Haddox J L, Pfister R R, Daniel R L, Slaughter S E, Lam K W
Eye Research Laboratories, Brookwood Medical Center, Birmingham, Alabama, USA.
Cornea. 1997 Jul;16(4):472-9.
The purpose of this study was to develop a classification system to predict keratomalacia after trauma in vitamin A-deficient eyes and to determine whether citrate impedes polymorphonuclear leukocyte infiltration into the cornea, thus preventing keratomalacia.
Preliminary classification studies showed that a 7.0-mm corneal epithelial scrape, before clinical findings of corneal xerosis, did not induce keratomalacia. Primary studies were conducted concurrently on the same animals to develop the classification system and test the effect of citrate in vitamin A deficiency. A 7.0-mm corneal epithelial scrape was performed on vitamin A-deficient eyes in various stages of corneal xerosis and treated as follows. Experiment 1: group 1, 10% citrate drops; group 2, phosphate buffer solution (PBS) drops; experiment II: group 3, drops and subconjunctival injection of 10% citrate; group 4, drops and subconjunctival injection of PBS.
Corneal abrasion in eyes with 2+ corneal xerosis yielded keratomalacia in 50% of cases; the remainder healed with xerotic epithelium. Eighty-three percent of eyes with > 2+ xerosis developed keratomalacia after corneal abrasion, whereas only 7.1% of eyes with < 2+ xerosis advanced to this stage. In experiment I, 27% of citrate-treated eyes and 38% of PBS-treated eyes developed keratomalacia (not significant). In experiment II, two of six citrate-treated eyes perforated and one eye developed keratomalacia. One of six control PBS eyes perforated and four developed keratomalacia.
We correlated the degree of corneal xerosis with the occurrence of keratomalacia after corneal trauma. This led to the development of a classification scale that is of research and clinical significance. Additionally, citrate did not significantly reduce keratomalacia or perforation in the vitamin. A-deficient eye.
本研究的目的是开发一种分类系统，以预测维生素A缺乏的眼睛在创伤后发生角膜软化症，并确定柠檬酸盐是否会阻碍多形核白细胞浸润到角膜中，从而预防角膜软化症。
初步分类研究表明，在角膜干燥症的临床症状出现之前，7.0毫米的角膜上皮刮除术不会诱发角膜软化症。在同一动物上同时进行了初步研究，以开发分类系统并测试柠檬酸盐在维生素A缺乏症中的作用。对处于不同角膜干燥症阶段的维生素A缺乏的眼睛进行7.0毫米的角膜上皮刮除术，并进行如下处理。实验一：第1组，滴注10%柠檬酸盐；第2组，滴注磷酸盐缓冲溶液（PBS）；实验二：第3组，滴注并结膜下注射10%柠檬酸盐；第4组，滴注并结膜下注射PBS。
角膜干燥症为2+的眼睛进行角膜擦伤后，50%的病例发生角膜软化症；其余病例角膜干燥上皮愈合。角膜干燥症>2+的眼睛在角膜擦伤后83%发生角膜软化症，而角膜干燥症<2+的眼睛只有7.1%发展到这一阶段。在实验一中，27%接受柠檬酸盐治疗的眼睛和38%接受PBS治疗的眼睛发生角膜软化症（无显著差异）。在实验二中，接受柠檬酸盐治疗的6只眼睛中有2只发生穿孔，1只眼睛发生角膜软化症。6只对照PBS眼睛中有1只发生穿孔，4只发生角膜软化症。
我们将角膜干燥症的程度与角膜创伤后角膜软化症的发生相关联。这导致开发出一种具有研究和临床意义的分类量表。此外，柠檬酸盐在维生素A缺乏的眼睛中并没有显著降低角膜软化症或穿孔的发生率。
