Lack of Activated Protein C Resistance in Healthy Hong Kong Chinese Blood Donors - Correlation with Absence of Arg506-Gln Mutation of Factor V Gene

Chan, Lewis; Bourke, Chase H.; Ck, Lam; Hw, Liu; Brookes, Steven J.; Jenkins, Valerie; Pasi, John

doi:10.1055/s-0038-1665404

Cited by 44 publications

(32 citation statements)

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“…Some studies attribute more than 95% of cases of APC resistance to the FV Leiden mutation [3,9,12]. FV Leiden is present in heterozygous form in 5% of the general Caucasian population and is less common or rare in other ethnic groups [13][14][15][16][17][18]. Homozygosity for FV Leiden occurs in about 1 in 5,000.…”

Section: Background and Molecular Basis Of Fv Leiden And Activated Prmentioning

confidence: 99%

Factor VLeiden

2015

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Factor V Leiden (FV Leiden ) is a common hereditary thrombophilia that causes activated protein C (APC) resistance. This review describes many of the most fascinating features of FV Leiden , including background features, mechanisms of hypercoagulability, the founder mutation concept, the "FV Leiden paradox," synergistic interaction with other thrombotic risk factors, the intertwined relationship between FV Leiden and APC resistance testing, and other, uncommon mutations implicated in causing APC resistance. In addition, there are several conditions where laboratory tests for APC resistance and FV Leiden are or can be discrepant, including lupus anticoagulants, anticoagulants such as direct thrombin inhibitors (dabigatran, argatroban, and bivalirudin) and rivaroxaban, as well as pseudohomozygous, pseudo-wildtype, liver transplant, and bone marrow transplant patients. The laboratory test error rate for FV Leiden is also presented.

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Section: Background and Molecular Basis Of Fv Leiden And Activated Prmentioning

confidence: 99%

Factor VLeiden

2015

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“…the discoveries of factor V Leiden, PT 20210A allele, MTHFR gene mutation and elevated factor VIII levels [1][2][3][4][5][6]17,18,20,21]. However, though factor V Leiden was found to be the most frequent cause of TED in the western countries, it was absent in the Chinese race [7,8]. Thus, the cause of TED in the Chinese is probably different and deserves our investigation.…”

Section: Discussionmentioning

confidence: 85%

“…More than 80% of the causes of TED had been unknown before 1993. After 1993, APC resistance to factor V Leiden was found to be a major cause of TED in the western countries [1][2][3][4][5][6], however, the same phenomenon was not found in the Chinese [7,8]. As the Chinese people are less prone to TED [9][10][11], possibly because of a difference in race, diet or other factors [12][13][14], the causes of venous thrombosis in the Chinese patients might be different from those of the Caucasians.…”

Section: Introductionmentioning

confidence: 99%

Causes of venous thrombosis in fifty Chinese patients

Chau

Hsu

et al. 2000

Am. J. Hematol.

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In a whole year from July 1997 to June 1998, a total of 50 patients with sonogram-proved venous thrombosis who called on our hematology clinic consecutively entered into the study. Their mean age was 59.1 +/- 17.5 years, range 18-83 years, and 29 were male. A series of examinations were performed in order to find out the cause of venous thrombosis. These examinations included antithrombin, protein C, protein S, plasminogen, heparin cofactor II, activated protein C ratio, factor V Leiden mutation, fibrinogen, factors VIII and XII, euglobulin lysis time, 677 C-->T mutation of methylenetetrahydrofolate reductase (MTHFR), prothrombin 20210 (PT 20210) A allele mutation, lupus anticoagulant, anticardiolipin antibody, and complete blood count. Five patients (10%) were found to have malignancy; an inferior vena cava thrombosis in one patient was due to venous compression by hydronephrosis; two patients had lupus anticoagulant; two had varicose veins of legs; two had protein C deficiency; four had protein S deficiency; two had plasminogen deficiency; two had antithrombin deficiency. No activated protein C resistance, elevated factor VIII level, factor V Leiden, PT 20210 A allele or heparin cofactor II deficiency was found in the present study. Homozygous MTHFR 677 C-->T gene mutation was found in 7 patients (14%); one of them also had a plasminogen deficiency. No possible risk factor of venous thrombosis could be found in 24 patients (48%). In conclusion, malignancy and protein S deficiency were the most frequent acquired and congenital causes of venous thrombosis in the Chinese, respectively.

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“…(8) One possible explanation for the lower incidence of VTE seen among Chinese patients may be related to the prevalence of activated protein C resistance, which is extremely low in Chinese populations. (9) However, evidence of the prognostic value of cTnI in Chinese patients with PE is scarce. Therefore, this retrospective study was conducted to assess whether cTnI levels could predict clinical outcomes and complications in…”

Section: Introductionmentioning

confidence: 99%

Raised troponin I in Chinese patients with acute pulmonary embolism suggests complicated clinical course and may predict intensive care unit admission

Kwok²,

Tsui³

2013

SMedJ

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were recruited. Information, including demographic data, presenting symptoms and vital signs at presentation, predisposing factors for PE, results of diagnostic procedures and clinical outcomes, was collected from the medical records of these patients. CONClUSION Elevated cTnI level was associated with a complicated clinical course in patients with acute PE. We suggest that measurements of cTnI levels be used for the early risk stratification of patients with PE in the emergency departments of hospitals. RESUlTS

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Lack of Activated Protein C Resistance in Healthy Hong Kong Chinese Blood Donors - Correlation with Absence of Arg506-Gln Mutation of Factor V Gene

Cited by 44 publications

References 0 publications

Factor VLeiden

Factor VLeiden

Causes of venous thrombosis in fifty Chinese patients

Raised troponin I in Chinese patients with acute pulmonary embolism suggests complicated clinical course and may predict intensive care unit admission

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