部分呼出气一氧化氮检测在肺炎支原体肺炎中的意义

Value of fraction exhaled nitric oxide detection in children with Mycoplasma pneumoniae pneumonia

目的 探讨部分呼出气一氧化氮（FeNO）检测在肺炎支原体肺炎（MPP）中的意义。方法 选取2012年8月至11月收治的住院前未使用过糖皮质激素及白三烯受体拮抗剂的下呼吸道感染患儿，从中筛选出69例单纯肺炎支原体（MP）感染为MPP组，33例非MPP组，MPP组按影像学表现再分为MPP大叶型组和MPP支气管型组。54例外科腹股沟斜疝择期手术儿童为对照组。入院后进行 FeNO 检测，同时留取外周血标本进行白细胞计数及测定嗜酸性粒细胞百分比。结果 MPP 组 FeNO 值［（6.28 ± 3.00）ppb］与非 MPP 组［（10.85±2.86）ppb］、对照组［（9.74 ±3.10）ppb］相比均显著降低，差异均有统计学意义（t=7.30、6.26，P均〈0.0001）；MPP支气管型组FeNO值［（5.78±3.06）ppb］与MPP大叶型组［（6.48±2.98）ppb］相比差异无统计学意义（t=0.88，P 〉0.05）。MPP组外周血嗜酸性粒细胞比例［（0.60 ±0.51）% ］与非 MPP组［（1.15±0.76）% ］比较显著降低，差异有统计学意义（t=4.14，P 〈0.000 1）；MPP支气管型组外周血嗜酸性粒细胞比例［（0.61±0.57）% ］与 MPP大叶性型组外周血嗜酸性粒细胞比例［（0.60±0.55）% ］比较差异无统计学意义（t= -0.05，P 〉0.05）。结论 MP感染致FeNO减少，可能与MP感染致呼吸道上皮纤毛系统破坏及细胞免疫反应失衡，从而影响一氧化氮生成有关，MPP后呼吸道炎性反应的发生及进展是呼吸道上皮纤毛系统损害及细胞免疫反应失衡互为因果的炎性反应损害过程。

Objective To explore the the role of fraction exhaled nitric oxide（FeNO） in airway inflammation of Mycoplasma pneumoniae pneumonia（MPP）. Methods Inpatients with low respiratory tract infection were enrolled from August to November in 2012,69 patients had MPP and 33 had no MPP（non - MPP）. Patients with MPP were further grouped into a bronchopneumonia group and the lobar pneumonia group. Fifty - four inguinal hernia patients without respiratory tract infection during the last 2 weeks were enrolled as a control group. FeNO was measured by nitric oxide analyzer. Eosinophile level was detected by blood cells analysator. Results The level of FeNO in patients with MPP [（6.28±3.00） ppbl was lower than that of patients of non- MPP [（10.85 ±2.86） ppb] and the control gToup [ （9.74 ±3. 10） ppb] （t =7.30,6.26,respectively,all P 〈0. 000 1 ） ;the level of FeNO between the bronchopneumouia group [ （ 5.78 ± 3.06 ） ppb ] and the lobar pneumonia group [ （6.48 ± 2.98） ppb ] with infection of Mycoplasma pneumoniae （MP） had no statistical significanee（t =0. 88 ,P 〉0.05）. The proportion of blood eosinophile in patients with MPP [ （0.60 ± 0.51 ） % ] was lower than that of non - MPP group [ （ 1.15 ± 0.76 ） % ] （ t = 4.14, P 〈 0：000 1 ） ; the proportion of blood eosinophile between bronchopneumonia group [ （ 0.61 ± 0.57 ） % ] and lobar pneumonia group [ （0.60± 0. 55 ） % ] with infection of MP had no discrepance （ t = - 0. 05,P 〉 0.05 ）. Conclusions MP infection decreases production of FeNO. The possible mechanism for this phenomenon is that the cilia loss and hypefimmune response to MP may affect the production of FeNO. The airway inflammation of mycoplasma pneumonia is associated with cilia loss and hypefimmune response.