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A case of pneumococcal sepsis with DIC is reported. The patient had hyposplenism from thorium dioxide administration 23 years previously. Evidences of consumptive coagulopathy were verified by clinical manifestations of shock, generalized petechiae, abnormal hemostatic studies, and autopsy findings. The possible pathogenetic mechanism(s) of DIC in hyposplenism and pneumococcemia are reviewed.
This report concerns four patients in a district general hospital who died from malignant liver tumours associated with Thorotrast (thorium dioxide) deposits in the liver. Three were known to have had diagnostic angiographic studies performed 36 to 43 years previously using Thorotrast as the contrast agent. In the fourth case no previous relevant information could be obtained. There were two men and one woman with hepatocellular carcinoma and one woman with cholangiocarcinoma. In one of the hepatoma cases there was associated hypercalcaemia of malignancy. Reported latency intervals suggest that cases of Thorotrast-related hepatic malignancy may present up to the second decade of the twenty-first century.
Exposure to ionizing radiation has long been well-recognized as a risk factor for cancer development. Since ionizing radiation can induce mutations, an accurate way of measuring somatic mutation frequencies could be a useful tool for evaluating cancer risks. In the present study, we have examined in vivo somatic mutation frequencies at the erythrocyte glycophorin A (GPA) and T-cell receptor (TCR) loci in 18 Thorotrast patients who have been continuously irradiated with alpha-particles emitted from the internal deposition of thorium dioxide and who thus have increased risks of certain malignant tumors. When compared with controls, the results showed a significantly higher frequency of mutants at the lymphocyte TCR loci but not at the erythrocyte GPA loci in the Thorotrast patients. The discrepancy between the results of the two assays is discussed.
To study the real phagocytic capacity of Sertoli cells the following experiments were carried out: carbon colloidal solution or thorium dioxide of particle size 0.01--0.03 micrometer as 2% solution were injected in rat testes at a speed of 50 microliter per minute by means of a infusion pump. The site of injection was made either in the intertubular species under the albuginea or in the lumen of seminiferous tubules using glass 120 micrometer-gauge needles connected to the pump syringe. 30 to 240 minutes after the injection the tissues were fixed by perfusion of 2% glutaraldehyde and embedded for EM. It was observed: 1) particles injected into the intertubular species were not able to pass through the tubular wall and were either trapped by the connective tissue macrophages or drained by the lymphatic vessels; 2) intraluminal particles were not phagocyted by the Sertoli cells and remained in the lumen. The behavior of the Sertoli cells did not match that of phagocytes since they did not show their devouring capacity for the inert particles. These results are consistent with the interpretation that the current disposal of either debris by Sertoli cells depends on autophagic dissolution rather than n macrophagic capacity.
Thorotrast (Thorium dioxide) has been used in the past as a radiological contrast medium. Its use resulted in serious side-effects, often after a delay of many years. There was an increased incidence of tumours and blood dyscrasias. Meningeal fibrosis, hydrocephalus and progressive lesions of the cauda equina have followed its injection into the sub-arachnoid spaces. A patient with such a cauda equina lesion is reported.
Autophagocytosis was induced in cultured, human glial cells by X-irradiation or exposure to vinblastine sulphate. A transmission electron microscopic investigation of the origin of the segregating membranes in the autophagic process was performed by labelling of endocytotic vacuoles and lysosomes with electron-dense marker particles (native and cationized ferritin, colloidal gold and thorium dioxide). Cytochemical demonstration of the lysosomal marker enzyme acid phosphatase and serial sectioning of the cells were also carried out. The majority of newly formed, double-membrane bounded autophagic vacuoles were devoid of markers for both lysosomes and endocytotic vacuoles. Moreover, no evidence of origin from the endoplasmic reticulum was found and the segregating membranes of this type of autophagic vacuoles were, by process of elimination, considered likely to be derived from Golgi vacuoles or, possibly, assembled de novo. Autophagy also appeared to be effected through an alternative pathway involving a lysosomal wrapping or microautophagic mechanism.
The lunar meteorite Sayh al Uhaymir 169 consists of an impact melt breccia extremely enriched with potassium, rare earth elements, and phosphorus [thorium, 32.7 parts per million (ppm); uranium, 8.6 ppm; potassium oxide, 0.54 weight percent], and adherent regolith. The isotope systematics of the meteorite record four lunar impact events at 3909 +/- 13 million years ago (Ma), approximately 2800 Ma, approximately 200 Ma, and <0.34 Ma, and collision with Earth sometime after 9.7 +/- 1.3 thousand years ago. With these data, we can link the impact-melt breccia to Imbrium and pinpoint the source region of the meteorite to the Lalande impact crater.
An important part of man's radioactive environment is the natural radioactivity of soils. This radioactivity varies with soil type and withdepth in the soil profile. The relation between gross gamma activity and soil depth for a particular soil (Miami silt loam) is presented, together with a discussion of the contribution of K(40) and the uranium and thorium series and of the effects of fallout from bomb tests in increasing the radioactivity of a thin layer of surface soil.
Uranium and thorium daughters are ten times more concentrated in thyroids from some bovine animals than in the teeth of the same animals. These radioactive isotopes are believed to be from natural sources, but their resulting annual dosage of thyroid radiation has exceeded that from iodine-131 fallout.
Mice carrying the gene Mx were resistant to the lethal action of a hepatotropic line of avian influenza A virus. In resistant animals, foci of liver necrosis were self-limiting, and maximal virus titers reached were much below those in susceptible animals. Resistance could not be abrogated by immunosuppressive treatment with cyclophosphamide, methotrexate, or procarbazine, although such treatment prevented cellular infiltration at sites of virus replication and appeared to delay virus clearance. Silica and thorium dioxide, thought to inhibit macrophage function, likewise failed to abolish resistance. Regenerating liver tissue did not support more extensive virus replication than did intact adult liver.
The invasion of Rickettsia tsutsugamushi, Gilliam strain, into guinea pig polymorphonuclear leukocytes (PMNs) and the localization and distribution of tracers were followed during the process by electron microscopy. The seven tracers used were: cationized ferritin, ferritin, thorium dioxide (ThO2), carbon particles, latex spheres, paraffin oil, and Escherichia coli. These markers were added to the incubation medium containing the PMNs before or simultaneously with R. tsutsugamushi-infected BHK-21 cells. Both morphologically intact and degenerating rickettsiae were present in the phagosomes in PMNs, but only the viable-appearing rickettsiae were free in the cytoplasm. The intact rickettsiae were singly and selectively phagocytized in tightly enclosed phagosomal membranes which usually excluded the tracers, except when ThO2 or ferritin was used. When ThO2, which labels the plasma membrane of PMNs, was used. ThO2-labeled phagosomal membranes enclosing rickettsiae were observed and short membrane fragments still labeled with this tracer were found in the vicinity of rickettsiae in the cytoplasmic matrix of PMNs. When ferritin or ThO2 was used as a tracer, some of the phagosomes contained rickettsiae still enclosed in an envelope of BHK-21 cytoplasm and cell membrane. Phagolysosomes preloaded with electron-dense markers fused with subsequently formed phagosomes containing degenerated rickettsiae but not with those containing intact rickettsiae. These results support our interpretation that viable rickettsial entry into PMNs is by selective phagocytosis and escape from these phagosomes.
Fusion of lysosomes with phagosomes containing Ehrlichia risticii, an obligate intracellular parasite, was evaluated in P388D1 murine macrophagelike cells. Lysosomes in cells ranging in infectivity from 30 to 70% were labeled cytochemically with acid phosphatase or via endocytosis of thorium dioxide or cationized ferritin to document phagosome-lysosome (P-L) fusion in untreated cells and cells treated with oxytetracycline. Regardless of the marker used, P-L fusion was generally not observed in E. risticii-containing vacuoles in untreated cells, while significantly greater P-L fusion with ehrlichia-containing vacuoles was observed after oxytetracycline treatment. When latex beads were introduced into uninfected cell cultures, P-L fusion was observed with vacuoles containing latex. Fusion of lysosomes with latex-containing vacuoles in cells was significantly greater than fusion of lysosomes with ehrlichia-containing vacuoles in the same infected cells. These findings indicate that E. risticii is able to inhibit P-L fusion, whereas oxytetracycline deprives organisms of this ability.
Four cases of thyrotoxicosis are reported among 35 patients who had been given Thorotrast during the investigation of intracranial haemorrhage. For the group as a whole Thorotrast had been given between 11 and 31 years (mean 23.4 years) before this study. Thyrotoxicosis occurred in four patients between six and 17 years (mean 11.8 years) after the injection of Thorotrast. The fact that thyrotoxicosis did not occur in a small control group of patients who had had a subarachnoid haemorrhage and in whom Thorotrast had not been used at angiography suggests that Thorotrast may be of aetiological significance. In view of the known association between thyrotoxicosis and changes in the lymphoreticular system it is possible that the irradiation of this system by retained thorium has resulted in an abnormality of function which renders these patients more liable to the development of thyrotoxicosis.A fifth patient developed non-toxic thyroid enlargement 16 years after Thorotrast angiography.
The use of Thorotrast (25% thorium dioxide), a radiologic contrast agent used up until the mid-1950s, was associated with a wide range of malignancies, mainly of hepatic origin. We report a case of Thorotrast-induced hepatocarcinoma in an 82-year-old woman.
A 63 year old woman developed progressive shortness of breath, pulmonary hypertension, and respiratory failure and died from pulmonary fibrosis 45 years after thoracic fistulography with Thorotrast. Bouts of acute respiratory failure occurred with features of noncardiogenic pulmonary oedema. Lung tissue obtained by biopsy and at necropsy showed abundant radioactive particles of thorium dioxide in the lungs. The particles were congregated in the walls of blood vessels and in perivascular fibrous zones, consistent with a causal role of Thorotrast in the development of lung fibrosis. It is suggested that the fibrosis was due to the combined effects of alpha radiation on the interstitial perivascular zones and of recurrent pulmonary oedema due to endothelial damage.
Thorotrast, a contrast medium containing radioactive thorium, was in use in the period 1930 to 1945. It is retained in the body after use, with harmful effects, including the induction of malignancies. Accidental, extravasal injection during carotid angiography results in cervical granulomas with progressive, local damage. A case is reported in which lesions of the vagus, glossopharyngeal, hypoglossal and facial nerves have developed over a 40-year period after carotid angiography. A limited removal of the injected Thorotrast was carried out and, in the postoperative period, rupture of the arterial wall necessitated ligation of the common carotid artery. No additional complications arose from this. The therapeutic implications are discussed
Extravasation of thorium dioxide after transcervical carotid angiography has resulted in persistent open draining neck wounds. These difficult problems have remained a challenge for the treating head and neck surgeon. Neck dissection has been the mainstay of treatment in the past; however, this has been fraught with complications. The application of doxycycline sclerosis is described in the successful resolution of a large thorotrast granulomatous neck wound. A review of the literature and the management options of Thorotrast granulomas are discussed.
Dose-response curves for chronic leukemia in A-bomb survivors and liver tumors in patients given Thorotrast (colloidal thorium dioxide) show large threshold effects. The existence of these threshold effects can be explained by the following hypothesis. A high dose of radiation causes a persistent wound in a cell-renewable tissue. Disorder of the injured cell society partly frees the component cells from territorial restraints on their proliferation, enabling them to continue development of their cellular functions toward advanced autonomy. This progression might be achieved by continued epigenetic and genetic changes as a result of occasional errors in the otherwise concerted healing action of various endogenous factors recruited for tissue repair. Carcinogenesis is not simply a single-cell problem but a cell-society problem. Therefore, it is not warranted to estimate risk at low doses by linear extrapolation from cancer data at high doses without knowledge of the mechanism of radiation carcinogenesis.