The hypercoagulable state places an individual at risk for, but does not in itself inevitably lead to, thrombosis. This article focuses on the mechanisms in the hypercoagulable state that enhance and maintain the production of thrombin in circulating blood while preventing its progression to thrombosis. These mechanisms include (1) reactions that produce thrombin from prothrombin, (2) feedback-loop mechanisms that affect the rate of thrombin production from prothrombin, and (3) the inactivation of thrombin in blood. The fibrinolytic system is involved in clot lysis but not in thrombin production and inactivation.

The hypercoagulable state has been defined as the potential to develop thrombosis in association with hereditary and noninherited genetic mutations and acquired disorders.<sup>2 Alessandri C., Basili S., Boili F. , e al. Hypercoagulability state in patients with chronic obstructive pulmonary disease Thromb Haemost 1994 ;  72 : 343-346

Cliccare qui per andare alla sezione Riferimenti, 3 Andrew H., David M., Adams M. , e al. Venous thromboembolic complications (VTE) in children: First analysis of the Canadian Registry of VTE Blood 1994 ;  83 : 1251-1257

Cliccare qui per andare alla sezione Riferimenti, 4 Azar A., Deckers J., Rosendaal P. , e al. Assessment of therapeutic quality control in a long-term anticoagulant trial in post-myocardial infarction patients Thromb Haemost 1994 ;  72 : 347-351

Cliccare qui per andare alla sezione Riferimenti, 5 Beving H., Eksborg S., Malmgren R. , e al. Inter-individual variation of the effect of low dose aspirin regime on platelet cyclooxygenase activity Thromb Res 1994 ;  74 : 39-51  [cross-ref]

Cliccare qui per andare alla sezione Riferimenti, 6 Boisclair M., Lane D., Philippou H. , e al. Mechanisms of thrombin generation during surgery and cardiopulmonary bypass Blood 1993 ;  82 : 3350-3357

Cliccare qui per andare alla sezione Riferimenti, 9 D Dahl, T Pedersen, P Klerulf et al. Sequential intrapulmonary and systemic activation of coagulation and fibrinolysis during and after total hip replacement surgery. Thromb Res 70:451–458.

Cliccare qui per andare alla sezione Riferimenti, 10 Dahlback B. The protein C anticoagulant system: Inherited defects a basis for venous thrombosis Thromb Res 1995 ;  77 : 1-43  [cross-ref]

Cliccare qui per andare alla sezione Riferimenti, 13 Finazzi G., Barbui T. Different incidence of venous thrombosis in patients with inherited deficiencies of antithrombin III, protein C and protein S Thromb Haemost 1994 ;  71 : 15-18

Cliccare qui per andare alla sezione Riferimenti, 19 Ginsberg J.S., Demers S., Brill-Edwards P. , e al. Increased thrombin generation and activity in patients with systemic lupus erythematosus and anticardiolpin antibodies: Evidence for a prothrombotic state Blood 1993 ;  81 : 2958-2963

Cliccare qui per andare alla sezione Riferimenti, 31 Jochmans K., Lissens W., Vervoort R. , e al. Antithrombin-Gly 424 Arg: A novel point mutation responsible for type 1 antithrombin deficiency and neonatal thrombosis Blood 1994 ;  83 : 146-151

Cliccare qui per andare alla sezione Riferimenti, 39 Minamikawa K., Wada H., Wakita Y. , e al. Increased activated protein C–protein C inhibitor complex levels in patients with pulmonary embolism Thromb Haemost 1994 ;  71 : 192-194

Cliccare qui per andare alla sezione Riferimenti, 40 Moor E., Hamsten A., Blomback M. , e al. Haemostatic factors and inhibitors and coronary artery bypass grafting: Preoperative alterations and relations to graft occlusion Thromb Haemost 1994 ;  72 : 335-342

Cliccare qui per andare alla sezione Riferimenti, 45 Pabinger I., Kyrle P., Heisteinger H. , e al. Risk of thromboembolism in asymptomatic patients with protein C and protein S deficiency Blood 1994 ;  83 : 683-690

Cliccare qui per andare alla sezione Riferimenti, 46 Pabinger I., Schneider B. Thrombotic risk of women with hereditary antithrombin II-protein C and proteins S benefit from taking oral contraceptive medication Thromb Haemost 1994 ;  71 : 548

Cliccare qui per andare alla sezione Riferimenti, 47 Petus M., Plaat B., Tencate H. , e al. Enhanced thrombin generation in children with sickle cell disease Thromb Haemost 1994 ;  71 : 169-172

Cliccare qui per andare alla sezione Riferimenti</sup> The most commonly encountered disorders include

The most intriguing aspect of the hypercoagulable states, and one which has received little attention, is the low frequency with which they are associated with thrombosis.<sup>46 Pabinger I., Schneider B. Thrombotic risk of women with hereditary antithrombin II-protein C and proteins S benefit from taking oral contraceptive medication Thromb Haemost 1994 ;  71 : 548

Cliccare qui per andare alla sezione Riferimenti</sup> For example, in pregnancy and other acquired and inherited hypercoagulable states, the calculated incidence of associated thrombosis, although slightly higher than in the general population, is less than 10%. This article provides information needed for the diagnosis and management of the hypercoagulable patient. It is divided in three sections: (1) a review of the regulatory systems that govern the hemostatic state; (2) a clinical presentation of the hypercoagulable anticoagulant deficiency genotype and the more common phenotype associated with disseminated intravascular coagulation; and (3) molecular markers.