Key result
Thrombophilic gene mutations (heterozygous factor V Leiden and homozygous MTHFR C677T) were identified as a potential cause of recurrent free functional muscle transfer failure due to thrombosis.
Case Report (n=1)
This case report suggests that underlying thrombophilic gene mutations may be a risk factor for free functional muscle transfer failure due to thrombosis.
The evolution of microsurgery popularized the free functioning muscle transfers as secondary procedures to reanimate paralyzed extremities after severance of the brachial plexus, especially when the surgeon deals with late cases. Studies considering transplantation, describe thrombophilic factors as a cause of severe complications after transplantation, such as acute or early rejection episodes, delayed graft function, or chronic graft dysfunction. It is the first time that thrombophilia associated with free muscle-graft rejection is reported. A young man who had two free functional muscle transfers for brachial plexus reconstruction in the same forearm within an interval of 6 months. The free functional muscle transfer was failed in both cases because of vein thrombosis and subsequent arterial clot. The possibility of thrombophilia was investigated and during the genetic investigation it was discovered that he was heterozygous for the mutations of factor V, G1691A-Leiden, A4070G and homozygous for the MTHFR C677T mutation.
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Vekris et al. (2007) conducted a case report in Brachial plexus reconstruction / Free functional muscle transfer failure (n=1). Thrombophilic gene mutations (factor V Leiden, A4070G, MTHFR C677T) was evaluated on Free functional muscle transfer failure due to vein thrombosis and subsequent arterial clot. Thrombophilic gene mutations (heterozygous factor V Leiden and homozygous MTHFR C677T) were identified as a potential cause of recurrent free functional muscle transfer failure due to thrombosis.
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