CAJ | 학술논문

目的利用活体共聚焦显微镜观察角膜内皮炎患者治疗前后各层细胞的形态学改变,探讨其发病机制.方法用海德堡Ⅲ代角膜共聚焦显微镜观察不同病变时期角膜内皮炎患者各层细胞的形态学改变,观察病变区前弹力层平面的朗格罕细胞(LCs)的密度,采用单因素方差分析比较患者LCs密度差异.结果 2008年3月至2010年4月共观察角膜内皮炎患者48例,年龄14～70岁,男性32例(32只眼),女性16例(16只眼).病毒性角膜炎病史:初发至23年,此次发病时间:4～180 d.48例角膜内皮炎患者中,弥漫型9例,盘状39例.临床表现特点:(1)角膜上皮水肿,部分患者上皮出现大泡.(2)基质弥漫或局限水肿,部分患者基质浸润.(3)病灶区角膜内皮粗糙,羊脂状角膜后沉积物(KP)形成.活体角膜共聚焦显微镜特点:(1)病变区角膜上皮细胞肿胀,细胞间出现大小不一的空泡.(2)基底细胞层可见树突状朗格罕细胞聚集,临床症状消退后,朗格罕细胞密度下降,但仍高于对侧眼.(3)患眼上皮下神经纤维丛密度明显下降甚至消失,神经纤维变细.(4)角膜基质细胞肿胀,活化、病情迁延患者基质内可见多量炎症细胞的浸润.(6)内皮细胞肿胀,失去多边形结构,边界不清,细胞间隙增宽,内皮细胞间可见大小不一,形态各异的KP,并可突破内皮细胞间的连接,出现内皮细胞缺损区.部分患者基底细胞肿胀,LCs密度为(143±37)个/nn2,对侧眼角膜中央LCs密度为(32±14)个/mm2,差异有统计学意义(F=4.164,P=0.014).结论角膜内皮炎时角膜各层组织均可发生改变.病情迁延患者,表现为内皮炎和基质炎同时存在的混合类型.上皮下神经纤维密度下降甚至消失,前弹力层朗格罕细胞活化,密度增高,是角膜内皮炎的特征性改变.KP对内皮细胞间连接的破坏可能是加重角膜水肿的原因之一.早期、正确的治疗至关重要.
목적 이용활체공취초현미경관찰각막내피염환자치료전후각층세포적형태학개변,탐토기발병궤제.방법 용해덕보Ⅲ대각막공취초현미경관찰불동병변시기각막내피염환자각층세포적형태학개변,관찰병변구전탄력층평면적랑격한세포(LCs)적밀도,채용단인소방차분석비교환자LCs밀도차이.결과 2008년3월지2010년4월공관찰각막내피염환자48례,년령14～70세,남성32례(32지안),녀성16례(16지안).병독성각막염병사:초발지23년,차차발병시간:4～180 d.48례각막내피염환자중,미만형9례,반상39례.림상표현특점:(1)각막상피수종,부분환자상피출현대포.(2)기질미만혹국한수종,부분환자기질침윤.(3)병조구각막내피조조,양지상각막후침적물(KP)형성.활체각막공취초현미경특점:(1)병변구각막상피세포종창,세포간출현대소불일적공포.(2)기저세포층가견수돌상랑격한세포취집,림상증상소퇴후,랑격한세포밀도하강,단잉고우대측안.(3)환안상피하신경섬유총밀도명현하강심지소실,신경섬유변세.(4)각막기질세포종창,활화、병정천연환자기질내가견다량염증세포적침윤.(6)내피세포종창,실거다변형결구,변계불청,세포간극증관,내피세포간가견대소불일,형태각이적KP,병가돌파내피세포간적련접,출현내피세포결손구.부분환자기저세포종창,LCs밀도위(143±37)개/nn2,대측안각막중앙LCs밀도위(32±14)개/mm2,차이유통계학의의(F=4.164,P=0.014).결론 각막내피염시각막각층조직균가발생개변.병정천연환자,표현위내피염화기질염동시존재적혼합류형.상피하신경섬유밀도하강심지소실,전탄력층랑격한세포활화,밀도증고,시각막내피염적특정성개변.KP대내피세포간련접적파배가능시가중각막수종적원인지일.조기、정학적치료지관중요.
Objective To study the cellular morphological characteristics and changes of corneal endotheliitis by corneal microstructure in vivo.Methods Forty-eight clinical diagnosed patients of corneal endotheliitis were examined by in vivo confocal microscopy.Confocal images of different layers were collected and observed.Of all the patients,39 were disciform and 9 were diffuse.The history of the 48 patients was from 7 days to 23 years and the duration was from 4 to 180 days.Results Epithelium revealed cellular edema,enlarged intercellular gaps,and bubble between the cells.The density of sub-basal nerve plexus was significantly lower than that of normal,even disappeared in 24 patients.A numerous dendritic cells (Langerhans cells,LCs ) presented in the basal epithelium layer and gradually abated with disease regression,but the density of LCs was significantly higher than that of the contralateral eye.The keratocyte revealed edema and to be activated.Inflammatory cell was found in stroma of the patients with long history and duration disease.Endothelium cells were observed edema,with enlarged intercellular gaps.Inflammatory cells was found to infiltrate into the endothelial layer,most them gathered to be keratic precipitates (KP),which were rounded or elliptic and inserted between the endothelium by pushing the endothelium away,and induced decayed area between the endothelium.Conclusion Corneal endotheliitis was not only the inflammation of endothelium,but also varied pathological changes of all layer of the cornea.Corneal endotheliitis patients with long history and duration presented the mixed type with stromal keratitis.The lower density of sub-basal nerve plexus and the higher density of dendritic LCs were the characteristics of endotheliitis.Impairment of intercellular junction by KP might be another important role of cornea edema.Sufficient and accurate treatment of endotheliitis was important.