Coagulation disorders in cancer. III.Fibrinolysis and inhibitors

Abstract

In a group of 100 unselected patients with disseminated malignancies, marked disturbances in the coagulation and fibrinolytic systems were found. Mean silicone coagulation time was shortened, and fibrinogen levels were markedly elevated. Fibrinolysis activation, as manifested by plasma clot lysis, euglobulin lysis, or the presence of fibrin degradation products, was noted in 9 cases. Mean plasminogen levels were normal. There was a significant elevation of urokinase inhibitor, but other inhibitors of fibrinolysis were normal.

Fibrinolytic activity in malignant disease.

“…In the present study the output of activator in response to venous occlusion or 'fibrinolytic capacity' (Robertson et al, 1972) was normal in the patients with malignant disease, indicating that the low circulating level is not due to decreased synthesis in the vessel wall or to some factor preventing its release. It is possible that it results from rapid neutralization by inhibitors in the plasma: indeed, high levels of fibrinolytic inhibitors have been described in patients with malignant disease (Soong and Miller, 1970).…”

“…A pathological increase in blood fibrinolytic activity was observed in some patients with carcinoma of the prostatewith metastases (Tagnon et al, 1952(Tagnon et al, , 1953, although Swan and Kerridge (1965)were unable to detect any increase in fibrinolytic activity in a series of 61 patients with carcinoma of the prostate. Soong and Miller (1970) observed increased fibrinolysis in nine of their 100 patients with disseminated malignancy.…”

Microangiopathic Haemolytic Anaemia and Experimental Tumour‐Cell Emboli

“…The lack of evidence for microclots at necropsy in patients with tumour cell emboli may be due to a spontaneous fibrinolysis between death and tissue fixation and only in very favourable conditions may they be observed (Bull & Kuhn, 1970;Cohan et al, 1972). A marked decrease of the fibrinolytic potential has been reported in patients with disseminated carcinoma (Thornes, 1967;Soong & Miller, 1970) and in autochthonous experimental tumours (Hilgard & Hiemeyer, 1970). It seems likely that the development of microangiopathic haemolytic anaemia in patients with tumour cell emboli is the coincidence of a variety of factors, producing an imbalance between fibrin formation and fibrinolysis which allows the persistence of intravascular microclots.…”

Thrombophlebitis migrans: a further systemic complication of ulcerative colitis

“…This has been attributed to the release of a thromboplastic substance from degenerating tumour cells (Soong and Miller, 1970), or alternatively to some tumour-induced immunological disturbance. Either mechanism might operate in ulcerative colitis, where the cell turnover rate is increased, and indeed other cutaneous complications 0032-5473/80/0300-0207 $02.00 (© 1980 (Camilleri and Fenech, 1977) describes a patient with severe and extensive ulcerative colitis of 13 years' duration.…”