Impact of short-term versus longterm topical steroid treatment on 'idiopathic' endothelial cell loss after normal-risk penetrating keratoplasty

被引:5
|
作者
Nguyen, Nhung Xuan
Pham, Huan Nguyen
Langenbucher, Achim
Cursiefen, Claus
Seitz, Berthold
机构
[1] Univ Erlangen Nurnberg, Dept Ophthalmol, Nurnberg, Germany
[2] Univ Tubingen, Dept Ophthalmol, Tubingen, Germany
[3] Univ Med, Dept Pharmacol, Ho Chi Minh City Eye Hosp, Ho Chi Minh City, Vietnam
来源
ACTA OPHTHALMOLOGICA SCANDINAVICA | 2007年 / 85卷 / 02期
关键词
normal-risk penetrating keratoplasty; topical steroid treatment; endothelial cell; subclinical immune reaction;
D O I
10.1111/j.1600-0420.2006.00763.x
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
Purpose: Chronic endothelial cell loss after penetrating keratoplasty (PK) is suspected to result from a subclinical immune reaction. The aim of this study was to investigate whether the prolonged use of a topical steroid after normal-risk PK has a favourable impact on chronic endothelial cell loss. Methods: The study included 305 eyes from the prospective Erlangen Normal-risk Keratoplasty Study, with a mean follow-up of 3.1 +/- 0.9 years. Postoperative treatment was initiated with prednisolone acetate 1% eyedrops five times a day and was tapered slowly over the first 6 months. Patients were then randomized into two treatment groups: a short-term group (n = 161), which stopped topical steroid treatment, and a longterm group (n = 144), which continued topical treatment with prednisolone acetate 1% eyedrops once a day until 12 months postoperatively. Endothelial cell counts were determined at each follow-up examination (after 6 weeks, then every 3 months until 2 years, then once a year). Results: Endothelial cell density in the short-term and longterm groups decreased significantly from 1941 +/- 550 cells/mm(2) and 1957 +/- 568 cells/mm(2) to 1535 +/- 535 cells/mm(2) and 1472 +/- 549 cells/mm(2), respectively, from 6 weeks to 2 years postoperatively (p < 0.001). In a linear regression model, cell count in the short-term group decreased by 216 +/- 93 cells/mm(2) and in the longterm group by 206 +/- 111 cells/mm(2) per year. There was no significant difference in endothelial cell loss between the short-term and longterm groups (p = 0.5). Conclusions: Longterm, low-dose, topical steroid treatment does not seem to prohibit chronic endothelial cell loss after normal-risk penetrating keratoplasty, in contrast to its favourable effect on immunological graft reactions. Our results may indicate that the aetiology of chronic endothelial cell loss is not of inflammatory origin. Further studies are needed to investigate this phenomenon.
引用
收藏
页码:209 / 212
页数:4
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