目的 提高对外源性过敏性肺泡炎的认识。 方法 回顾分析2011年10月报道1例外源性过敏性肺泡炎（过敏性肺炎）患者的诊断及治疗经过，总结其临床特征、诊疗要点及预后评价。 结果 患者数次误诊后最终诊断为外源性过敏性肺泡炎，予脱离变应原及激素治疗后痊愈，随访半年无复发。结论 该病临床表现无特异性，需结合患者病史、临床症状、血清学检查、影像学表现，甚至肺泡灌洗液及肺活检综合判断；脱离变应原为该病治疗的最根本、最重要措施；对于病情严重患者，短期全身性使用糖皮质激素可缩短病程或改善症状。
ObjectivesTo detect expressions of trefoil factor 1 (TFF1) and TFF3 in the mice with acute allergic airway disease (AAD) after different interventions, and explore primitively the effect of recombinant TFF3 on airway inflammation and mucous secretion.MethodsForty BALB/c mice were randomly divided into 5 groups, each group with 8 mice, ie. a normal saline control group (group A), an AAD group (group B), a budesonide intervention group (group C), a recombinant TFF3 intervention group (group D), and a budesonide+recombinant TFF3 intervention group (group D). The BALB/c mice were sensitized and challenged with ovalbumin to induce AAD. Lung tissue sections were stained with hematoxylin-eosin staining for assessment of airway inflammation, and immunohistochemistry was used for detecting TFF1/TFF3 expression in the airway. Alcian blue stain was applied to determine mucous secretion.ResultsAirway inflammation score and airway mucous secretion: Group B was significantly more than group A (P<0.01); Group C was less than group B (P<0.05), and there was no significant difference between group D and group B (P>0.05); There was no significant difference between group C and group E (P>0.05). Expression of TFFs: TFF1 and TFF3 were expressed in epithelial cells, goblet cells and submucosal gland cells of bronchi and bronchioles in all groups; The expressions of TFF1 and TFF3 in group B were significantly higher than those in group A (P<0.01), while the expressions of TFF1 and TFF3 in group C were lower than those in group B (P<0.05). TFF1 expression in airway epithelium was positively correlated with inflammatory score (r=0.876, P=0.000) and mucin expression (r=0.807, P=0.000). TFF3 level was positively correlated with inflammatory score (r=0.654, P=0.006) and mucin expression (r=0.666, P=0.005).ConclusionsOvalbumin-induced acute allergic airway inflammation significantly increases TFF1/TFF3 expression. Intranasal TFF3 treatment may not influence airway inflammation and mucus secretion. Inhaled corticosteroids to some extent inhibit expressions of TFF1 and TFF3, simultaneously suppress airway inflammation and mucus secretion in the mouse model of acute AAD .
摘要:目的:评价孟鲁司特用于过敏性鼻炎的临床疗效和安全性。方法:计算机检索PubMed、维普及CNKI数据库,手工收集有关孟鲁司特用于过敏性鼻炎治疗的临床研究,根据纳入和剔除标准汇集文献,采用Jadad量表进行纳入文献质量评价,对总体治疗有效性使用Revman4.2软件进行Meta分析。结果:疗效评价共纳入9个临床随机对照研究共650例。有效率孟鲁司特组高于对照组,异质性检验显示各亚组及其合并总有效率P值均大于0.1,I2lt;50%,采用固定效应模型计算。2周时孟鲁司特组和对照组无统计学差异(Pgt;0.1),但2月、3月时二组均有显著性统计学差异(Plt;0.000 01),三个亚组综合分析孟鲁司特组和对照组有显著性统计学差异(Plt;0.000 01),不良反应差异无统计学意义。结论:现有临床证据显示孟鲁司特较传统抗过敏药物对过敏性鼻炎的治疗有效,但由于纳入研究存在选择性偏倚和测量性偏倚的可能性,势必影响结果的论证强度。故期待更多高质量的随机双盲对照试验性研究,以提供更高质量的证据。Abstract: Objective: To evaluate montelukast for allergic rhinitis clinical efficacy and safety. Methods: We searched the PubMed,VIP and CNKI databases, manual collection of clinical study about allergic rhinitis treatment of montelukast, based on inclusion and exclusion criteria for pooling of literature, Jadad scale used for quality assessment of the literature. Then use Revman4.2 Meta analysis software to evaluate the overall effectiveness. Results: Nine RCT clinical study have been included, The results showed that montelukast group was higher than control group on efficient control, Heterogeneity test showed that the subgroup and its total effective rate is Pgt;01,I2lt;50%. Therefore, we adopted a fixed effects model. After 2 weeks montelukast group and the control group no significant difference (Pgt;0.1). But after 2,3 month the two groups were statistically significant differences(Plt;0.000 01). On a comprehensive analysis of the three subgroups, montelukast group and the control group statistically significant differences(Plt;0.000 01), adverse drug reactions was no significant difference. Conclusion: The available clinical evidence to show that montelukast for the treatment of allergic rhinitis and effective, However, due to the existence of selection and measurement bias, This may affect the outcome of the argument strength.Therefore look forward to more highquality randomized and doubleblind controlled trials to provide highquality evidence.
摘要:目的:探讨复方丹参加西咪替丁治疗过敏性紫癜(HSP)临床疗效。方法:60例患儿随机分为对照组和治疗组各30例。对照组常规治疗,治疗组加用复方丹参和西咪替丁治疗。结果:治疗组总有效率为90.0%,明显高于对照组53.3%,且治疗组紫癜性肾炎(HSPN)发生率(10.0%)明显低于对照组(36.7%),Plt;0.01。结论:复方丹参加西咪替丁能提高HSP患儿疗效,减少肾损害,促进患儿病情康复。
【摘要翻译】 一 氧化氮合酶( NOS) -2( NOS-2) 的诱导和一氧化氮产物增加是过敏性气道疾病的共同特征。严重哮喘与气道S-亚硝基硫醇减少相关。S-亚硝基硫醇是NO的生化产物, 可通过促炎症转录因子NF-κB 的S-亚硝基化抑制炎症反应。因此, 重建气道S-亚硝基硫醇对治疗可能有益。我们对此假设在以卵清蛋白诱导的过敏性炎症大鼠模型中进行验证。未使用或使用卵清蛋白致敏的动物均在卵清蛋白激发前于气管内灌注S-亚硝基谷胱甘肽( GSNO;50 μl, 10 mM) , 并在48 h 以后进行分析。GSNO 给药增加了肺组织S-亚硝基硫醇水平。与对照组比, GSNO 降低了卵清蛋白致敏动物NF-κB 的活性, 但对支气管肺泡灌洗细胞总数、分类计数及杯状细胞化生标记物均无显著影响。GSNO给药也改变了HIF-1 的活性, 导致未致敏大鼠HIF-1 活化,但抑制卵清蛋白致敏大鼠的HIF-1 活性。我们使用NOS-2基因敲除小鼠来评价内源性一氧化氮合成酶-2 在调节NF-κB和( 或) HIF-1 活性及气道过敏性炎症的作用。尽管在NOS-2 基因敲除小鼠中卵清蛋白诱导的NF-κB 活力轻度增高, 这与支气管肺泡灌洗中性粒细胞轻度增加有关, 其他的过敏性炎症指标和HIF-1 活性在NOS-2 基因敲除及野生型小鼠之间却无明显相差。总体来说, 我们的研究表明GSNO灌注能抑制气道过敏性炎症中NF-κB 活性, 但是并不能显著地影响大部分炎症及杯状细胞化生指标, 这样可能因为对其他信号通道( 比如HIF-1) 的影响而限制了它的治疗价值。【述评】 GSNO 是近年哮喘治疗研究的热点。既往的研究发现GSNO 在哮喘治疗中有一定前景。本研究却发现GSNO 气管内滴注虽能抑制过敏性气道炎症中NF-κB 活性,但并不能显著抑制气道炎症反应及杯状细胞化生这两个哮喘关键病理改变, 可能与GSNO 同时影响了HIF-1 等其他信号通路有关。该研究表明GSNO 对哮喘气道炎症治疗效果有限, 同时表明哮喘气道炎症调控机制较为复杂, 治疗药物的设计需考虑多种信号通路对哮喘气道炎症的影响。
ObjectiveTo investigate the common inhalant allergens causing allergic rhinitis in underage patients, and provide references for clinical prevention of allergic rhinitis. MethodsUnderage patients with allergic rhinitis admitted to our hospital between January 2010 and June 2013 were screened and skin prick test (SPT) was applied to investigate the response intensity to 22 kinds of common inhalant allergens and analyze the correlation of the positive rates and grades of allergens with age and sex. ResultsA total of 402 patients were included, and 77.6% (312/402) of them reported positive reaction of SPT; and the top five allergens were dust mites (242/402, 60.2%), house dust (235/402, 58.5%), housefly (142/402, 35.3%), spring pollen Ⅲ (133/402, 33.1%) and mulberry silk (121/402, 30.1%), respectively. Compared with patients whose age was younger than 5 years, both the positive rates and grades of SPT were significantly higher in patients above 5 years old. Additionally, the higher positive rates and grades of SPT were also observed much more in male patients than female patients. ConclusionThe most common inhalant allergens causing allergic rhinitis in underage patients are dust mites and house dust. And the SPT response intensity of inhalant allergens can be affected by age and gender.
Objective To investigate the expression of aquaporin-1( AQP-1) in pulmonary tissues of asthma mice and the effects of acetazolamide( AZ) on AQP-1 expression. Methods Forty C57BL/6 mice were randomly divided into five groups. Group A was treated with phosphate buffer as a non-asthmatic group.The mice in group B, C, D, and E were sensitized with ovalbumin( OVA) and challenged with aerosol OVA to establish asthma model. The mice in group B, C, and D were interperitoneally injected with AZ at doses of 300, 200, 100 mg/kg, respectively during the challenge period. Results ①Wet/dry weight ratio of lung tissues in group E was significantly higher than that in group A( P lt;0. 05) , while it was lower in B, C and D groups than group E. ②The total number of cells, the number of eosinophils, and interleukin-5( IL-5) inBALF of group E were higher than those in group A( P lt;0. 05) , and interferon-γ( IFN-γ) level was lower in group E than in group A ( P lt; 0. 05) . After AZ treatment, the total number of cells, the number of eosinophils, neutrophils and lymphocytes were significantly decreased( P lt; 0. 05) , which were positively correlated with the dose of AZ. ③AQP-1 were expressed in tracheal epithelium, microvascular endothelial cell and bronchial peripheral vascular bed, and the expression in group E was significantly higher than that in group A( P lt;0. 01) . AQP-1 expression was significantly decreased after the intervention of AZ ( P lt;0. 05) .The decrease was positively correlated with the dose of AZ. The expression of AQP-1 mRNA showed no significant difference among these groups( P gt;0. 05) . Conclusions AQP-1 was over-expressed in the lung tissue of mice with asthma. AZ can inhibit the expression of AQP-1 and relieve lung inflammatory cells infiltrationin a dose-dependent manner. It is the protein expression of AQP-1 not the AQP-1 mRNA which were significantly different in different groups, suggesting that AZ affected AQP-1 in the post-transcriptional stage.