Journal Information
Vol. 35. Issue 7.
Pages 329-333 (July - August 1999)
Share
Share
Download PDF
More article options
Vol. 35. Issue 7.
Pages 329-333 (July - August 1999)
Full text access
Búsqueda de marcadores clínicos de hipercoagulabilidad patológica según los factores desencadenantes de enfermedad tromboembólica venosa (ETV)
The search for clinical markers of abnormal hypercoagulable States among factors that trigger venous thromboembolic disease
Visits
4262
R. Otero Candelera
Corresponding author
rotero@separ.es

Correspondencia: Castillo de Marchenilla, 5, 2, 1.° A. 41013 Sevilla.
, M. Arenas Gordillo, J.E. Hurtado Ayuso
Servicios de Neumología. Hospital Virgen del Rocío. Sevilla
R. Moralesaa, M. Monederoaa, J. Digonaa
a Hematología. Hospital Virgen del Rocío. Sevilla
This item has received
Article information
Abstract
Bibliography
Download PDF
Statistics

Nos propusimos buscar marcadores de hipercoagulabilidad patológica atendiendo a la edad, sexo o factores desencadenantes de enfermedad tromboembólica venosa (ETV) en el seguimiento de un grupo de pacientes que habían sido diagnosticados de ETV. Consideramos los siguientes datos de los pacientes: edad, sexo y factores desencadenantes de la ETV, que categorizamos en: coyunturales o transitorios, permanentes y desconocidos. Se practicó estudio de hipercoagulabilidad a los menores de 55 años, a aquellos en los que el factor desencadenante de la ETV fue desconocido o a aquellos con historia familiar y/o personal previa de ETV. El estudio de hipercoagulabilidad se llevó a cabo a los 3 meses aproximados tras el episodio agudo trombótico y fue repetido en los casos patológicos para confirmar el diagnóstico.

Desde abril del 1993 hasta julio del 1996 hemos seguido en nuestra consulta externa a 297 pacientes, diagnosticados de ETV. De los 297 pacientes, se realizó estudio de hipercoagulabilidad a 187 (63%) de los que 86 (46%) fueron normales y 101 (54%) patológicos. No se encontró ninguna relación significativa entre edad, sexo o factores desencadenantes con los resultados del estudio de hipercoagulabilidad realizado en el seguimiento.

Concluimos que no hay que atender solamente a los factores desencadenantes de ETV para asentar la indicación del estudio de hipercoagulabilidad, puesto que la presencia de hipercoagulabilidad patológica no se limita a aquellos pacientes con supuestos marcadores clínicos.

Palabras clave:
Embolismo pulmonar
Marcadores clínicos de hipercoagulabilidad
Pruebas a seguir

We proposed to search for markers of hypercoagulable States in function of age, sex or factors that trigger venous thromboembolic disease (VTD) in a group of patients so diagnosed. The following patient data were analyzed: age, sex and triggering factors of VTD categorized as associativetransient, permanent or unknown. In patients under age 55 years of age in whom the triggering factor of VTD was unknown, and in those who had a family and/or personal history of VTD, coagulability was assessed approximately three months after the episode of acute thrombosis and was repeated during follow-up.

From April 1993 to July 1996 we saw 297 patients diagnosed of VTD and performed 187 coagulability tests (63%). Eighty-six were normal (46%) and 101 (54%) abnormal. No significant relations were found for age, sex or triggering factors and the results of follow-up coagulability testing.

We conclude that factors known to trigger VTD are not the only ones relevant for indicating the need to order the assessment of coagulability, given that the presence of coagulopathy is not confined to patients with supposed clinical markers.

Key words:
Pulmonary embolism
Hypercoagulable states
Follow-up testing
Full text is only aviable in PDF
Bibliografía
[1.]
E. Strandeness.
Deep venous thrombosis and the postrhrombotic syndrome.
Duplex scanning vascular disorders, pp. 167-184
[2.]
W.S. Gross, R.E. Burney.
Therapeutic and economic implication of emergency department evaluation for venous thrombosis.
J Am Coll Emerg Phys, 8 (1979), pp. 110
[3.]
Ventilation-Perfusion Scan- PIOPED Investigators.
JAMA, 263 (1990), pp. 2.755-2.759
[4.]
P.D. Alderson, E.C. Martin.
Pulmonary embolism diagnosis with multiple imaging modalities.
Radiology, 164 (1987), pp. 297-312
[5.]
C. Philip.
Congenital and acquired hypercoagulable States.
Disorders of thrombosis, pp. 339-347
[6.]
C. Korninger, K. Lechner, H. Niessner, H. Gössinger, M. Kundi.
Impareid fibrinolytic capacity predisposes for recurrence of venous thrombosis.
Thromb Haemost, 52 (1984), pp. 127-130
[7.]
S.V. Pizzo, H.E. Fuchs, K.A. Doman, D.B. Petruska, H. Berger.
Release of tissue plasminogen activator and its fast-acting inhibitor in defective fibrinolysis.
Areh Intern Med, 146 (1986), pp. 188
[8.]
M. Kolodziej, P.C. Comp.
Hypercoagulable States due to natural anticogulant deficiencies.
Curr Opinion in Hematology, pp. 301-307
[9.]
J.S. Ginsberg, P.S. Wells, P. Brill-Edwards, D. Donovan, K. Moffatt, M. Johnston, et al.
Antiphospholipid antibodies and venous thromboembolism.
Blood, 86 (1995), pp. 3.685-3.691
[10.]
W.A. Wilson, A.E. Gharavi.
Hughes syndrome: perpectives on thrombosis and antiphospholipid antibody.
Am J Med, 101 (1996), pp. 574-575
[11.]
D.E. Sprengers, C. Kluft.
Plasminogen activator inhibitors.
Blood, 69 (1987), pp. 381-387
[12.]
B. Latham, E.A. Kufoy, O. Barret, M.F. Gonzalez.
Deficient tissue plasminogen activator release and normal tisssue plasminogen activator inhibitors.
Am J Med, 88 (1990), pp. 199-200
[13.]
L. Engesser, E.J.P. Brommer, C. Kluft, E. Briet.
Elevated plasminogen activator inhibitor (PA1): a cause of thrombophilia?.
Thromb Haemost, 62 (1989), pp. 673-680
[14.]
M. Tabernero, A. Estelles, V. Vicente, I. Alberca, J. Aznar.
Incidence of incresed plasminogen activator inhibitor in patients with deep thrombosis venous and/or pulmonary embolism.
Thromb Res, 56 (1989), pp. 565-570
[15.]
P.M. Ridker, D.E. Vaugham, M.J. Stampfer, J.E. Manson, C. Shen, L.M. Newcomer, et al.
Baseline fibrinolytic State and the risk of future venous thrombosis.
Circulation, 85 (1992), pp. 1.822-1.827
[16.]
F. Andreotti, G.J. Davies, D.R. Hackett, M.I. Khan, A.C.W. DeBart, V.R. Aber, et al.
Major circadian fluctuations in fibrinolytic factors and possible relevance to time of onset of myocardial infartion, sudden cardiac death and stroke.
Am J Cardiol, 62 (1988), pp. 635-637
[17.]
C. Kluft, J.H. Verheijen, A.F.H. Jie, D.C. Rijken, F.E. Preston, H.M. Sue-Ling, et al.
The postoperative fibrinolytic shut-down: a rapidly reverting acute phase pattern for the fast acting inhibitor of tissue type plasminogen activator after trauma.
Scan J Clin Lab Invest, 45 (1985), pp. 605-610
[18.]
S. Shulman, A.S. Rhedin, P. Lindmarker.
A comparison of six weeks with six months of oral anticoagulant therapy after a first episode of venous thromboembolism.
N Engl J Med, 332 (1995), pp. 1.661-1.669
Copyright © 1999. Sociedad Española de Neumología y Cirugía Torácica
Archivos de Bronconeumología
Article options
Tools

Are you a health professional able to prescribe or dispense drugs?