Szeghy G
Jász-Nagykun-Szolnok County Hetényi Géza Hospital and Clinic, Hungary.
Acta Physiol Hung. 1991;77(3-4):279-91.
The author presents a so far unknown pathological process interrupting permanently the regeneration of the superficially damaged cornea, and its consequences and therapy of the condition as well. The process occurs only in 5.6% of the injured individuals. The occurrence is in no correlation with the quality or extent of the damage. Also it is independent of the form and duration of therapy. The essence of the pathological changes is the slowing of corneal epithelisation within 2-4 days, followed by a complete cessation. After that a thin membrane-like layer develops simultaneously and evenly within 12 days on the area without epithelium, the surface of which is dull, transparent and whitish in colour. Within weeks or months an individually varying thickening of the membrane occurs, but the area does not grow. The surface becomes whitish-grey and is without any epithelium and with no adherence to tear. The deposits are closely and inseparably adherent to their base, their substance is rigid, being brittle only at the margins. The lesion is staining greenish-yellow with Na-fluorescein, and lively blue with toluidine blue. It is staining in small reddish-brown with rose bengal. In vivo the deposits are not measurably influenced by hyaluronidase, trypsin, alpha-chymotrypsin and papain. The microbes play no role in the process. Histological and electron-microscopical examinations suggest the corneal deposit are the product of the necrobiotic process occurring on the corneal surface during regeneration. The specific treatment consists of local application of corticoid-heparin. On the basis of the results of the examinations and literary data the author suggests that the corneal deposition and the similarly rare KCV (keratoconjunctivitis vernalis) plaque formation is the same specific process, i.e. the peculiar manifestation of the atopic state of the organism occurring independently of age.
作者提出了一种迄今为止尚不为人知的病理过程,该过程会永久性地阻断表层受损角膜的再生,以及这种情况的后果和治疗方法。此过程仅发生在5.6%的受伤个体中。其发生与损伤的性质或程度无关,也与治疗的形式和持续时间无关。病理变化的本质是角膜上皮化在2 - 4天内减缓,随后完全停止。此后,在无上皮的区域,12天内会同时均匀地形成一层薄膜状层,其表面暗淡、透明且呈白色。数周或数月内,薄膜会出现个体差异的增厚,但面积不会增大。表面变为灰白色,无任何上皮,不与泪液粘连。沉积物紧密且不可分离地附着于其基底,其质地坚硬,仅边缘处易碎。该病变用荧光素钠染色呈绿黄色,用甲苯胺蓝染色呈鲜蓝色,用孟加拉玫瑰红染色呈小的红棕色。在活体中,沉积物不受透明质酸酶、胰蛋白酶、α - 糜蛋白酶和木瓜蛋白酶的显著影响。微生物在这个过程中不起作用。组织学和电子显微镜检查表明,角膜沉积物是再生过程中角膜表面发生的坏死过程的产物。具体治疗方法是局部应用皮质类固醇 - 肝素。根据检查结果和文献资料,作者认为角膜沉积物和同样罕见的春季角结膜炎(KCV)斑块形成是相同的特定过程,即机体特应状态的特殊表现,与年龄无关。