Microangiopathic Haemolytic Anaemia and Experimental Tumour‐Cell Emboli

Hilgard, P.; Gordon‐Smith, E. C.

doi:10.1111/j.1365-2141.1974.tb00508.x

Cited by 45 publications

(11 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Clotting activation was greatly reduced by anticoagulation with either warfarin or heparin and was abolished by blocking tumour cell PCA in vitro. 1973: Hilgard & Gordon-Smith, 1974. 1992) the prevention of intravascular coagulation as presently described may provide the biochemical basis of the 'antimetastatic' effect of these agents, at least in this experimental system.…”

Section: Discussionmentioning

confidence: 88%

Procoagulant activity of the MC28 fibrosarcoma cell line in vitro and in vivo

Amirkhosravi

Francis

1993

Br J Haematol

View full text Add to dashboard Cite

Experimental evidence suggests that many tumours can activate blood coagulation and that such interaction is part of the pathology of metastatic tumour growth. This study aimed to study the procoagulant activity of the methylcholanthrene-induced (MC28) fibrosarcoma to determine whether coagulation activation by these cells could explain the previously reported effects of oral anticoagulants on lung seeding in this model. MC28 cells shortened the recalcification times of normal and factor VII-deficient plasma and directly activated factor X in a chromogenic assay, but did not aggregate platelets in vitro in either whole blood or platelet-rich plasma. Cellular coagulant activity was calcium-dependent, blocked by DFP and concanavalin A but not inhibited by iodoacetamide, E-64 or antibodies to human tissue factor or factor VII. Injection of viable MC28 cells into hooded Lister rats induced a decrease in platelet count (P < 0.001), plasma factor X (P < 0.001) and fibrinogen (P < 0.05) and a marked increase in plasma haemoglobin (P < 0.001). These effects were either not observed or were considerably less marked in heparinized or warfarinized animals. Injection of MC28 cells treated with concanavalin A in vitro completely abolished the clotting changes observed with untreated cells. In conclusion, MC28 cells possessed a potent factor X-activating serine proteinase procoagulant in vitro, which had some of the characteristics of a tissue factor/factor VIIa complex. In vivo, MC28 cells caused clotting activation and intravascular fibrin generation. Since thrombocytopenia was abolished by heparin and the cells lacked platelet aggregating activity in vitro, thrombocytopenia was probably secondary to intravascular coagulation and thrombin generation. The trigger for intravascular clotting activation appeared to be the cellular procoagulant activity since it was abolished by prior in vitro blockade of the latter with concanavalin A.

show abstract

Section: Discussionmentioning

confidence: 88%

Procoagulant activity of the MC28 fibrosarcoma cell line in vitro and in vivo

Amirkhosravi

Francis

1993

Br J Haematol

View full text Add to dashboard Cite

show abstract

“…Although several studies have suggested that fibrinoid necrosis of the bone marrow and tumor cell emboli of the arteries, arterioles, and capillaries are the causes of CA-MAHA, the pathogenesis of CA-MAHA remains unclear [14, 15]. Tumor-derived factors, procoagulants, and some anti-cancer drugs are also considered causative agents of CA-MAHA [16].…”

Section: Discussionmentioning

confidence: 99%

Microangiopathic Hemolytic Anemia as the First Manifestation of Metastatic Signet Ring Cell Carcinoma of Unknown Origin: A Case Report and Review of Literature

et al. 2011

View full text Add to dashboard Cite

Microangiopathic hemolytic anemia (MAHA) occurs occasionally as a paraneoplastic syndrome in some solid tumors, but MAHA accompanied by signet ring cell carcinoma of an unknown origin is very rare. In this study, we present the case of an 80-yr-old man who was admitted to the hospital because of a 1-month history of lower back pain and dyspnea. He was diagnosed with MAHA on the basis of the laboratory findings that revealed anemia with schistocytes, decreased haptoglobin levels, and a negative direct Coombs' test. Bone marrow examination, which was performed because of the progression of anemia, revealed bone marrow metastases of signet ring cell carcinoma with extensive bone marrow necrosis. However, the primary origin of this signet ring cell carcinoma was not found. When the cause of progressive MAHA is unknown, the possibility of cancer-associated MAHA must be excluded by performing additional tumor workup, including the detection of tumor markers, gastric and colorectal endoscopic examinations, bone marrow examinations, and positron emission tomography-computed tomography or bone scans.

show abstract

“…The present patient demonstrated the fact that the MAHA can be due to benign tumours, 0032-5473/82/0600-0362 $02.00 C 1982 The Fellowship of Postgraduate Medicine especially if they are large and necrotic, as has been described infrequently before (Conley, Lambird and Biesecker, 1970). MAHA is thought to occur with tumours from erythrocytes shearing on fibrin strands produced by intravascular coagulation, a mechanism that has been demonstrated experimentally as well (Hilgard and Gordon-Smith, 1974). An alternative mechanism for the development of MAHA is shearing of erythrocytes secondary to direct contact with abnormal pulmonary vessels as has been described in the presence of pulmonary hypertension (Stuard et al, 1972).…”

Section: Discussionmentioning

confidence: 96%

Microangiopathic haemolytic anaemia associated with recurrent pulmonary emboli and benign pelvic tumours

Blau¹,

Kaplinsky

1982

Postgraduate Medical Journal

View full text Add to dashboard Cite

SummaryA 42-year-old woman presented with a huge benign pelvic tumour and recurrent pulmonary emboli associated with severe microangiopathic haemolytic anaemia (MAHA). Following removal of the tumour and anticoagulation, all signs of MAHA disappeared. MAHA may occur when red blood cells pass through abnormal blood vessels in tumours. This patient is unusual in that the tumour was benign, rather than malignant. A further site of microangiopathy was the pulmonary vasculature. IntroductionMicroangiopathic haemolytic anaemia (MAHA) is well recognized as a rare complication of malignant tumours (Brain, Dacie and Hourihane, 1962;Antman et al., 1979). It was also described in primary pulmonary hypertension (Stuard, Heuskinkveld and Moss, 1972). We describe a woman with MAHA associated with a benign tumour, and pulmonary hypertension due to recurrent pulmonary emboli.

show abstract

Microangiopathic Haemolytic Anaemia and Experimental Tumour‐Cell Emboli

Cited by 45 publications

References 18 publications

Procoagulant activity of the MC28 fibrosarcoma cell line in vitro and in vivo

Procoagulant activity of the MC28 fibrosarcoma cell line in vitro and in vivo

Microangiopathic Hemolytic Anemia as the First Manifestation of Metastatic Signet Ring Cell Carcinoma of Unknown Origin: A Case Report and Review of Literature

Microangiopathic haemolytic anaemia associated with recurrent pulmonary emboli and benign pelvic tumours

Contact Info

Product

Resources

About