title: Impact of short-term versus longterm topical steroid treatment on 'idiopathic' endothelial cell loss after normal-risk penetrating keratoplasty.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Ophthalmology, University of Erlangen-Nürnberg, Erlangen-Nürnberg, Germany. nhung.nguyen@med.uni-tuebingen.de
authors.forename: Nhung Xuan
authors.initials: NX
authors.lastname: Nguyen
authors.forename: Huan Nguyen
authors.initials: HN
authors.lastname: Pham
authors.forename: Achim
authors.initials: A
authors.lastname: Langenbucher
authors.forename: Claus
authors.initials: C
authors.lastname: Cursiefen
authors.forename: Berthold
authors.initials: B
authors.lastname: Seitz
mesh_terms: D002452:Cell Count; D003316:Corneal Diseases / Q000601:surgery; D004728:Endothelium, Corneal / Q000187:drug effects / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D005938:Glucocorticoids / Q000008:administration & dosage*; D006801:Humans; D015948:Keratoplasty, Penetrating; D008297:Male; D008875:Middle Aged; D009883:Ophthalmic Solutions / Q000008:administration & dosage; D011239:Prednisolone / Q000008:administration & dosage / Q000031:analogs & derivatives*; D011446:Prospective Studies
chemical_list: D005938:Glucocorticoids; D009883:Ophthalmic Solutions; C009935:prednisolone acetate; D011239:Prednisolone