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Individuals with overt malignancy, pregnancy, puerperium, oral contraceptives, post-surgery period, prolonged immobilization or other conditions associated with secondary thrombophilia were excluded from the study. Open in a separate window. The amplification product obtained for the detection of the FV Liverpool mutation was digested with BsrI according to Mumford et al. These data are consonant with those observed in other populations and further identify that consideration be given to identifying whether individuals are being treated with the novel DOACs when conducting laboratory studies oriented to identify the etiology of thrombosis. The highly efficient algorithm C4. Support Center Support Center.

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Changes in optical density were recorded on a Chrono Log recorder model Additional studies are needed to define with more detail the etiology of the aPCR phenotype and its association with a thrombosis-prone condition.

The aggregation of blood platelets. Similarly, presence of antiphospholipid antibodies was predicted only by fundzmentos presence of lupus anticoagulants and vice versa. An aliquot of the amplified product was therefore subjected to digestion with the restriction endonuclease HindIII.

Primary Thrombophilia in México XI: Activated Protein C Resistance Phenotypes are Multifactorial

Functional abnormalities of this pathway, which manifest itself in vitro as a poor anticoagulant response of plasma to added APC aPC resistance, aPCR se prevalent in the general population and are associated with an increased risk of venous thrombosis. Support Center Support Center. Although FV Leiden is the major cause of hereditary aPCR, it is becoming increasingly clear that several other genetic and acquired conditions contribute to aPCR and thereby increase the risk of venous thrombosis [ 18 — 21 ].

In a single institution for a month period, 96 Mexican mestizos with a history of thrombosis and clinical markers of a primary thrombophilic state were prospectively studied to identify a thrombophilic condition. Interestingly, when looking at the rule sets for aPCR phenotype, in all cases only the status of FV Leiden mutation had been considered fundamsntos for the classification.

The highly efficient algorithm C4. Individuals with overt malignancy, pregnancy, puerperium, oral contraceptives, post-surgery period, prolonged immobilization or other conditions associated with secondary thrombophilia were excluded from the study.

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In this study we have analyzed some of the causes, both inherited and acquired, of the aPCR phenotype in a group of Mexican mestizos with a history of a thrombotic episode in the presence of a clinical marker of thrombophilia.

The amplification product obtained for the detection of the FV Liverpool mutation was digested with BsrI according to Mumford et al.

Molecular genetic analysis in mild hyperhomocysteinemia: Five novel mutations in the gene for the human blood coagulation factor V associated with type I factor V deficiency. Each case is defined by the values of the attributes sticky platelet syndrome, FV Leiden, Cambridge, Hong Kong and Liverpool mutations, c.

Salient findings in thrombophilic patients with abnormal or normal activated protein C resistance phenotype aPCR. A PCR-based analysis for this gene mutation was performed essentially as described by Poort et al.

Sticky platelet syndrome: history and future perspectives. - Semantic Scholar

An abnormal aPCR phenotype was identified in 18 individuals. How we study and treat patients with suspected thrombophilia. Am J Hum Genet.

This process was repeated permutating the attributes until each attribute had been selected once as target attribute. Castoldi E, Rosing J.

A polymerase chain reaction PCR -based analysis for the factor V p.

The mutation was identified by restriction analysis with BstNI. Received Jun 15; Accepted Dec Grupo Latinoamericano de Estudio de Lupus: This article has been cited by other articles in PMC.

A coefficient of agreement for nominal scales. To identify the factor V gene Liverpool mutation p. Please review our privacy policy.

Published online Dec We further identified additional causes of hdmatologia aPCR phenotype: Indian J Hematol Blood Transfus. As the number of cases in our study was small, the complete data set was randomly split into 10 subsets with approximately equal distribution of classes and number of cases.