Effect of short-term systemic glucocorticoid treatment on human nasal mediator release after antigen challenge.
Effect of short-term systemic glucocorticoid treatment on human nasal mediator release after antigen challenge.
复制标题
短期全身糖皮质激素治疗对抗原攻击后人鼻介质释放的影响。
DOI：
10.1172/jci113188
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Naclerio,RM
中科院分区：
文献类型：
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作者：
Pipkorn,U;Proud,D;Lichtenstein,LM;Schleimer,RP;Peters,SP;AdkinsonJr,NF;Kagey-Sobotka,A;Norman,PS;Naclerio,RM
在13名过敏个体中进行的双盲、交叉研究中，确定了全身性糖皮质激素治疗对过敏原激发后早期和晚期鼻过敏反应的影响。受试者在激发前用60 mg泼尼松/d或匹配的安慰剂预处理2 d。利用先前描述的使用重复鼻灌洗来测量体内介质释放的模型。记录攻毒前、攻毒期间和攻毒后反复获得的症状评分以及打喷嚏的次数和时间。测量的介质是组胺。N-α-对甲苯磺酰基-L-精氨酸甲酯（驯服）-酯酶活性、激肽、PGD 2和LTC 4/D4。还测量了白蛋白作为血浆漏出的标志物。采集血样，测定白色血细胞总数、分类计数和血组胺总含量。在过敏反应的早期阶段，除了激肽减少外，未发现类固醇治疗对症状或任何介质的外观有影响。但在晚期，强的松减少了喷嚏次数（P <0.01），以及组胺（P <0.05）、TAME-酯酶活性（P <0.05）、激肽（P <0.05）和白蛋白（P <0.05）水平。只有低水平的白三烯被发现在晚期阶段，但这些介质的数量似乎减少了糖皮质激素治疗（P = 0.06）。在LPR期间，PGD 2没有增加，因此不受糖皮质激素的影响。还评价了第一次激发后11 h对第二次激发的即时反应。而在安慰剂治疗的受试者中，介质的出现比对相同激发剂量的初始反应增强，这种增强在泼尼松治疗后消失。由于已知该剂量的药物在治疗花粉热方面具有临床有效性，因此本研究证实了其他人的早期发现，即短期全身性糖皮质激素治疗抑制抗原激发的晚期而非即刻。此外，即时反应的二次增强被抑制。本研究表明，糖皮质激素在晚期反应和生理反应中抑制炎症介质的产生或释放。
The effect of systemic glucocorticoid treatment on early- and late-phase nasal allergic reactions after allergen challenge was determined in a double-blind, cross-over study in 13 allergic individuals. The subjects were pretreated for 2 d before challenge with 60 mg prednisone per day or a matching placebo. A previously described model using repeated nasal lavages for measuring mediator release in vivo was utilized. Symptom scores obtained repeatedly before, during, and after the challenge and the number and timing of sneezes were recorded. The mediators measured were histamine. N-alpha-p-tosyl-L-arginine methyl ester (TAME)-esterase activity, kinins, PGD2, and LTC4/D4. Albumin was also measured as a marker of plasma transudation. Blood samples were taken for determination of total number of white blood cells, differential count, and total blood histamine content. No effect of steroid therapy was found on the appearance of symptoms or any of the mediators, except a reduction in kinins, in the early phase of the allergic reaction. However, in the late phase, the prednisone reduced the number of sneezes (P less than 0.01), as well as the level of histamine (P less than 0.05), TAME-esterase activity (P less than 0.05), kinins (P less than 0.05), and albumin (P less than 0.05). Only low levels of leukotrienes were found in the late phase, but the quantities of these mediators seemed to be decreased by the glucocorticoid treatment (P = 0.06). PGD2 did not increase during the LPR and thus was not affected by glucocorticosteroids. The immediate response to a second challenge 11 h after the first was also evaluated. Whereas the appearance of mediators was enhanced over the initial response to the same challenge dose in placebo-treated subjects, this enhancement was abrogated after prednisone treatment. As this dose of drug is known to be clinically effective in treating hay fever, the present study confirms the earlier findings of others that short-term systemic glucocorticoid treatment inhibits the late phase but not the immediate phase of antigen challenge. Furthermore, secondary enhancement of immediate responses is inhibited. This study shows that glucocorticoids inhibit the generation or release of inflammatory mediators during the late reaction and the physiologic response.