Thromb Haemost 1990; 64(02): 216-221
DOI: 10.1055/s-0038-1647288
Original Article
Schattauer GmbH Stuttgart

Increased Monocyte Procoagulant Activity Independent of the Lupus Anticoagulant in Patients with Systemic Lupus Erythematosus

D de Prost
The Inserm U.294 and Laboratoire d–lmmunologie et d–Hématologie, CHU X. Bichat, Paris, France
,
V Ollivier
The Inserm U.294 and Laboratoire d–lmmunologie et d–Hématologie, CHU X. Bichat, Paris, France
,
C Ternisien
The Inserm U.294 and Laboratoire d–lmmunologie et d–Hématologie, CHU X. Bichat, Paris, France
,
S Chollet-Martin
The Inserm U.294 and Laboratoire d–lmmunologie et d–Hématologie, CHU X. Bichat, Paris, France
› Author Affiliations
Further Information

Publication History

Received 08 January 1990

Accepted after revision 07 May 1990

Publication Date:
25 July 2018 (online)

Summary

Monocytes can play a role in the activation of coagulation via increased procoagulant activity (PCA). We investigated the level of monocyte PCA in 19 patients with systemic lupus erythematosus (SLE), given the high rate of thrombotic events in this condition. Nine of these subjects also presented the lupus anticoagulant (LA). The PCA generated by patient monocytes was significantly higher than control values and was identified as tissue factor-like. Moreover, the number of monocytes with membrane-associated D dimer, a parameter whieh we have shown to be correlated with the PCA expressed in vitro by endotoxin-activated monocytes, was also significantly increased. Serum from both groups of patients (i.e. SLE and SLE + LA) stimulated the generation of PCA by control monocytes. By contrast, purified IgG from both patient groups had the same effect as control IgG on PCA generation by control monocytes. The nature of the stimulating agent in the serum was not identified. In conclusion, increased monocyte PCA may account for the increased incidence of thrombosis in SLE patients, although other, superimposed, factors would appear to exist in SLE + LA patients, given the higher incidence of thrombosis in this subgroup.

 
  • References

  • 1 Pauzner R, Rosner E, Many A. Circulating anticoagulant in systemic lupus erythematosus. Acta Haematol 1986; 76: 90-94
  • 2 Derksen RH W M, Kater L. Lupus anticoagulant. Revival of an old phenomenon. Clin Exp Rheumatol 1985; 3: 849-851
  • 3 Feinstein DI. Lupus anticoagulant, thrombosis and fetal loss. N Engl J Med 1985; 313: 1348-1350
  • 4 Derksen RH W M, Bouma BN, Kater L. The striking association between lupus anticoagulant and fetal loss in systemic lupus erythematosus. Arthritis Rheum 1986; 29: 695-696
  • 5 Lechner K, Pabinger-Fasching I. Lupus anticoagulants and thrombosis. A study of 25 cases and review of the literature. Haemostasis 1985; 15: 254-262
  • 6 Carreras LO, Vermylen JG. “Lupus” anticoagulant and thrombosis. Possible role of inhibition of prostacyclin formation. Thromb Haemos-tas 1982; 48: 38-40.
  • 1 Comp PC, De Bault LE, Esmon NL, Esmon CT. Human thrombomodulin is inhibited by IgG from two patients with nonspecific anticoagulants. Blood 1983 suppl 1 1099
  • 8 Cariou R, Tobelem G, Soria C, Caen J. Inhibition of protein C activation by endothelial cells in the presence of lupus anticoagulant. N Engl J Med 1986; 314: 1193-1194
  • 9 Hasselaar P, Derksen RH W M, Blokzijl L, De Groot PhG. Thrombosis associated with antiphospholipid antibodies cannot be explained by effects on endothelial and platelet prostanoid synthesis. Thromb Haemostas 1988; 59: 80-85
  • 10 Geczy CL, Farram E, Moon DK, Meyer PA, McKenzie IC. Macrophage procoagulant activity as a measure of cell-mediated immunity in the mouse. J Immunol 1983; 130: 2743-2749
  • 11 Osterud B, Olsen JO, Benjaminsen AW. The role of complement in the induction of thromboplastin synthesis. Haemostasis 1984; 14: 386-392
  • 12 Rivers RP A, Hathaway WE, Weston WL. The endotoxin-induced coagulant activity of human monocytes. Br J Haematol 1975; 30: 311-316
  • 13 Rothberger HT, Zimmerman HL, Spiegelberg HL, Vaughan JH. Leucocyte procoagulant activity. Enhancement of production in vitro by IgG and antigen-antibody complexes. J Clin Invest 1977; 5: 549-557
  • 14 Lyberg T, Prydz H. Thromboplastin (factor III) activity in human monocytes induced by immune complexes. Eur J Clin Invest 1982; 12: 229-234
  • 15 Maier RV, Ulevitch RJ. The induction of a unique procoagulant activity in rabbit hepatic macrophages by bacterial lipopolysac-charides. J Immunol 1981; 127: 1596-1600
  • 16 Schwartz BS, Levy GA, Curtiss LK, Fair DS, Edgington TS. Plasma lipoprotein induction and suppression of the generation of cellular procoagulant activity in vitro. Two procoagulant activities are produced by peripheral blood mononuclear cells. J Clin Invest 1981; 67: 1650-1658
  • 17 Shands JW. The endotoxin-induced procoagulant of mouse exudate macrophages: a factor-X activator. Blood 1983; 62: 333-340
  • 18 Hogg N. Human monocytes are associated with the formation of fibrin. J Exp Med 1983; 157: 473-485
  • 19 Shelley WB, Juhlin L. Induction of fibrin thrombi by monocytes. Nature 1977; 270: 343-344
  • 20 Edwards RL, Rickies FR, Cronlund M. Abnormalities of blood patients with cancer. Mononuclear tissue factor generation. J Lab Clin Med 1981; 98: 917-28
  • 21 Lyberg T, Prydz H, Baklien K, Hoyeraal HM. Effect of immune complex-containing sera from patients with rheumatic diseases on thromboplastin activity of monocytes. Thromb Res 1982; 25: 193-202
  • 22 østerud B, Flaegstad T. Increased tissue thromboplastin activity in monocytes of patients with meningococcal infection: related to an unfavourable prognosis. Thromb Haemostas 1983; 49: 5-7
  • 23 Cole EH, Schulman J, Urowitz M, Keystone E, Williams C, Levy GA. Monocyte procoagulant activity in glomerulonephritis associated with systemic lupus erythematosus. J Clin Invest 1985; 75: 861-868
  • 24 Chollet-Martin S, Ollivier V, Amiral J, de Prost D. Binding of an anti D dimer monoclonal antibody to endotoxin-activated monocytes. Demonstration by immunogold-silver staining. Thromb Res 1988; 52: 1-10
  • 25 Tan EM, Cohen AS, Fries JF. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum 1982; 11: 1271-1277
  • 26 Schleider MA, Nachman RL, Jaffe EA, Coleman M. A clinical study of the lupus anticoagulant. Blood 1976; 48: 499-509
  • 27 Rosove MH, Ismail M, Kozid BJ, Runge H, Kasper CK. Lupus anticoagulant: improved diagnosis with a kaolin clotting time using rabbit brain phospholipid in standard and high concentrations. Blood 1986; 68: 472-478
  • 28 Meyer O, Piette JC, Bourgeois P, Fallas P, Bletry O, Jungers P, Kahn MF, Ryckewaert A. Antiphospholipid antibodies: a disease marker in 25 antinuclear antibody negative systemic lupus erythematosus (SLE). Comparison with a group of 91 antinuclear antibody positive SLE. J Rheumatol 1987; 14: 502-506
  • 29 Altieri DC, Manucci PM, Capitanio M. Binding of fibrinogen to human monocytes. J Clin Invest 1986; 159: 1042-1057
  • 30 Tucker SB, Pierre RV, Jordon RE. Rapid identification of monocytes in mixed mononuclear preparations. J Immunol Method 1977; 14: 267-269
  • 31 Lorenzet R, Niemetz J, Marcus AJ, Broekman MJ. Enhancement of mononuclear procoagulant activity by platelet 12-hydroxyeicosa-tetraenoic acid. J Clin Invest 1986; 78: 418-423
  • 32 Rickies FR, Rick PD. Structural features of Salmonella typhimurium lipopolysaccharide required for activation of tissue factor in human mononuclear cells. J Clin Invest 1977; 59: 1188-1195
  • 33 Tsao BP, Fair DS, Curtiss LK, Edgington TS. Monocytes can be induced by lipopolysaccharide-triggered T lymphocytes to express functional factor VH/VIIa protease activity. J Exp Med 1984; 159: 1042-1057
  • 34 Caen J, Larrieu MJ. Samama M. L,hémostase - Méthodes d,explora-tion et diagnostic pratique. L,expansion Scientifique; Paris: 1975. p 313
  • 35 Hardin JA, Cronlund M, Haber E, Bloch KJ. Activation of blood clotting in patients with systemic lupus erythematosus. Relation to disease activity. Am J Med 1978; 65: 430-436
  • 36 Van Ginkel CJ W, Van Aken WG, Oh JI H, Vreeken J. Stimulation of monocyte procoagulant activity by adherence to different surfaces. Br J Haematol 1977; 37: 35-45
  • 37 Edwards RL, Rickies FR. The role of human T cells (and T cell products) for monocyte tissue factor generation. J Immunol 1980; 125: 606-609
  • 38 Ollivier V, Sheibani A, Chollet-Martin S, Vie P, Benacerraf R, Duparc J, de Prost D. Monocyte procoagulant activity and membrane-associated D dimer after Knee replacement surgery. Thromb Res 1989; 55: 179-185
  • 39 Rylatt DB, Blake AS, Cottis LE, Massingham DA, Fletcher WA, Masci PP, Whitaker AN, Elms M, Bunce I, Webber AJ, Wyatt D, Bundesen PG. An immunoassay for human D Dimer using monoclonal antibodies. Thromb Res 1983; 31: 767-778
  • 40 Rajagopalan S, Pizzo SV. Characterization of murine peritoneal macrophage receptors for fibrin(ogen) degradation products. Blood 1986; 67: 1224-1228
  • 41 Edwards RL, Perla D. The effect of serum on monocyte tissue factor generation. Blood 1984; 64: 707-714
  • 42 Rustin MH A, Bull HA, Machin SJ, Isenberg DA, Snaith ML, Dowd PM. Effects of the lupus anticoagulant in patients with systemic lupus erythematosus on endothelial cell prostacyclin release and procoagulant activity. J Invest Dermatol 1988; 90: 744-748
  • 43 Thomas L. Studies on the intravascular thromboplastic effect of tissue suspensions in mice. II. A factor in normal rabbit serum which inhibits the thromboplastic effect of the sedimentable tissue component. Bull Johns Hopkins Hosp 1947; 81: 26
  • 44 Carson SD. Tissue factor (coagulation factor III) inhibition by apolipoprotein A-II. J Biol Chem 1987; 262: 718-721
  • 45 Rao LV, Rapaport SI. Studies of a mechanism inhibiting the initiation of the extrinsic pathway of coagulation. Blood 1987; 69: 645-651
  • 46 Gramzinski RA, Broze GJ, Carson SD. Human fibroblast tissue factor is inhibited by lipoprotein-associated coagulation inhibitor and placental anticoagulant protein but not by apolipoprotein A-II. Blood 1989; 73: 983-989
  • 47 Bajaj MS, Rana SV, Wysolmerski RB, Bajaj P. Inhibitor of the factor Vlla-tissue factor complex is reduced in patients with disseminated intravascular coagulation but not in patients with severe hepatocellular disease. J Clin Invest 1987; 79: 1874-1878