Vinyl chloride-associated disease.
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Biomedical subjects
Publications and source records attributed to H J Marsteller.
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The results of angiography of the hand in workers in the vinyl chloride industry are described. Amongst 93 patients, there were 19 on whom angiograms of the hand were performed because of Raynaud-like changes, pain or other pathological findings. All patients examined by angiography showed abnormalities in the vessels in the hands and fingers of varying severity. Vascular occlusions (17 patients), stenoses (9 patients) and thread-like narrowing of the digital arteries (6 patients) with the development of a collateral circulation, were prominent findings. In addition there was elongation and tortuosity of the digital arteries (14 patients) which were regarded as cirsoid aneurysms. The angiographic findings have been correlated with the known histological changes.
Gastric rinsing during gastroscopy is presented as a new, effective, uncomplicated method of primary elimination of poison, as a part of a new diagnostic and therapeutic concept for patients intoxicated with hypnotics. The advantage of this active therapy is a fast elimination of the toxic substance and prevention of secondary complications. The diagnostic value of gastroscopy and radiological examination in patients with unexplained comatous states is emphasized.
Direct antegrade cholangiography via transjugular access or as transcutaneous, transhepatic fine-needle cholangiography reduces the examination risk involved in the direct visualisation of the bile duct via needles of thick calibre. The article reports on the results obtained with 83 patients. Direct puncture of the bile duct by means of a fine needle is superior to transjugular antegrade cholangiography in respect of the required technical equipment and cost, and also as far as the proportion of accurate results is concerned, since visualisation of cholangiectasis will always be successful, whereas the visualisation of undilatated bile ducts can be effected in 50% of the examinations. Transvenous access should be chosen in such cases where liver tissue biopsy is necessary. Dilatation of the transcutaneous, transhepatic bile duct access via the temporary transcutaneous, transhepatic bile duct drainage, is necessary in those situations where the bile flow cannot be ensured by surgery, or where surgery is ruled out on account of the patient's general condition.
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.
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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.
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.
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Peculiar clinical symptoms observed in polyvinyl chloride production workers of a nearby chemical plant arose the suspicion of liver and spleen disease in these workers before first reports on vinyl chloride-induced angiosarcoma of the liver became known. Starting at the end of 1972, 44 workers were followed up by biochemical investigations, peritoneoscopy and liver biopsy. As early as 1973 it could be ascertained, that advanced vinyl chloride-induced liver damage presents as hepatic fibrosis with splenomegaly, portal hypertension, and thrombocytopenia without conspicuous deterioration of hepatic parenchyma function. Similar symptoms have been observed after chronic intoxication by arsenic and thorium dioxide (thorotrast). The clinical and peritoneoscopic aspects of the disease are described.
The monomer vinyl chloride in its gaseous form is used as basic product for industrial synthesis of polyvinyl chloride; it does cause lesions of the liver depending on the dose and the time of exposure. Lesions found on histological examination are: 1. degenerative alterations of liver parenchyma; 2. focal adaptive changes in the cytoplasma of hepatocytes; 3. enlargement of liver cells and polymorphy of cell nuclei; 4. slowly progressive fibrotic and to a lesser degree cirrhotic changes of liver parenchyma, localized in part around the sinus, in part in the septal-periportal areas; 5. activation and proliferation of sinusoidal cells. Sarcoma of the liver due to a probable oncogenic effect of vinyl chloride could be diagnosed in three patients exposed to the toxic agent.
In three patients with occupational vitiligo caused by paratertiary butylphenol--the first cases observed in the BRD--a functional disorder of the liver was found. In two of these patients splenomegaly was seen. The laboratory findings, the laparoscopic examination and the result of the liver-biopsy are described. It is assumed that these changes as well as the depigmentation and a functional disorder of the thyroid (described elsewhere) are caused by the systemic action of inhaled paratertiary butylphenol.
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Explore the source record for details and available documents.
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