Thrombosis in the Young: Epidemiology and Risk Factors. A Focus on Venous Thrombosis

Thrombosis occurs most often as myocardial infarction, cerebral infarction or venous thromboembolism, ie, deep-vein thrombosis and pulmonary embolism. The incidence of all types of thrombosis is strongly dependent on age. Among young individuals, up to age 40, venous thrombosis is the most common form of thrombosis. The risk factors for arterial and venous thrombosis differ, and among the latter disorders of hemostasis appear to be more prominent. In children venous thrombosis appears almost exclusively in association with venous catheters, with an exception of the renal vein thrombosis of the newborn, which has an unknown etiology. In young adults, the risk factors for venous thrombosis are essentially the same as in older individuals, excepting oral contraceptives, pregnancy and puerperium which are limited to young women. In young women, most venous thrombotic events can be attributed to oral contraceptives. Venous thrombosis is a multicausal disease: more than one risk factor needs to be present before thrombosis occurs. The younger an individual, the more risk factors are required to precipitate thrombosis: in children often three or four, and in young adults often two or more.

[1]  M. Prins,et al.  Frequency of Pregnancy-Related Venous Thromboembolism in Anticoagulant Factor-Deficient Women: Implications for Prophylaxis , 1996, Annals of Internal Medicine.

[2]  P. Prandoni,et al.  Hyperhomocysteinemia and deep-vein thrombosis. A case-control study. , 1996, Thrombosis and haemostasis.

[3]  P. Reitsma,et al.  Apparent different thrombotic tendency in patients with factor V Leiden and protein C deficiency due to selection of patients. , 1996, Blood.

[4]  P. Reitsma,et al.  A common genetic variation in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. , 1996, Blood.

[5]  P. Mannucci,et al.  Inherited Thrombophilia: Part 1 , 1996, Thrombosis and Haemostasis.

[6]  S. Goldhaber,et al.  Pulmonary embolism and deep venous thrombosis during pregnancy or oral contraceptive use: prevalence of factor V Leiden. , 1996, American heart journal.

[7]  C. Mannhalter,et al.  ORAL CONTRACEPTIVES ENHANCE THE RISK OF CLINICAL MANIFESTATION OF VENOUS THROMBOSIS AT A YOUNG AGE IN FEMALES HOMOZYGOUS FOR FACTOR V LEIDEN , 1996, British journal of haematology.

[8]  W. Spitzer,et al.  CSM should rethink its approach for such announcements , 1996, BMJ.

[9]  W M O'Fallon,et al.  Stroke incidence, prevalence, and survival: secular trends in Rochester, Minnesota, through 1989. , 1996, Stroke.

[10]  W. Spitzer,et al.  Third generation oral contraceptives and risk of venous thromboembolic disorders: an international case-control study , 1996, BMJ.

[11]  M. Blombäck,et al.  Arg506–Gln mutation in factor V and risk of thrombosis during pregnancy , 1996, British journal of haematology.

[12]  P. Reitsma,et al.  Hyperhomocysteinemia as a risk factor for deep-vein thrombosis. , 1996, The New England journal of medicine.

[13]  T. Farley,et al.  Effect of different progestagens in low oestrogen oral contraceptives on venous thromboembolic disease , 1995 .

[14]  H. Jick,et al.  Risk of idiopathic cardiovascular death and rionfatal venous thromboembolism in women using oral contraceptives with differing progestagen components , 1995, The Lancet.

[15]  J. Vandenbroucke,et al.  Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation progestagen , 1995, The Lancet.

[16]  B. Schmidt,et al.  Neonatal thrombosis: report of a prospective Canadian and international registry. , 1995, Pediatrics.

[17]  B. Dahlbäck,et al.  Resistance to activated protein C as a basis for venous thromboembolism associated with pregnancy and oral contraceptives. , 1995, American journal of obstetrics and gynecology.

[18]  P. Reitsma,et al.  Protein C deficiency in a controlled series of unselected outpatients: an infrequent but clear risk factor for venous thrombosis (Leiden Thrombophilia Study) , 1995, Blood.

[19]  P. Ridker,et al.  Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men. , 1995, The New England journal of medicine.

[20]  P. Reitsma,et al.  High risk of thrombosis in patients homozygous for factor V Leiden (activated protein C resistance) , 1995, Blood.

[21]  J. Vandenbroucke,et al.  Role of clotting factor VIII in effect of von Willebrand factor on occurrence of deep-vein thrombosis , 1995, The Lancet.

[22]  T. Farley,et al.  Venous thromboembolic disease and combined oral contraceptives: results of international multicentre case-control study. World Health Organization Collaborative Study of Cardiovascular Disease and Steroid Hormone Contraception. , 1995, Lancet.

[23]  M. Manco-Johnson,et al.  Childhood thrombosis. , 1995, Pediatrics.

[24]  P. Reitsma,et al.  Increased risk of venous thrombosis in oral-contraceptive users who are carriers of factor V Leiden mutation , 1994, The Lancet.

[25]  P. Reitsma,et al.  Activated protein C resistance as an additional risk factor for thrombosis in protein C-deficient families. , 1994, Blood.

[26]  P. Mannucci,et al.  High prevalence of hyperhomocyst(e)inemia in patients with juvenile venous thrombosis. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[27]  T. Barbui,et al.  Thrombosis during Pregnancy and Surgery in Patients with Congenital Deficiency of Antithrombin III, Protein C, Protein S , 1994, Thrombosis and Haemostasis.

[28]  P. Reitsma,et al.  Factor VII and Fibrinogen Levels as Risk Factors for Venous Thrombosis , 1994, Thrombosis and Haemostasis.

[29]  Pieter H. Reitsma,et al.  Mutation in blood coagulation factor V associated with resistance to activated protein C , 1994, Nature.

[30]  B. Lämmle,et al.  Thrombotic Risk of Women with Hereditary Antithrombin III-, Protein C- and Protein S-Deficiency Taking Oral Contraceptive Medication , 1994, Thrombosis and Haemostasis.

[31]  M. Bernstein,et al.  Venous thromboembolic complications (VTE) in children: first analyses of the Canadian Registry of VTE , 1994 .

[32]  B. Dahlbäck,et al.  Resistance to activated protein C as a basis for venous thrombosis. , 1994, The New England journal of medicine.

[33]  M. M. Rees,et al.  Homocysteinemia: association of a metabolic disorder with vascular disease and thrombosis. , 1993, Thrombosis research.

[34]  M. Andrew,et al.  Venous thromboembolic complications in children. , 1993, The Journal of pediatrics.

[35]  B. Dahlbäck,et al.  Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[36]  P. Reitsma,et al.  Citations from the Literature , 2003 .

[37]  B. Lindblad,et al.  A prospective study of the incidence of deep‐vein thrombosis within a defined urban population , 1992, Journal of internal medicine.

[38]  M. Marmot,et al.  Primary prevention of stroke , 1992, The Lancet.

[39]  K. Mcintyre Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep-vein thrombosis: Heijboer H, Brandjes DPM, Büller HR, Sturk A, Wouter ten Cate J. N Engl J Med 1990;323:1512–6 , 1991 .

[40]  H. Büller,et al.  Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep-vein thrombosis. , 1990, The New England journal of medicine.

[41]  A. Chuansumrit,et al.  Homozygous protein S deficiency in an infant with purpura fulminans. , 1990, The Journal of pediatrics.

[42]  M. Samama,et al.  Thrombosis and Pregnancy in Congenital Deficiencies in AT III, Protein C or Protein S: Study of 78 Women , 1990, Thrombosis and Haemostasis.

[43]  P. Callas,et al.  The clinical spectrum of heterozygous protein C deficiency in a large New England kindred. , 1989, Blood.

[44]  S. Daeschner Pulmonary embolism. , 1988, Nursing.

[45]  J. Miletich,et al.  Absence of thrombosis in subjects with heterozygous protein C deficiency. , 1987, The New England journal of medicine.

[46]  P. Hopkins,et al.  Identification and relative weight of cardiovascular risk factors. , 1986, Cardiology clinics.

[47]  J. Katz,et al.  INHERITED PROTEIN C DEFICIENCY AND COUMARIN-RESPONSIVE CHRONIC RELAPSING PURPURA FULMINANS IN A NEWBORN INFANT , 1983, The Lancet.

[48]  G. J. Kloosterman,et al.  Epidemiological observations of thrombo‐embolic disease during pregnancy and in the puerperium, in 56,022 women , 1983, International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics.

[49]  A. Kierkegaard Incidence and Diagnosis of Deep Vein Thrombosis Associated with Pregnancy , 1983, Acta obstetricia et gynecologica Scandinavica.

[50]  B. Stadel Oral contraceptives and cardiovascular disease (first of two parts). , 1981, The New England journal of medicine.

[51]  J. Dalen,et al.  Oral contraceptives and cardiovascular disease. , 1981, American heart journal.

[52]  M. Graffar [Modern epidemiology]. , 1971, Bruxelles medical.

[53]  D. W. Neill,et al.  Metabolic Abnormalities Detected in a Survey of Mentally Backward Individuals in Northern Ireland , 1962, Archives of disease in childhood.