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A severe haemophiliac patient with acute coronary syndrome admitted to cardiac rehabilitation

subjects prior to the collection of blood samples. The allele frequencies, observed heterozygosity frequencies, are shown in Table 1. It was observed that BclI and HindIII are in strong linkage disequilibrium and this has also been reported earlier by other authors [4]. The combination of Hind III and BclI alone showed 48.6% (18/37) informativity in unrelated Nepali subjects. The exon 14 BslI marker has shown 40.5% in the 37 females analysed and this marker is also in linkage disequilibrium with the remaining two markers. Only two females were informative exclusively with BslI marker. The cumulative heterozygosity of BclI, HindIII and BslI was 54%. In the f9 gene, the MseI polymorphism showed 0% heterozygosity, whereas DdeI and HhaI showed 15% and 41% respectively with a cumulative heterozygosity of 53%. Thus, in conclusion, Nepali population shows considerable deviation from most of the other populations as far as the heterozygosity of some of the markers in f8 and f9 genes is concerned. Based on the present study, an algorithm may be drawn as follows: BclI, HindIII and BslI sequentially in haemophilia A families, and in case of haemophilia B, HhaI and DdeI markers should be used, while MseI marker may not be used in Nepali population. Other RFLP markers like VNTR at intron 7, intron 13 and intron 22 need to be studied to look for the cumulative heterozygosity and to draw a cost-effective algorithm for indirect RFLP-based genetic diagnosis in affected families.