title: HLA class I/II matching and chronic endothelial cell loss in penetrating normal risk keratoplasty.
abstract: OBJECTIVE
  Chronic endothelial cell loss of the graft is very common after penetrating keratoplasty. The aetiology of this is unknown. Clinically, non-identifiable immune reactions have been suspected. Recently, we were able to demonstrate that proper human leucocyte antigen (HLA) matching is a suitable means to reduce classical immune reactions in normal risk keratoplasty patients. In this study, we therefore investigated whether HLA-matched grafts also experience less chronic endothelial cell loss.
  
  
  METHODS
  A homogenous group of 223 normal risk keratoplasty patients was divided into six groups with different degrees of HLA matching (group 1 with unknown HLA data, group 2 with up to two mismatches, group 3 with three mismatches, group 4 with four mismatches, group 5 with five mismatches and group 6 with six mismatches on the HLA A, B, DR loci). All serological HLA A, B, C and all moleculargenetic HLA DRB, DRQB typings of donors and recipients were performed in a single laboratory accredited by the American Society for Histocompatibility and Immunogenetics. Only patients with at least three postoperative endothelial cell density values were included in the study. The slopes of the regression lines for each individual scatterplot of endothelial cell density values plotted against postoperative time (linear regression, lost cells/mm2/day), and after logarithmic transformation (exponential regression, annual relative loss of cells) were evaluated, respectively.
  
  
  RESULTS
  There were no statistically significant differences between the six groups.
  
  
  CONCLUSIONS
  Whereas proper HLA matching at present standards is already a suitable means to reduce identifiable immune reactions and to prolong graft survival even in normal risk keratoplasty patients, the same HLA matching procedures are not effective in reducing the extent of chronic endothelial cell loss. For several reasons this does not yet exclude, however, the possibility that the underlying cause of chronic endothelial cell loss is immunological.
authors.affiliation: Eye Hospital, Albert-Ludwigs University, Freiburg, Germany. Reinhard@aug.ukl.uni-freiburg.de
authors.forename: Thomas
authors.initials: T
authors.lastname: Reinhard
authors.forename: Daniel
authors.initials: D
authors.lastname: Böhringer
authors.forename: Jürgen
authors.initials: J
authors.lastname: Enczmann
authors.forename: Gesine
authors.initials: G
authors.lastname: Kögler
authors.forename: Peter
authors.initials: P
authors.lastname: Wernet
authors.forename: Stefan
authors.initials: S
authors.lastname: Böhringer
authors.forename: Rainer
authors.initials: R
authors.lastname: Sundmacher
mesh_terms: D002452:Cell Count; D002908:Chronic Disease; D004728:Endothelium, Corneal / Q000473:pathology*; D005260:Female; D006085:Graft Survival / Q000502:physiology; D015395:Histocompatibility Antigens Class I / Q000276:immunology*; D000949:Histocompatibility Antigens Class II / Q000276:immunology*; D006650:Histocompatibility Testing; D006801:Humans; D015948:Keratoplasty, Penetrating / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications; D012307:Risk Factors; D014019:Tissue Donors
chemical_list: D015395:Histocompatibility Antigens Class I; D000949:Histocompatibility Antigens Class II