Increased production of mononuclear cell procoagulant activity in Hodgkin's disease

Viero, Piera; Cortellazzo, S.; Casarotto, Costanza; Barbui, Tiziano; Colucci, Mario; Semeraro, Nicola

doi:10.1016/0277-5379(83)90083-4

Cited by 14 publications

(10 citation statements)

References 17 publications

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“…However, the endotoxin-stimulated monocytes from patients with PV showed a 21-fold increase in TF levels compared to unstimulated monocytes, and a 5.5-fold increase compared to stimulated monocytes from normal controls and apparent and secondary polycythemia (P < 0.001). Similar results, namely normal levels of TF in unstimulated monocytes and a significant increase in TF following stimulation of the cells had been shown also in other diseases associated with thrombus formation such as Hodgkin's disease [31], toxemia of pregnancy [32], and Crohn's disease [27]; (3) There is a significant correlation between TF activity and antigen in the stimulated monocytes and plasma F 1+2 in PV (r ‫ס‬ 0.77 and 0.87, respectively). When combining all these findings, it is possible that stimulation of monocytes in patients with PV by endotoxin during episodes of infections, or by other substances such as immune complexes [25], interleukins [23], and complement [24], which induce monocyte TF by the same mechanism as endotoxin, induce a potent TF in monocytes.…”

Section: Discussionsupporting

confidence: 83%

Enhanced generation of monocyte tissue factor and increased plasma prothrombin fragment1+2 levels in patients with polycythemia vera: Mechanism of activation of blood coagulation

et al. 1997

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Polycythemia vera (PV) is associated with a high incidence of thrombosis. The association of apparent and secondary polycythemia with thrombosis is not clear. It was suggested that activation of the coagulation system contributes to thrombus formation in PV. However, the mechanism of activation is unknown. Monocytes generate a potent tissue factor (TF) upon stimulation with various substances, which is involved in thrombus formation in various disorders. Therefore, we studied the possibility that the factor is involved in the activation of coagulation and thrombus formation also in PV. Unstimulated peripheral blood mononuclear cells (PBMC) from each of the different types of polycythemia expressed weak TF activity (2 U) and antigen (41.4 to 52.9 pg/ml), which were similar to normal controls. Following stimulation with endotoxin, PBMC from normal controls and from apparent and secondary polycythemia showed a 3.9-to 4.5-fold increase in TF, while cells from PV showed a 21-fold increase (P < 0.001). Similar levels were generated by PBMC after treatment of PV and at the spent phase. TF was generated by monocytes but not by lymphocytes. Plasma prothrombin fragment 1+2 (F 1+2 ) levels, assayed at the same time, were significantly higher in PV (2.46 nm) compared to normals and apparent and secondary polycythemia (0.22 to 0.32 nm), and were in a significant correlation with monocyte TF activity and antigen levels (r = 0.77, 0.87). The high levels of F 1+2 confirm that the coagulation system is activated in PV. The increased capacity of monocytes to generate TF may be responsible for the activation of the coagulation system and thrombus formation. The hypercoagulability state that is induced by this mechanism suggests that long-life oral anticoagulation should be considered once thrombosis has been developed in PV. Am.

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Section: Discussionsupporting

confidence: 83%

Enhanced generation of monocyte tissue factor and increased plasma prothrombin fragment1+2 levels in patients with polycythemia vera: Mechanism of activation of blood coagulation

et al. 1997

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“…Edwards et al (1981) and Morgan et al (1988) reported that blood monocytes from patients with advanced lung carcinoma generated increased amounts of PCA (tissue factor), as compared with normal cells, when incubated in short-term culture with or without endotoxin. A similar observation was made by Viero et al (1983) in patients with Hodgkin's disease. Other investigators, however, either failed to detect changes in monocyte PCA or found a decreased procoagulant response to various stimuli (Osterud and Due, 1984;Geczy et al, 1986).…”

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confidence: 80%

Procoagulant activity of mononuclear phagocytes from different anatomical sites in patients with gynecological malignancies

Semeraro

Montemurro

Conese

et al. 1990

Intl Journal of Cancer

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Mononuclear phagocytes exhibit complex interactions with cancer cells and might contribute to fibrin formation associated with malignancy through the production of procoagulant activity (PCA). We have studied the PCA of peritoneal macrophages in 8 patients with advanced (stages III or IV) ovarian cancer and of macrophages from regional lymph nodes in 14 patients with limited (stages I or II) uterine cancer; peritoneal and lymph-node macrophages from patients with benign gynecological tumors were used as reference cell populations. In all patients, PCA of blood monocytes was also studied. Peritoneal and lymph-node macrophages obtained from patients with ovarian and uterine cancer, respectively, expressed far higher levels of basal PCA than the corresponding cell populations from patients with benign tumors (p less than 0.001). PCA of blood mononuclear cells from patients with ovarian, but not with uterine cancer, was significantly higher (p less than 0.001) than that of control cells. High levels of D-dimer, a specific product derived from plasmin-induced degradation of stabilized fibrin, were found in all ascitic fluids and in all plasma samples but one from patients with ovarian cancer. In contrast, all controls and all uterine cancer patients but one had normal plasma D-dimer. Our findings suggest that local activation of host macrophages for PCA production might contribute to fibrin formation within the tumoral mass. In advanced cancer, blood monocytes may also be activated to produce PCA and thus contribute to activation of intravascular coagulation and, possibly, to thrombo-embolic complications frequently associated with disseminated malignancy.

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“…Cancer by itself has an important role in promoting thrombosis either directly, through tumor-associated procoagulants agents [3,4], or as an indirect effect, through macrophages [5,6], platelets [7], and cytokines [8]. Neverthless thromboembolism is increasingly recognized as a multifactorial disease, caused by the combination of different genetic abnormalities and environmental stimuli [9].…”

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confidence: 99%

THROMBIN GENERATION IN CHILDREN WITH ACUTE LYMPHOBLASTIC LEUKEMIA: Effect of Leukemia Immunophenotypic Subgroups

Giordano

Vecchio

Santoro

et al. 2000

Pediatric Hematology and Oncology

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Elevated plasma concentrations of endogenous thrombin generation markers and thrombotic events have been reported in children with leukemia. The aim of this study was to evaluate the effects of cancer and its treatment on thrombin generation (TAT levels) in children with acute lymphoblastic leukemia (ALL). The authors evaluated 32 children (23 M, 9 F) aged between 1 and 15 years (mean 6) affected by ALL (immunophenotypic subgroups: 16 common, 7 T, and 9 pre-B type). In all patients TAT levels at onset and after 5-6 doses of L-asparaginase were evaluated. TAT levels were higher in patients both at onset (13.04 +/- 10.90 ng/L) and after the 5-6 doses of L-asp (19.41 +/- 11.05 ng/L) with respect to controls (4 +/- 1 ng/L) (p < .001 and p < .001). TAT levels after 5-6 doses of L-asp were higher than those at onset (p < .001). Factorial ANOVA showed that at onset there was a significant effect of leukemia immunophenotypic subgroups upon TAT levels (p < .05) and no effect of inherited thrombotic risk factors. These results indicate that in children with ALL an important role is played by acquired thrombotic risk factors, among which the indirect cancer procoagulant activity has its importance.

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Increased production of mononuclear cell procoagulant activity in Hodgkin's disease

Cited by 14 publications

References 17 publications

Enhanced generation of monocyte tissue factor and increased plasma prothrombin fragment1+2 levels in patients with polycythemia vera: Mechanism of activation of blood coagulation

Enhanced generation of monocyte tissue factor and increased plasma prothrombin fragment1+2 levels in patients with polycythemia vera: Mechanism of activation of blood coagulation

Procoagulant activity of mononuclear phagocytes from different anatomical sites in patients with gynecological malignancies

THROMBIN GENERATION IN CHILDREN WITH ACUTE LYMPHOBLASTIC LEUKEMIA: Effect of Leukemia Immunophenotypic Subgroups

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