Schattenberg P J, Totović V, Gedigk P, Marsteller H J
Virchows Arch A Pathol Anat Histol. 1977 Apr 6;373(3):233-47. doi: 10.1007/BF00432239.
Liver biopsies taken from 15 workers at a PVC-producing factory were examined by electron microscopy. The hepatocytes showed focal hydropic swelling, disseminated toxic steatosis, peculiar para-crystalline inclusions in enlarged mitochondria, focal cytoplasmic degradations, and occasional single cell necroses. These regressive changes were more prominent in cases with a shorter interval of non-exposure prior to the biopsy. Further, a focal compensatory hyperplasia of the smooth endoplasmatic reticulum was found. With increase of the non-exposure time interval, a regression of the degree of steatosis as well as an age-independent excessive lipofuscin deposition was seen in the hepatocytes. Apparently, these are sequelae of increased autophagia of lipids and increased lipid oxidation by the vinylchloride. In the sinusoids, activation, enlargement and proliferation of Kupffer cells was noted. The tendency of these cells to proliferate is apparently caused by the cancerogenic stimulation by vinylchloride. The prominent hyperplasia of lipocytes is probably connected with the deposition of collagen and the peculiar perisinusoidal fibrosis.
对一家聚氯乙烯生产工厂的15名工人进行了肝脏活检,并通过电子显微镜检查。肝细胞显示出局灶性水样肿胀、弥漫性中毒性脂肪变性、扩大的线粒体中出现特殊的副结晶包涵体、局灶性细胞质降解以及偶尔的单细胞坏死。这些退行性变化在活检前非暴露间隔较短的病例中更为明显。此外,还发现了光滑内质网的局灶性代偿性增生。随着非暴露时间间隔的增加,肝细胞中脂肪变性程度有所消退,并且出现了与年龄无关的过量脂褐素沉积。显然,这些是脂质自噬增加和氯乙烯导致脂质氧化增加的后遗症。在肝血窦中,观察到库普弗细胞活化、增大和增殖。这些细胞的增殖趋势显然是由氯乙烯的致癌刺激引起的。脂肪细胞的显著增生可能与胶原蛋白沉积和特殊的肝血窦周围纤维化有关。