Bavbek S, Demirel Y S, Erekul S, Kalayctoglu O, Beder S, Misirligil Z, Gürbüz L
Department of Allergic Disease, School of Medicine, Ankara University, Turkey.
Allergol Immunopathol (Madr). 1996 Mar-Apr;24(2):45-53.
Epidemiological data indicated that allergic rhinitis often coexists with and may precede the development of reactive airway disease. In particular, ARP with BHR are more likely to develop asthma. However, the pathogenesis of BHR associated with allergic rhinitis is still remains uncertain. Therefore we designed the study on ARP with/without BHR. The aim of this study were to investigate the presence of an inflammatory process in lower respiratory tract in ARP and to relate these changes to airway responsiveness Eleven ARP with BHR (Group I), eleven ARP without BHR (Group II) and two control patients (Control group) were studied. All of the ARP were judged atopic on the basis of positive skin prick test to common inhalant allergens. Bronchial challenges were performed with increasing concentration of M. All the subjects underwent fiberoptic bronchoscopy, BAL and bronchial biopsies were obtained for pathologic examination. The mean total cell and the mean percentage of macrophages, lymphocytes, neutrophils and eosinophils in BAL fluid were in normal range in all groups without any significant differences between the groups. There weren't any correlation between PC20 to M and the total cell counts and percentage counts of these cells. In bronchial biopsy samples, the absolute numbers of lymphocytes, neutrophils, eosinophils and mast cells in the submucosa showed no differences between the three groups. The epithelial shedding was more extensive in ARP than control subjects (p = 0.05). The thickness of the epithelium was prominent in Group I (p < 0.05) but there was no significant differences in the basement membrane thickening between the three groups. We could only find an inverse correlation between PC20 to M and the mast cell counts in the submucosa (r xy:-0.815 p < 0.05). In conclusion, we couldn't observe any prominent morphological changes which indicate that may cause of BHR in ARP except the increased epithelial shedding in Group I. However, the increased epithelial shedding is not a reliable criterion to comment because of the possibility of mechanical damage of bronchial biopsies caused by the forceps.
流行病学数据表明，过敏性鼻炎常与反应性气道疾病共存，且可能先于其发生。特别是，伴有支气管高反应性（BHR）的变应性鼻炎患者更易发展为哮喘。然而，与过敏性鼻炎相关的支气管高反应性的发病机制仍不确定。因此，我们设计了这项关于伴有/不伴有支气管高反应性的变应性鼻炎的研究。本研究的目的是调查变应性鼻炎患者下呼吸道炎症过程的存在情况，并将这些变化与气道反应性相关联。我们研究了11例伴有支气管高反应性的变应性鼻炎患者（第一组）、11例不伴有支气管高反应性的变应性鼻炎患者（第二组）和2例对照患者（对照组）。所有变应性鼻炎患者根据对常见吸入性过敏原皮肤点刺试验阳性判断为特应性。用递增浓度的甲酰甲胆碱进行支气管激发试验。所有受试者均接受纤维支气管镜检查，获取支气管肺泡灌洗（BAL）样本和支气管活检组织进行病理检查。所有组支气管肺泡灌洗液中的平均总细胞数以及巨噬细胞、淋巴细胞、中性粒细胞和嗜酸性粒细胞的平均百分比均在正常范围内，各组之间无显著差异。甲酰甲胆碱激发试验的PC20与这些细胞的总细胞计数和百分比计数之间无相关性。在支气管活检样本中，三组之间黏膜下层淋巴细胞、中性粒细胞、嗜酸性粒细胞和肥大细胞的绝对数量无差异。变应性鼻炎患者的上皮脱落比对照受试者更广泛（p = 0.05）。第一组上皮厚度显著增加（p < 0.05），但三组之间基底膜增厚无显著差异。我们仅发现甲酰甲胆碱激发试验的PC20与黏膜下层肥大细胞计数呈负相关（r xy: -0.815，p < 0.05）。总之，除了第一组上皮脱落增加外，我们未观察到任何表明可能导致变应性鼻炎患者支气管高反应性的显著形态学变化。然而，由于活检钳可能对支气管活检造成机械损伤，上皮脱落增加并不是一个可靠的评判标准。
