Effect of Anabolic Steroids on Plasma Antithrombin III

SummaryThe effect of seven different anabolic steroids (Ethyloestrenol, Methenolone acetate, Norethandrolone, Methylandrostenediol, Oxymetholone, Methandienone, and Stanozolol) on three α-globulin antiprotease inhibitors of thrombin and plasmin was studied in men with ischaemic heart disease. In distinct contrast to the oral contraceptives, five of the six 17-α-alkylated anabolic steroids studied produced increased plasma Antithrombin III levels and five produced decreased levels of plasma α2-macroglobulin. The effect on plasma α1antitrypsin levels was less clear-cut but three of the steroids examined produced significantly elevated levels. The increased plasma fibrinolytic activity which the 17-α-alkylated anabolic steroids induce is therefore unlikely to be secondary to disseminated intravascular coagulation.

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Plasma Fibrinolytic Activity Following Oral Anabolic Steroid Therapy

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651371 ◽

1975 ◽

Vol 34 (01) ◽

pp. 236-245 ◽

Cited By ~ 3

Author(s):

I. D Walker ◽

J. F Davidson ◽

P Young ◽

J. A Conkie

Keyword(s):

Heart Disease ◽

Ischaemic Heart Disease ◽

Anabolic Steroid ◽

Fibrinolytic Activity ◽

Anabolic Steroids ◽

Long Term Effects ◽

Lysis Time ◽

Detailed Evaluation ◽

Euglobulin Lysis Time

SummarySix anabolic steroids were assessed for their ability to enhance plasma fibrinolytic activity in males with ischaemic heart disease. Five 17α-alkylated steroids (Ethyloestrenol, Norethandrolone, Methandienone, Methylandrostenediol and Oxymetholone) were examined and all produced a significant increase in plasma plasminogen activator as measured by the euglobulin lysis time. The only non-17α-alkylated steroid studied (Methenolone acetate) failed to enhance fibrinolysis. The 17α-alkylated steroids studied all deserve more detailed evaluation of their long term effects on plasma fibrinolytic activity.

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The Effects of Cigarette Smoking on the Haemostatic System

10.1055/s-0039-1680757 ◽

1977 ◽

Author(s):

T.W. Meade ◽

R. Chakrabarti ◽

A.P. Haines ◽

W.R.S. North ◽

Yvonne Stirling

Keyword(s):

Regression Analysis ◽

Platelet Count ◽

Heart Disease ◽

Cigarette Smoking ◽

Factor Viii ◽

Oral Contraceptives ◽

Fibrinolytic Activity ◽

Antithrombin Iii ◽

Platelet Adhesiveness ◽

Heart Study

The main purposes of the Northwick Park Heart Study (NPHS) are to improve the prediction of ischaemic heart disease (IHD) and to elucidate its pathogenesis. Measures of haemostatic function are made along with those of variables already known to be associated with IHD; one such variable is cigarette smoking. It is clearly of interest to know whether the smoking effect may be mediated through changes in haemostatic function; data at recruitment in 1392 men and 580 women have therefore been examined in order to study such changes. Since certain characteristics in NPHS, particularly age and social class, are correlated with both cigarette smoking and with levels of some haemostatic variables, multiple regression analysis has been used to identify smoking effects independent of associations between smoking and these other characteristics. The haemostatic variables included in this, analysis are factors V, VII and VIII, fibrinogen, antithrombin III, fibrinolytic activity, platelet count and platelet adhesiveness. In men, factor VIII levels and fibrinolytic activity are significantly lower in smokers than non-smokers; fibrinogen levels are significantly higher. In women, factor VIII levels are also significantly lower in smokers, but there is no difference in fibrinogen; for fibrinolytic activity there is an interaction between smoking and the use of oral contraceptives (OC). Activity in non-smokers on OC is substantially higher than in those not on OC, but activity in smokers on OC is the same as in women not on OC. It therefore seems that smoking abolishes the protective rise in fibrinolytic activity caused by OC. In men, cigarette smoking may promote thrombosis through effects on fibrinogen and fibrinolytic activity.

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Plasma Prekallikrein, Factor XII, Antithrombin III, C1−-Inhibitor and α2-Macroglobulin in Critically III Patients with Suspected Disseminated Intravascular Coagulation (DIC)

American Journal of Clinical Pathology ◽

10.1093/ajcp/82.4.396 ◽

1984 ◽

Vol 82 (4) ◽

pp. 396-404 ◽

Cited By ~ 38

Author(s):

Bernhard Lämmle ◽

Tri H. Tran ◽

Rudolf Ritz ◽

Francois Duckert

Keyword(s):

Disseminated Intravascular Coagulation ◽

Antithrombin Iii ◽

Factor Xii ◽

C1 Inhibitor ◽

Intravascular Coagulation ◽

Α2 Macroglobulin

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Activation of Protein C and Its Distribution between Its Inhibitors, Protein C Inhibitor, α1-Antitrypsin and α2-Macroglobulin, in Patients with Disseminated intravascular Coagulation

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651631 ◽

1993 ◽

Vol 69 (05) ◽

pp. 448-453 ◽

Cited By ~ 50

Author(s):

M F Scully ◽

C H Toh ◽

H Hoogendoorn ◽

R P Manuel ◽

M E Nesheim ◽

...

Keyword(s):

Western Blotting ◽

Disseminated Intravascular Coagulation ◽

Protein C ◽

Antithrombin Iii ◽

Clinical Course ◽

Factor Xa ◽

Intravascular Coagulation ◽

Α2 Macroglobulin ◽

Protein C Inhibitor ◽

The Face

SummaryActivation and inactivation of protein C during the clinical course of disseminated intravascular coagulation (DIC) was studied in three patients by qualitative (Western blotting) and quantitative (ELISA) analysis and the intensity of procoagulant activity monitored by the measurement of thrombin and factor Xa antithrombin III complexes. In one patient, inhibitor complexes of APC with protein C inhibitor (PCI) and α1-antitrypsin (α1-AT) were observed and the latter predominated at presentation. Both disappeared during the development of remission but the loss of α1-AT complexes preceded PCI complexes which on Western blotting appeared to increase in intensity prior to disappearance. The two other patients bled to death from uncontrollable haemorrhage. In both cases, APC/inhibitor complexes with α2-macroglobulin (α2-M) in addition to PCI and αr-AT were detected and persisted until death. Although PCI appeared to be the primary inhibitor in all three cases, α1-antitrypsin and particularly α2-macroglobulin appeared to assume greater roles in the two fatal cases. These data are similar to previous findings in an experimental animal model of DIC that suggested that α2-macroglobulin and α1-antitrypsin become more important inhibitors of APC as the primary inhibitor PCI is consumed in the face of a sustained procoagulant challenge.

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