Combined Modalities in Surgical Patients

An, Nicolaides; Fareed, Jawed; Kakkar, Ajay K.; Comerota, Anthony J.; Goldhaber, Samuel Z.; Hull, R D; Myers, Kelly; Samama, Meyer-Michel; Fletcher, J.; Kalodiki, Evi; Bergqvist, David; Bonnar, J.; Caprini, Joseph A.; Carter, C.; Conard, J.; Eklöf, Bo; Elalamy, Ismaı̈l; Gerotziafas, G.; Geroulakos, George; Giannoukas, A.; Greer, Ian A.; Griffin, Maura; Kakkos, S.; M, Lassen; Lowe, G. D. O.; Markel, Arie; Prandoni, Paolo; Raskob, Gary E.; Spyropoulos, Alex C.; Turpie, Alexander G. G.; Walenga, Jeanine M.; Warwick, David

doi:10.1177/1076029612474840l

Cited by 3 publications

(5 citation statements)

References 3 publications

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“…The OR for G20210A PTM was 2.80 (95% CI 2.25-3.48) for heterozygotes and 6.74 (95% CI 2.19-20.72) for homozygotes. The presence of combined heterozygosis is a rare condition generally considered to be associated with a 10-20 increase of the risk of VTE [4]; however, in this analysis, its presence did not appear to confer additional risk for first VTE beyond the sole presence of FVL (OR: 3.42, CI 95% 1.65-7.13) [6].…”

Section: Introductioncontrasting

confidence: 65%

“…Numerous case-control, cohort studies and meta-analyses have established that the two of these mutations are connected to an increased risk of venous thromboembolic events (VTE), especially in patients with homozygosity or double heterozygosity [2][3]. Indeed, combined hereditary thrombophilias, homozygous FVL or G20210A PTM, antithrombin deficiency, antiphospholipid syndrome, homozygous deficiency of Protein C and homozygous deficiency of Protein S are generally considered strong risk factors for VTE [4][5]. In a recent meta-analysis [6], FVL was associated with an increased risk of VTE in both heterozygotes and homozygotes (odds ratio…”

Section: Introductionmentioning

confidence: 99%

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Association between inherited thrombophilia and venous thromboembolism in patients with Non-O Blood Type: a meta-analysis

Pomero¹,

Dentali²,

Nicoletto³

et al. 2022

Polish Archives of Internal Medicine

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The risk of venous thromboembolism determined by the presence of a single inherited thrombophilic alteration, such as factor V Leiden or prothrombin mutation, is difficult to estimate. Nevertheless, the coexistence of these disorders with a blood group different than O considerably increases the risk of venous thromboembolism in the general population. Since the analysis of the blood group can be easily performed, in all patients with other risk factors for venous thromboembolism particular attention should be given to the presence of blood groups different than O.

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Section: Introductioncontrasting

confidence: 65%

Section: Introductionmentioning

confidence: 99%

Association between inherited thrombophilia and venous thromboembolism in patients with Non-O Blood Type: a meta-analysis

Pomero¹,

Dentali²,

Nicoletto³

et al. 2022

Polish Archives of Internal Medicine

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show abstract

“…Las trombofilias, definidas como la tendencia a desarrollar fenómenos de trombosis arterial o venosa recurrente, espontáneas o con mínima provocación, a edades menores de las habituales, en territorios poco comunes ya sea de origen congénito o adquirido [166,167], en los últimos años se han documentado como causa íntima de pérdidas fatales recurrentes [168][169][170][171][172]. Dentro las trombofilias congénitas asociadas con pérdidas fetales recurrentes la que más se ha encontrado en nuestro medio [173,174] y en otros países latinoamericanos [175][176][177] es el síndrome de plaqueta pegajosa situación que se controla efectivamente con aspirina a bajas dosis.…”

Section: Aspirina Y Pérdidas Fetalesunclassified

“…Síndromes de hiperagregabilidad plaquetaria (trombocitosis primaria y secundaria [bibliografías], síndromes mielodisplásicos [bibliografías], síndrome de plaqueta pegajosa [166])…”

Section: Agregación Eritrocitaria Elevada [203]unclassified

Resistencia a la aspirina: un problema latente de alto riesgo

Campuzano-Maya¹

2016

Med. Lab.

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La aspirina es la piedra angular del tratamiento en pacientes con enfermedades cardiovasculares y cerebrovasculares; sin embargo, varios estudios sobre la respuesta in vitro de las plaquetas a la administración de aspirina mostraron que esta respuesta es variable, encontrando algunos pacientes con falta de respuesta o resistencia a la aspirina. La resistencia a la aspirina puede ser ”clínica” o "de laboratorio". La resistencia clínica a la aspirina se define como el fracaso para evitar la aparición de los episodios isquémicos aterotrombóticos en pacientes a los que se les administra. La resistencia de laboratorio a la aspirina se define como el fracaso de la aspirina para inhibir la producción de tromboxano A2 por las plaquetas o para inhibir la activación de las plaquetas dependiente de la producción de tromboxano A2. Hasta el momento no hay ningún método general para la evaluación ex vivo de la activación plaquetaria o del grado de activación de las plaquetas después de la administración de aspirina, y los datos relativos al impacto clínico de la resistencia a la aspirina son conflictivos. Por esto, no es posible sugerir directrices específicas para el tratamiento de pacientes que muestran altos niveles de activación plaquetaria o un bajo nivel de inhibición de las plaquetas después del tratamiento con aspirina. El objetivo de esta revisión es presentar los datos de estudios clínicos y de laboratorio que están relacionadas con la resistencia a la aspirina y discutir las posibles causas, importancia clínica y formas de manejo clínico de dicha resistencia.

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“…3 Up-to-date indications for thrombophilia testing in patients with VTE have been summarized in various guidelines and reviews; however, validated guidance is still lacking on whom and what to test. [5][6][7][8][9][10][11][12][13][14][15] As no single well-standardized and widely accepted method exists for heritable thrombophilia screening, a list of investigations has to be performed in a patient suspected of thrombophilia. Thrombophilia screening usually includes tests for APC resistance or FVL, FII20210A, as well as assays for AT, PC, and PS.…”

mentioning

confidence: 99%

Inherited thrombophilia and the risk of myocardial infarction: current evidence and uncertainties

2019

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thrombophilia and the risk of myocardial infarction 419 large arteries, sometimes with coexistent VTE, and linked the events to hypercoagulability of the patients' plasma. 2,3 Some decades later, research on thrombophilia expanded by investigating families with frequent or unusual events of VTE. Today, due to this field of extensive research, the term thrombophilia is used to describe a hemostasis disorder leading to an elevated risk of developing VTE that can be inherited, acquired, or both. The well-established factors of inherited thrombophilia are as follows: different loss-of-function mutations of the inhibitors of plasma coagulation that cause deficiencies of antithrombin (AT), protein C (PC), and protein

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Combined Modalities in Surgical Patients

Cited by 3 publications

References 3 publications

Association between inherited thrombophilia and venous thromboembolism in patients with Non-O Blood Type: a meta-analysis

Association between inherited thrombophilia and venous thromboembolism in patients with Non-O Blood Type: a meta-analysis

Resistencia a la aspirina: un problema latente de alto riesgo

Inherited thrombophilia and the risk of myocardial infarction: current evidence and uncertainties

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