Dobbie J W
Baxter R & D Europe, Advanced Scientific Development, Nivelles, Belgium.
Perit Dial Int. 1992;12(1):14-27.
Drawing from diverse sources including epidemiological and clinical data, surgical observations, histopathology, serosal healing responses to fibrin and fibrinolysis, tissue reaction to chronic exposure, and to exo- and endotoxins, new information on mesothelial stem cells, autocrine and paracrine influences on their proliferation and collagen synthesis, and the effect of glucose on fibroconnective tissue, we have begun to piece together the pathogenetic jigsaw of fibrosis in continuous ambulatory peritoneal dialysis (CAPD). The reaction of peritoneal mesothelium and stroma to the stress of continual dialysis results in a spectrum of alterations ranging from opacification through a tanned peritoneum syndrome to sclerosing encapsulating peritonitis (SEP). Any agent that causes irritation of the mesothelial layer and induces serositis, or single severe or multiple episodes of peritonitis resulting in mesothelial loss, predisposes the peritoneum to fibroneogenesis. An accurate definition of the histopathological changes of peritoneal thickening is a prerequisite for defining pathogenesis. This paper is the first attempt to create such a framework. It is evident from many areas of study that fibrin deposition and fibrinolysis, hyalinization of the superficial stromal collagen possibly tanned through nonenzymatic glycosylation by dialysate glucose and the proliferative potential of mesothelial stem cells play an important and possibly interdependent role in excessive fibroneogenesis in certain patients on CAPD. Many of the pieces of the jigsaw are obviously still missing, and the picture is most surely incomplete. Nevertheless, the outline of the pathologic and etiologic landscape should now be discernible.
我们综合了多种来源的信息，包括流行病学和临床数据、手术观察结果、组织病理学、浆膜对纤维蛋白和纤维蛋白溶解的愈合反应、组织对慢性暴露以及对内毒素和外毒素的反应、间皮干细胞的新信息、自分泌和旁分泌对其增殖和胶原蛋白合成的影响，以及葡萄糖对纤维结缔组织的影响，开始拼凑持续性非卧床腹膜透析（CAPD）中纤维化的发病机制拼图。腹膜间皮和基质对持续透析压力的反应导致一系列改变，从腹膜浑浊到“晒黑腹膜综合征”，再到硬化性包裹性腹膜炎（SEP）。任何引起间皮层刺激并诱发浆膜炎的因素，或导致间皮丢失的单次严重或多次腹膜炎发作，都会使腹膜易于发生纤维蛋白生成。准确界定腹膜增厚的组织病理学变化是明确发病机制的前提。本文首次尝试构建这样一个框架。从许多研究领域可以明显看出，纤维蛋白沉积和纤维蛋白溶解、浅表基质胶原的透明变性（可能是由透析液葡萄糖通过非酶糖基化作用“晒黑”）以及间皮干细胞的增殖潜能，在某些CAPD患者的过度纤维蛋白生成中发挥着重要且可能相互依存的作用。拼图的许多碎片显然仍缺失，这幅图肯定不完整。然而，现在应该可以看出病理和病因的大致轮廓了。
