Three patients with industrial exposure to PVC are described, who developed angio-sarcomas of the liver; in one patient this was combined with a multi-lobular primary hepato-cellular carcinoma. The epidemiology, clinical features and diagnosis are discussed, with particular reference to angiography, sonography and computerized tomography. The non-invasive methods, such as computerized tomography and sonography, are the techniques of choice if an angiosarcoma is suspected after long exposure to PVC.
In 11 patients with hepatic coma (stage IV and V according to Abouna) extracorporeal haemoperfusion using the Scribner shunt (radial or profunda femoris artery) was performed over 12 to 27 hours with 22 baboon and one human livers. Eight patients emerged from coma, six of them showed sufficient regeneration of the diseased liver. Four patients were discharged as cured, one patient died of acute pancreatic necrosis, a further one due to bleeding from an old gastric ulcer. In the 2 remaining patients the coma recurred within 48 hours. Tree patients never came round from coma. After perfusion no antibodies against baboon proteins were demonstrable in the patients. Thus there is very little danger of an anaphylactic reaction when perfusion is repeated. The titre of preformed cytotoxic antibodies against baboon cells in patients' serum rises only after 1-2 weeks and decreases again after 4 weeks. In our experience extracorporeal liver perfusion with baboon or human livers is the most promising method for treatment of hepatic coma.
For almost a century now numerous examples of acute and subacute hepatic injury from exposure to toxic agents in the occupational or non-occupational environment have been extensively studied and are well documented, but such events are comparatively rare. In contrast, epidemiological data associating exposure to environmental chemicals with chronic liver disease or primary hepatic malignancies in the human is scarce as compared with the vast body of literature concerning chronic pulmonary disease as a consequence of exposure at the workplace. Large-scale industrial production of many newly synthesized organic chemicals began during the period 1930-1940 but it was not until the 1960s that the output increased exponentially. Consequently, the spectrum of environmental influences is gaining increasing complexity since simultaneous or sequential exposure to a variety of pollutants is becoming the rule rather than the exception. Possible interaction or synergism of environmental agents--even of those which in themselves or for their low dosage level may be considered "harmless" - and particularly latency periods of more than one decade further complicate preventive strategies. The liver, as the central site for the biotransformation of xenobiotics, deserves special attention when new chemicals which are to be introduced into the environment are being tested for their potential toxicity, especially since many hepatotoxic agents have been shown to undergo bioactivation in the liver. Currently available information on hepatic injury due to environmental agents is briefly reviewed and comprises solvents and degreasing agents, pesticides, polyhalogenated biphenyls, dioxins and dibenzofuranes, epoxy resin hardeners, vinyl chloride, naturally occurring hepatotoxins in plants and fungi, herbal medicines and traditional remedies and a side-light on the Reye syndrome and the Spanish "toxic oil syndrome".
Occurence of severe liver damage including angiosarcoma in polyvinyl chloride production workers necessitates regular control investigations of liver and spleen. Radioisotope techniques with small irradiation doses which give valid results should be used. Investigations of 15 patients with PVC-induced liver disease showed that hepatic perfusion as demonstrated by 99mTc pertechnate does not correlate with the uptake of sulphide colloid in the hepatic reticuloendothelial system. This provides evidence that in VC disease specific damage of the reticuloendothelial system of the liver occurs. Sequential scintigraphy also proved that the liver perfusion quotient can be considered as a measure of portal pressure. In practice this may be used for follow-up controls. Vascularized tumours described in VC disease can also be demonstrated by scintigraphy.
The computer tomographic appearances of very rare sarcomas of the liver have been demonstrated in five cases (four haemangiosarcomas, one spindle-cell sarcoma). On the plain scan, all the tumours appeared less dense than the liver parenchyma, but in haemangiosarcomas there was a marked increase in density after the infection of contrast up to an isodense level. During angio-CT, densities equal to intrahepatic vessels were observed. There was only a slight increase in density of the spindle cell sarcoma after contrast injection. The CT appearances have been compared with the pathological and anatomical structure of the tumour.
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