中华耳鼻咽喉科杂志
中華耳鼻嚥喉科雜誌
중화이비인후과잡지
CHINESE JOURNAL OF OTORHINOLARYNGOLOGY
2001年
1期
42-43
,共2页
张盛忠%卢志达%倪鑫%张勇%洪明理
張盛忠%盧誌達%倪鑫%張勇%洪明理
장성충%로지체%예흠%장용%홍명리
鼻硬结病%免疫组织化学%显微镜检查,电子
鼻硬結病%免疫組織化學%顯微鏡檢查,電子
비경결병%면역조직화학%현미경검사,전자
目的观察鼻硬结病的组织病理学和临床特点,探讨鼻硬结杆菌对宿主造成组织损伤的机理。方法以24例鼻硬结病患者的组织标本为研究对象,用HE及组织化学W-S(Warthin-Starry)染色,其中11例组织分别用CD43(T淋巴细胞)、CD20(B淋巴细胞)、CD68(巨噬细胞)、溶菌酶抗体免疫组化ABC法染色,2例进行透射电镜观察。结果肉芽肿期15例,纤维瘢痕期9例。 W-S染色和电镜观察均在Mikulicz细胞内检测出大量鼻硬结杆菌,细胞外偶见。电镜下Mikulicz细胞内出现大量吞噬体,将细胞器挤到一侧,粗面内质网及溶酶体很少。在病变组织内T淋巴细胞很少,Mikulicz细胞的溶菌酶抗体表达较弱。结论鼻硬结病患者显示细胞免疫功能障碍的特点,宿主的免疫反应是导致组织损伤的主要原因。
目的觀察鼻硬結病的組織病理學和臨床特點,探討鼻硬結桿菌對宿主造成組織損傷的機理。方法以24例鼻硬結病患者的組織標本為研究對象,用HE及組織化學W-S(Warthin-Starry)染色,其中11例組織分彆用CD43(T淋巴細胞)、CD20(B淋巴細胞)、CD68(巨噬細胞)、溶菌酶抗體免疫組化ABC法染色,2例進行透射電鏡觀察。結果肉芽腫期15例,纖維瘢痕期9例。 W-S染色和電鏡觀察均在Mikulicz細胞內檢測齣大量鼻硬結桿菌,細胞外偶見。電鏡下Mikulicz細胞內齣現大量吞噬體,將細胞器擠到一側,粗麵內質網及溶酶體很少。在病變組織內T淋巴細胞很少,Mikulicz細胞的溶菌酶抗體錶達較弱。結論鼻硬結病患者顯示細胞免疫功能障礙的特點,宿主的免疫反應是導緻組織損傷的主要原因。
목적관찰비경결병적조직병이학화림상특점,탐토비경결간균대숙주조성조직손상적궤리。방법이24례비경결병환자적조직표본위연구대상,용HE급조직화학W-S(Warthin-Starry)염색,기중11례조직분별용CD43(T림파세포)、CD20(B림파세포)、CD68(거서세포)、용균매항체면역조화ABC법염색,2례진행투사전경관찰。결과육아종기15례,섬유반흔기9례。 W-S염색화전경관찰균재Mikulicz세포내검측출대량비경결간균,세포외우견。전경하Mikulicz세포내출현대량탄서체,장세포기제도일측,조면내질망급용매체흔소。재병변조직내T림파세포흔소,Mikulicz세포적용균매항체표체교약。결론비경결병환자현시세포면역공능장애적특점,숙주적면역반응시도치조직손상적주요원인。
Objective To investigate the clinicopathologic characteristics and reason of tissue injury caused by klebsiella rhinoscleromatis(KR) infection. Methods Twenty-four cases of rhinoscleromas in the nasal and pharyngeal region in this hospital from March 1983 to March 1998 were studied retrospectively. Warthin-Starry(W-S) stain was used in all cases and CD43、CD20、CD68、Lysozyme mark were observed in eleven specimens by ABC immunochemical method. Two cases were studied further with transmission electron microscopy. Results A great number of KR were found in Mikulicz cells and were confirmed further in the phagosomes in cytoplasm of Mikulicz cells, where a small number of endoplasmic reticulums and lysozymes was squeezed to the side of cells. A few of T-lyphocytes was found within the granuloma. Conclusion Cellular immunity function of the patient with rhinoscleroma was depressed and the response to immunization of host which regards to KR was the major cause of tissue injury.