Reactive airways dysfunction syndrome due to chlorine: Sequential bronchial biopsies and functional assessment
Reactive airways dysfunction syndrome due to chlorine: Sequential bronchial biopsies and functional assessment
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DOI：
10.1183/09031936.97.10010241
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发表时间：
1997-01-01
影响因子：
24.3
通讯作者：
Boutet, M
中科院分区：
文献类型：
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作者：
Lemiere, C;Malo, JL;Boutet, M
关于反应性气道功能障碍综合征（RADS）引起的急性组织病理学支气管改变的信息非常少。我们有机会对因氯而患有 RADS 的受试者（急性接触后 60 小时、15 天、2 和 5 个月）进行连续支气管活检，并评估肺活量测定和支气管对乙酰甲胆碱的反应性。 1994 年 9 月 12 日，水过滤厂的一名 36 岁工人（不吸烟）突然吸入高浓度的氯。他立即感到鼻腔和喉咙烧灼感、胸骨后烧灼感和喘息，这些症状在轮班期间和轮班后持续存在。两天后，他主诉胸骨后烧灼感、呼吸困难和喘息。记录吸气性哮鸣音。他的一秒用力呼气量 (FEV(1)) 为预测值的 66%，导致 FEV(1) (PC20) 下降 20% 的乙酰甲胆碱激发浓度略有异常 (2.5 mg.mL-1)。第二天，患者接受了支气管活检，结果显示上皮几乎完全被纤维蛋白出血性渗出物取代。受试者被开了吸入类固醇。事故发生15天后，PC20改善至6毫克。毫升（-1）。支气管活检显示大量上皮脱落，伴有炎性渗出物和上皮下间隙肿胀。事故发生五周后，PC20 正常（57 mg·mL(-1)）。停止吸入类固醇。事故发生两个月后，PC20 恶化至 4 毫克。毫升（-1）。然后活检显示基底细胞使上皮再生(1)，并且仍然存在明显的炎症浸润。重新开始吸入类固醇。三个月和五个月后，PC20 正常（24 mg·mL(-1)）。支气管活检显示上皮细胞大大改善，炎症浸润减少。该病例报告表明，反应性气道功能障碍综合征可导致急性、显着但部分可逆的组织学异常。在这种情况下，吸入类固醇可能会调节支气管反应性的变化。
Very little information is available on the acute histopathological bronchial alterations caused by reactive airways dysfunction syndrome (RADS). We had the opportunity to carry out sequential bronchial biopsies in a subject with RADS due to chlorine (60 h, 15 days, 2 and 5 months after the acute exposure), and also to assess spirometry and bronchial responsiveness to methacholine.A 36 year old worker in a water-filtration plant (nonsmoker) abruptly inhaled high concentrations of chlorine on September 12, 1994. He experienced immediate nasal and throat burning, retrosternal burning and wheezing, and these symp toms persisted during and after the workshift. Two days later, he complained of retrosternal burning, dyspnoea and wheezing. Inspiratory wheezing was documented. His forced expiratory volume in one second (FEV(1)) was 66% of predicted and the provocative concentration of methacholine causing a 20% fall in FEV(1) (PC20) was slightly abnormal (2.5 mg . mL-1). On the following day, the patient underwent bronchial biopsies, which showed almost complete replacement of the epithelium by a fibrinohaemorhagic exsudate. The subject was prescribed inhaled steroids.Fifteen days after the accident, the PC20 was improved to 6 mg . mL(-1). Bronchial biopsies showed considerable epithelial desquamation with an inflammatory exudate and swelling of the subepithelial space. Five weeks after the accident, the PC20 was normal (57 mg . mL(-1)). Inhaled steroids were stopped. Two months after the accident, the PC20 deteriorated to 4 mg . mL(-1). Biopsies then showed regeneration(1) of the epithelium by basal cells and there was still a pronounced inflammatory infiltrate. Inhaled steroids were restarted. Three and five months later, the PC20 was normal (24 mg . mL(-1)). Bronchial biopsies showed a greatly improved epithelium and reduction of the inflammatory infiltrate.This case report shows that reactive airways dysfunction syndrome can cause acute, marked, though partially reversible, histological abnormalities. Inhaled steroids may modulate changes in bronchial responsiveness in this condition.