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Biomedical subjects

W K Lelbach

Publications and source records attributed to W K Lelbach.

At least 19 recordsLinked to original sources
PubMed1996

A 25-year follow-up study of heavily exposed vinyl chloride workers in Germany.

The course of vinyl chloride-induced disease observed in 21 polyvinyl chloride (PVC) production workers, covering the period from first exposure to diagnosis and finally to death, and the difficulties in elucidating the true character of the lesions and their occupational origin are described. In 19 cases death was due to malignant hepatoma, predominantly angiosarcoma of the liver, but hepatocellular and cholangiocellular carcinoma were also found. Two workers died of complications of noncirrhotic portal fibrosis with portal hypertension. Except for the final stages, there was strikingly little impairment of hepatic function. Latency periods in workers with malignant hepatoma ranged from 12 to 34 years; mean latency was 22 years, and younger age at first exposure (here age < 27) seemed to have been accompanied by shorter latency periods.

Adult↗
PubMed1989

Multiple nodular foci in the liver associated with chronic hepatic porphyria after previous treatment of breast cancer.

More than 7 years after the diagnosis and treatment of breast cancer (T1N1aM0), multiple nodular foci were observed in the liver of a 40-year-old woman at ultrasonographic examination. The lesions were confirmed by CT scan, but CT-guided liver biopsy revealed only non-specific alterations. At subsequent peritoneoscopic examination, bluish-brown foci were indeed visible on the liver surface, but guided liver biopsies again failed to corroborate the suspected metastases. Instead, histology showed mild portal fibrosis, moderate steatosis and siderosis of hepatocytes, as before. Only the intense red fluorescence of part of the biopsy material under Wood's light suggested the diagnosis of chronic hepatic porphyria or porphyria cutanea tarda, here presumably as a consequence of prolonged alcohol consumption. Subsequent porphyrin studies in urine, faeces and plasma yielded the typical constellation of latent porphyria cutanea tarda (chronic hepatic porphyria type C). The activity of erythrocyte uroporphyrinogen decarboxylase was normal, which argued against a genetic predisposition. After 1 year of strict alcohol abstinence and low-dose chloroquine treatment the "nodular foci" in the liver were no longer visible on ultrasonogram and CT scan; only proton-weighted NMR imaging (SE 1500/30) still showed ill-defined areas of higher signal intensity. The renal excretion of porphyrins had decreased considerably. The levels are now consistent with the diagnosis of subclinical chronic hepatic porphyria type A. Modern non-invasive imaging techniques are tremendously useful, but they have their pitfalls. Focal liver lesions may present serious diagnostic problems, especially when they are found in a patient with a history of carcinoma at an extrahepatic primary site. A rare example is described.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

[Fulminant liver failure in tuberculostatic therapy. A contribution to clinical aspects and pharmacokinetics].

A 23-year old female patient on a prolonged regimen of tuberculostatic chemotherapy finally developed fulminant hepatic failure shortly after addition of hormonal contraception. The pathophysiology of this almost fatal drug reaction is described as a pharmacokinetic interaction: the inherent hepatotoxicity of prothionamide-the drug finally prescribed during convalescence-was significantly potentiated by the Cyt-P-450-inducing effect of the progestagen component of the hormonal contraceptive. Potentiation of hepatotoxicity in connection with tuberculostatic regimes containing rifampicin is well known and this pharmacokinetic phenomenon also pertains to the combination with other Cyt-P-450-inducing drugs such as, for instance, anticonvulsants. However, since the maximum of rifampicin-related Cyt-P-450-inducing effect is limited to the initial 2-3 weeks of therapy, the hepatotoxic risk triggered by this rifampicin-related induction may decline during continuation of therapy. This, unfortunately, does not pertain to the other Cyt-P-450-inducers, whose inductive effect is not time-limited. Progressive severe hepatic damage may follow from such interaction as demonstrated in this case report.

Adult↗
PubMed1985

[The liver and environmental poisons].

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".

Carcinoma, Hepatocellular↗
PubMed1983

[Malignant mesenchymal liver tumors in the computed tomogram].

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.

Adult↗
PubMed1981

[Vinyl chloride-induced angiosarcoma and hepato-cellular carcinoma of the liver (author's transl)].

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.

Angiography↗
PubMed1977

[Extracorporeal perfusion with baboon liver in the treatment of hepatic coma (author's transl)].

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.

Adult↗
PubMed1977

[Corrosive lesions of the upper intestinal tract in gastrectomized patients (author's transl)].

Lesions of the upper gastrointestinal tract caused by acid or alkaline solutions are generally limited to the esophagus and the stomach, because of physiological blocking mechanisms. In patients partially gastrectomized noxious solutions however can enter into lower parts of the gastrointestinal tract and cause severe lesions. Among 74 patients observed with corrosive lesions of the gastrointestinal tract two had undergone partial gastrectomy (Billroth II) previously. In these 2 patients very severe lesions of the intestinal mucosa were initiated; one of these patients died in spite of two resections of parts of the small intestine after massive gastrointestinal hemorrhage. These additional complications have to be foreseen in gastrectomized patients with corrosive lesions of the gastrointestinal tract.

Adult↗
PubMed1976

[Treatment of hepatic coma using extracorporeal perfusion with baboon and human liver as well as with activated charcoal].

In the 6 patients with hepatic coma hemoperfusions with 8 baboon and 2 human livers were carried out. Four awoke from the coma, one women could be discharged, but the others died of various complications and liver insufficiency. In the 4 patients with hepatic coma, 11 hemoperfusions with activated charcoal columns were performed. Two awoke from the coma, but they died of liver insufficiency. We were able to detect the elevation of preforming antibodies in a discharged patient.

Acute Disease↗
PubMed1975

[Sequential scintigraphy of liver and spleen in patients with polyvinyl chloride disease (author's transl)].

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.

Chemical and Drug Induced Liver Injury↗
PubMed1975

[Liver disease in polyvinyl chloride production workers - Clinical and peritoneoscopic aspects (author's transl)].

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.

Chemical Industry↗
PubMed1975

[Morphological changes of the liver after chronic vinyl chloride intoxication (author's transl)].

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.

Adult↗