Microangiopathic Haemolytic Anaemia Associated with Hypercakaemia in an Experimental Rat Tumour

Hilgard, P.; Hohage, Roderich; Schmitt, W; W, Köhle

doi:10.1111/j.1365-2141.1973.tb05745.x

Cited by 24 publications

(6 citation statements)

References 24 publications

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“…Early animal experiments with parathyroid hormone intoxication revealed multiple thromboses at necropsy (Hueper, 1927) and intravascular coagulation was found in our hypercalcaemic tumour animals (Hilgard et al, 1973). These data, in conjunction with the results reported here, seem to indicate that the development of thrombosis may be favoured by an increase in the serum calcium level if additional trigger mechanisms are involved.…”

Section: Discussionsupporting

confidence: 83%

Experimental hypercalcaemia and whole blood clotting

Hilgard

1973

J Clin Pathol

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SYNOPSIS Experimental hypercalcaemia was induced in rats by (1) transplantation of the solid Walker 256 tumour, and (2) intraperitoneal injections of calcium gluconate. Whole blood clotting was studied by means of thromboelastography and whole blood clotting times in polystyrene and glass test tubes. At serum calcium levels between 10-3 and 115 m-equiv/l a slight delay in clot formation was found which was reversible by the addition of EDTA to whole blood. Acute, calciumgluconate-induced hypercalcaemia, however, leads to a significant shortening of the clotting time in the polystyrene tube and to a lesser degree in the glass tube. Maximal factor XII activation in vitro with ellagic acid levels the difference of clotting times again. From these experiments it is concluded that acute hypercalcaemia induces a hypercoagulable state, possibly by partial contact activation, and thus may favour thrombus formation in vivo.

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Section: Discussionsupporting

confidence: 83%

Experimental hypercalcaemia and whole blood clotting

Hilgard

1973

J Clin Pathol

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“…Among the various diseases in which microangioyathic haemolytic anaemia occurs, disseminated carcinomatosis is of particular interest since widespread vascular lesions are rarely found at necropsy. There is, however, experimental evidence that fibrin deposition in the tumour vessels can cause red cell fragmentation (Hilgard et al, 1973) aiid a similar mechanism in certain human tumours was suggtsted by Hopfner et al (1972). However, the lack of histological evidence for iiitravascular fibrin in patients with malignancies aiid microangiopathic haemolytic anaemia led to the conclusion that mechanical damage to the red cells might be caused just by contact with the malignant endothelial lining of the tumour vessels (Donald & Dawson, 1971).…”

Section: Discussionmentioning

confidence: 84%

“…Fibrinogen labelling. Animonium-sulphate-precipitated rat fibrinogen was prepared as previously described (Hilgard et al, 1973) and labelled with "' I by the iodine-monochloride method (Helmkamp et al, 1960), the iodineffibrinogen ratio being less than 0.5. Then 0.5 ml of the radioiodinated fibrinogen solution, containing 20 mg of protein and approximately 10 pCi radioactivity, was injected intravenously into the lateral tail vein of 24 rats.…”

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confidence: 99%

Microangiopathic Haemolytic Anaemia and Experimental Tumour‐Cell Emboli

Hilgard

Gordon‐Smith

1974

Br J Haematol

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Summary. The mechanism by which disseminated carcinoma may induce microangiopathic haemolytic anaemia has been studied in rats using intravenous injections of Walker carcinosarcoma‐256 cells. Following the injection of tumour cells there was sequestration of radio‐labelled fibrinogen and platelets in the lungs and a simultaneous fall in peripheral platelet count and rise in free plasma haemoglobin. Anti‐fibrinolytic treatment (EACA) and triamcinolone accentuated the changes whereas heparin abolished the effect. Electron microscopy demonstrated fibrin and platelet deposition around tumour cells. It is concluded that intravascular coagulation around tumour cell emboli is an important mechanism in the production of microangiopathic haemolytic anaemia in disseminated carcinoma.

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“…It should also be noted that in some advanced neo plastic patients the hypercalcémie state [35,36] was associated with the increased rate of fibrin monomer polymerization [37,38] and the state of DIC [38][39][40]. The effect of AzUR on the calcium homeostasis has been known for some time [41][42][43].…”

Section: Discussionmentioning

confidence: 99%

Effect of 6-Azauridine and Pyrazofurin on Fibrinolysis by L1210 Leukemic Cells

Novak¹

1982

Oncology

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The expression of plasminogen activator activity (PA) by L1210 leukemic ascitic cells, obtained from the peritoneum of BDF₁ mice, increases in the terminal stages of the disease. Treatment of mice carrying advance leukemia (day 6 following inoculation with 10⁶ cells i.p.) with 6-azauridine (AzUR) results in prolonged survival (2–3 days) and also in increased expression of PA activity by the ascitic cell population. Similar treatment with pyrazofurin (PF), another inhibitor of orotidylate decarboxylase and of de novo pyrimidine synthesis, fails to produce either of these effects. Neither AzUR or PF, given at the early stage of tumor growth (day 3), extend the life span nor do they cause increase of the PA activity. Thus, the elevation in PA activity following treatment with AzUR is associated with the asymptotic stage of the disease and this phenomenon correlates positively with the life-prolonging effects of this drug. An analysis of the PA activity elicited by intact cells, secretions, and cellular digests suggests that most of the activity originates on the surface of the cells. The results indicate that the described in vivo effect of AzUR, but not that of PF, on late-stage leukemia, is mediated by the changes in the fibrinolytic potential of the tumor or host cells rather than through the inhibition of the de novo pyrimidine synthesis.

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Microangiopathic Haemolytic Anaemia Associated with Hypercakaemia in an Experimental Rat Tumour

Cited by 24 publications

References 24 publications

Experimental hypercalcaemia and whole blood clotting

Experimental hypercalcaemia and whole blood clotting

Microangiopathic Haemolytic Anaemia and Experimental Tumour‐Cell Emboli

Effect of 6-Azauridine and Pyrazofurin on Fibrinolysis by L1210 Leukemic Cells

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