 cases in the control group, 25 cases were cured, 6 cases were basically cured and 9 cases were effective. Among the 40 cases in the treatment group, 34 cases were cured, 5 cases were basically cured and 1 case was effective. The difference was statistically significant (P <0.05 ), The treatment group than the control group. The days of hospitalization in the treatment group were significantly shorter than those in the control group, with significant difference (P <0.01). The levels of cytokines (TNF-α, IL-6 and IL-8) in the two groups after treatment were significantly lower than those before treatment (P <0.01), and the treatment group decreased more significantly compared with the control group , The difference was statistically significant (P <0.05 or P <0.01). Conclusion Ultrashort wave treatment of children with mycoplasma pneumonia can accelerate the absorption of lung inflammation, shorten the course of treatment may be related to the mechanism of its influence on the secretion of cytokines, which regulate the body’s immune response to inflammation.