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By A. Batorova

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2001). Somatic mosaicism in hemophilia A: a fairly common event. American Journal of Human Genetics. Vol. 69 (July 2001), pp. 75–87. ISSN 0002-9297/2001/6901-0009. S. (1998). Single-tube polymerase chain reaction for rapid diagnosis of the inversion hotspot of mutation in haemophilia A. Blood. Vol. 92. pp. 1458-1459. R. (2009). Clinical variability of haemophilia A and B in Mexican families by factor V Leiden G1691A, prothrombin G20210A and MTHFR C677T/A1298C. Haemophilia. Vol. 15. pp. 1342-1345.

Vol. 6. (January 2008). pp. 830-836. S. (1995). Recent human germ-line mutation: inferences from patients with hemophilia B. Trends in Genetics. Vol. 11, No. 4. (April 1995). pp. 141-147. J. (2002). Lack of expression of XIST from a small ring X chromosome containing the XIST locus in a girl with short stature, facial dysmorphism and developmental delay. European Journal of Human Genetics. Vol. 10. (November 2001). pp. 44-51. J. (2011). Detección de las inversiones de los intrones 1 y 22 por PCR inversa cambiante (IS-PCR) en pacientes con hemofilia A grave.

At the time it was only possible to rule out Factor VIII inversions with breakpoints within the repeated intron 22 unit so the nature of the mutation remained unknown. Since the patients were first cousins and came from an ethnic group with a long-standing tradition of consanguineous marriages, there was a high chance that the two patients also shared common polymorphisms in other genes that play a role in the risk of inhibitor development. It is possible that the one cousin developed antibodies to Factor VIII because of more frequent encounters with this protein than the other cousin but the reason why one had more severe phenotype than the other was not identified.

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