Reinhard Thomas, Böhringer Daniel, Enczmann Jürgen, Kögler Gesine, Wernet Peter, Böhringer Stefan, Sundmacher Rainer
Eye Hospital, Albert-Ludwigs University, Freiburg, Germany.
Acta Ophthalmol Scand. 2004 Feb;82(1):13-8. doi: 10.1046/j.1600-0420.2003.00188.x.
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.
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.
There were no statistically significant differences between the six groups.
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.
穿透性角膜移植术后移植物内皮细胞慢性丢失非常常见。其病因尚不清楚。临床上，人们怀疑存在无法识别的免疫反应。最近，我们能够证明适当的人类白细胞抗原（HLA）配型是降低正常风险角膜移植患者经典免疫反应的一种合适方法。因此，在本研究中，我们调查了HLA配型的移植物是否也经历较少的慢性内皮细胞丢失。
将223例正常风险角膜移植患者的同质组分为六组，HLA配型程度不同（第1组HLA数据未知，第2组最多有两个错配，第3组有三个错配，第4组有四个错配，第5组有五个错配，第6组在HLA A、B、DR位点有六个错配）。供体和受体的所有血清学HLA A、B、C以及所有分子遗传学HLA DRB、DRQB分型均在一个获得美国组织相容性和免疫遗传学协会认可的单一实验室进行。本研究仅纳入术后至少有三个内皮细胞密度值的患者。分别评估内皮细胞密度值与术后时间的每个个体散点图的回归线斜率（线性回归，细胞丢失/mm²/天）以及对数转换后的斜率（指数回归，细胞年度相对丢失率）。
六组之间无统计学显著差异。
尽管按照目前的标准进行适当的HLA配型已经是降低可识别免疫反应并延长移植物存活时间的合适方法，即使在正常风险角膜移植患者中也是如此，但相同的HLA配型程序在减少慢性内皮细胞丢失程度方面无效。然而，由于多种原因，这尚未排除慢性内皮细胞丢失的潜在原因是免疫性的可能性。
