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。
Objective To investigate whether the peri pheral administration of amitri ptyl ine produces antihyperalgesiceffect following the chronic constriction injury (CCI) of the sciatic nerve in rats. Methods Forty-eight maleCCI rats weighing (220 ± 20) g were randomly divided into 6 groups (n=8)：group NS, group A2.5, group A5, group A10,group A15.9 and group Aip. In the group NS, group A2.5, group A5, group A10 and group A15.9, sciatic nerve blockade was locally performed with 0.5 mL normal sal ine, and 2.5, 5.0, 10.0, 15.9 mmol/L amitriptyl ine respectively through implanted cannulas on the 7th day after operation. In the group Aip, amitriptyl ine (2.5 mg) was administered by intraperitoneal injection. The mechanical withdrawal threshold (MWT), thermal withdrawal latency (TWL) and motor function were measured before and 1, 2, 4, 8, 12, 24 and 48 hours after sciatic nerve blockade. Results Forty-eight CCI rats were all survival without infection palsy and catheter fall ing off. The rats of group A2.5, group NS and group Aip didn’t produce ambulation deficits. There were no significant difference in these 3 groups (P gt; 0.05). However compared with group A2.5, group NS and group Aip, the rats of group A5, group A10, group A15.9 all produced significant ambulation deficits (P lt; 0.05). The ambulation deficits lasted 2 hours (group A5), 4 hours (group A10), 8 hours (group A15.9) respectively. But the ambulation deficits of CCI rats were all reversible. The MWT and TWL of groups with local injection of amitriptyl ine increased when conpared with group NS, group Aip and those of before injection (P lt; 0.05). Sciatic nerve blockade with amitriptyl ine significantly suppressed mechanical hyperalgesia and thermal hyperalgesia in neuropathic rats. The peripheral anti-hyperalgesic effects lasted 2 hours (A2.5 group), 4 hours (group A5), 24 hours (group A10), 24 hours (group A15.9) respectively. But there were no significant difference between A10 group and A15.9 group (P gt; 0.05). There were no significant difference between group NS and group Aip (P gt; 0.05). Conclusion The peri pheral anti-hyperalgesic effects can be found in sciatic nerve blockade of amitri ptyl ine on CCI rats. And this effect of amitri ptyl ine has concentration dependent and ceil ing effect. Amitri ptyl ine of 5.0-15.9 mmol/L can produce significantambulation deficits which are reversible.
ObjectiveTo investigate the role of interleukin-25 (IL-25) and its receptor during allergen challenge test in allergic asthmatics as well as its underlining mechanism.MethodsFifteen allergic asthmatic patients with dual response in allergen challenge test were enrolled and blood samples were collected before and after challenge test. The expression levels of IL-25 receptor on the surface of eosinophils, plasma and intracellular IL-25 levels were measured by flow cytometry and enzyme-linked immunosorbent assay. Besides, the function of eosinophils from these patients was evaluated through the expression of type 2 cytokines, degranulation and chemotaxis after stimulation with IL-25.ResultsUpon allergen challenge, the expression of IL-17RB on the surface of eosinophils were increased from (7 426±2 824)/106 white blood cells to (19 446±5 593)/106 white blood cells (P<0.001). The expression of IL-17RA/RB on eosinophils were significantly increased from (4 508±1 360)/106 white blood cells to (9 025±3 166)/106 white blood cells (P<0.001). The plasma level of IL-25 increased from (650±45) pg/ml to (851±43) pg/ml (7 hours after allergen challenge) and (813±56) pg/ml (24 hours after allergen challenge) (P<0.001). The intracellular IL-25 expression of eosinophils was also upregulated from (10 398±1 909)/106 white blood cells to (147 684±46 222)/106 white blood cells (P<0.05). In vitro study, IL-25 (1 ng/ml) stimulated eosinophils for 2 hours promoted its expression of peroxidase [(12.5±4.2) ng/ml compared to control (1.26±0.4) ng/ml, P<0.05). The intracellular expression of IL-5 and IL-13 in eosinophils were also increased after stimulated by IL-25. IL-25 (1 pg/ml) stimulation compared to control could increase eosinophil migration in eotaxin [(36±3) vs. (69±5), P<0.05).ConclusionIL-25 and its receptor play a critical role in eosinophilic aggregation, activation and mobilization during allergic inflammation in allergic asthmatics.
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.
Sleep deprivation can cause hyperalgesia, and the mechanisms involve glutamic acid, dopamine, serotonin, metabotropic glutamate receptor subtype 5, adenosine A2A receptor, nicotinic acetylcholine receptor, opioid receptor, brain-derived neurotrophic factor, melatonin, etc. The mechanisms of hyperalgesia caused by sleep deprivation are complex. The current treatment methods are mainly to improve sleep and relieve pain. This paper reviews the mechanism and treatment progress of hyperalgesia induced by sleep deprivation, and aims to provide scientific evidence for the treatment of hyperalgesia caused by sleep deprivation.
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.