scholarly journals Activated Protein C Resistance and Factor V Leiden in Mexico

2007 ◽  
Vol 14 (4) ◽  
pp. 428-437 ◽  
Author(s):  
Abraham Majluf-Cruz ◽  
Manuel Moreno-Hernández ◽  
Adriana Ruiz-de-Chávez-Ochoa ◽  
Rosario Monroy-García ◽  
Karim Majluf-Cruz ◽  
...  

A common cause of hereditary thrombophilia is activated protein C resistance (APCR), and most cases result from factor V Leiden mutation. An APCR phenotype without association with factor V Leiden has been described. This transversal, observational, nonrandomized study evaluated these 2 phenomena in healthy indigenous and mestizo Mexican subjects (n = 4345), including 600 Mexican natives. No indigenous subjects had APCR, but 82 mestizo subjects did. After retesting, 50 subjects had a negative test. The remaining 32 subjects had factor V Leiden, giving a 0.85% prevalence of factor V Leiden in the mestizo Mexican population. Only 31% of APCR carriers had factor V Leiden. These results show a very low prevalence of APCR and factor V Leiden in Mexico. Except for factor V Leiden, there are no other mutations in the factor V gene responsible for the APCR phenotype. Acquired APCR is nearly twice as prevalent as the inherited variant.

1998 ◽  
Vol 80 (08) ◽  
pp. 344-345 ◽  
Author(s):  
Pasra Arnutti ◽  
Motofumi Hiyoshi ◽  
Wichai Prayoonwiwat ◽  
Oytip Nathalang ◽  
Chamaiporn Suwanasophon ◽  
...  

1994 ◽  
Vol 88 (1) ◽  
pp. 219-222 ◽  
Author(s):  
Nicholas J. Beauchamp ◽  
Martina E. Daly ◽  
K. K. Hampton ◽  
Peter C. Cooper ◽  
F. Eric Preston ◽  
...  

2018 ◽  
Vol 3 (3) ◽  

This case was presented due to development of DVT and pulmonary embolism after VZV infection and determination of Factor V Leiden mutation and activated protein C resistance. A 19-year old male patient presented with fever at the 10th day of varicella zoster virus (VZV) infection, and pruritic vesicopustular skin lesions and increased leukocyte and CRP levels. Acyclovir and ampicillin-sulbactam therapy were started. On the fourth day of hospitalization, left leg DVT and pulmonary embolism developed. Anticoagulant therapy was started. Tests revealed activated protein C resistance and Factor V Leiden mutation. The patient was discharged after the relief of symptoms with anticoagulant therapy. Thrombosis rarely develops in the course of VZV infection. It is essential to investigate the factors contributing to predisposition to thrombosis in patients with thrombosis.


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