Open AccessImpact of short‐term versus longterm topical steroid treatment on ‘idiopathic’ endothelial cell loss after normal‐risk penetrating keratoplasty
Author(s) -
Nguyen Nhung Xuan,
Pham Huan Nguyen,
Langenbucher Achim,
Cursiefen Claus,
Seitz Berthold
Publication year - 2007
Publication title -
acta ophthalmologica scandinavica
Language(s) - English
Resource type - Journals
eISSN - 1600-0420
pISSN - 1395-3907
DOI - 10.1111/j.1600-0420.2006.00763.x
Subject(s) - medicine , subclinical infection , prednisolone , endothelial stem cell , topical steroid , endothelium , prospective cohort study , surgery , steroid , ophthalmology , gastroenterology , hormone , biochemistry , chemistry , in vitro
. 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.