Polypoid mucosa with eosinophilia and glandular hyperplasia in chronic sinusitis: A histopathological and immunohistochemical study
Polypoid mucosa with eosinophilia and glandular hyperplasia in chronic sinusitis: A histopathological and immunohistochemical study
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DOI：
10.1097/00005537-200204000-00026
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发表时间：
2002-04-01
期刊：
影响因子：
2.6
通讯作者：
Ophir, D
中科院分区：
文献类型：
--
作者：
Berger, G;Kattan, A;Ophir, D
目的：探讨慢性鼻窦炎的组织病理学和免疫组化特点，并结合鼻窦受累的程度进行分析。研究设计：一项非随机、回顾性、对照的定性和定量研究。方法. 29名患有难治性慢性鼻窦炎的成年人接受了功能性内窥镜鼻窦手术。计算机断层扫描的评分用于确定疾病的程度。6例正常鼻窦粘膜患者作为对照组。标本进行常规组织学处理和苏木精-伊红和高碘酸-希夫染色。应用免疫组化法检测T和B淋巴细胞。低倍显微镜用于观察典型的病理特征，高倍镜用于计数各种炎性细胞。结果如下：根据其主要病理特征将患者分为两组：16例为息肉样粘膜和嗜酸性粒细胞增多，13例为腺体增生。息肉样粘膜和嗜酸性粒细胞增多症患者固有层中嗜酸性粒细胞、T和B淋巴细胞的数量显著高于腺体增生和正常对照组，而腺体增生患者与对照组之间的差异不显著。尽管总体炎症反应相对温和，鼻息肉病在息肉样粘膜和嗜酸性粒细胞增多的患者中更普遍;同样，计算机断层扫描显示，与腺体增生患者相比，这些患者的疾病范围更广。结论：提示有两种病理生理学途径，诱导窦分泌物流出的长期阻塞并最终导致慢性炎症：1）息肉样粘膜肿胀，嗜酸性粒细胞活化，损害上皮细胞; 2）粘膜下浆液粘液腺增生导致粘液分泌持续增加。
Objective: To evaluate the histopathological and immunohistochemical characteristics of chronic sinusitis, with reference to the extent of sinus involvement. Study Design: A nonrandomized, retrospective, controlled qualitative and quantitative study. Methods. Twenty-nine adults with refractory chronic sinusitis underwent functional endoscopic sinus surgery. The score of computed tomography scans was used to determine the extent of disease. Six patients with normal sinus mucosae served as control subjects. Specimens underwent routine histological processing and hematoxylin-eosin and periodic acid-Schiff staining. Immunohistochemistry for T and B lymphocytes was applied. Low-magnification microscopy was designed to yield typical pathological features, and high magnification to count various inflammatory cells. Results: Patients were divided into two groups according to their dominant pathological features: 16 had polypoid mucosa and eosinophilia, and 13 had glandular hyperplasia. The number of eosinophils, T and B lymphocytes in the lamina propria was significantly higher in patients with polypoid mucosa and eosinophilia, compared with those with glandular hyperplasia and with normal control subjects, whereas the difference between patients with glandular hyperplasia and control subjects was insignificant. Although the overall inflammatory reaction was relatively modest, nasal polyposis was more prevalent in patients with polypoid mucosa and eosinophilia; likewise, computed tomography revealed a significantly more extensive disease in these patients compared with the patients with glandular hyperplasia. Conclusion: Two pathophysiological pathways, inducing prolonged obstruction to the outflow of sinus secretion and ultimately causing chronic inflammation, are suggested: 1) swollen polypoid mucosa with activation of eosinophils that damage the epithelium and 2) continued increased mucus secretion originated from hyperplastic submucosal seromucous glands.