1591 Letters to the Editor Dear Sir, Factor V Leiden has a presumed lifelong prothrombotic tendency with 5- to 10-fold risk for heterozygotes and 80-fold for homozygotes (1). It occurs with high prevalence in the western world, highest among Greeks (2, 3). Paucity of reports on prevalence of FVL in the Indian population prompted us to undertake the present study. We studied a cohort of 1118 subjects of which 578 belonged to different caste and tribal groups, and 540 cases of thromboembolic disorders from India. Routine screening was normal. FVL was identified by amplification of factor V gene, Mnl I digestion (Roche Biomedicals, Germany) (4) and then 10% PAGE. Table 1 gives the prevalence of FVL in India. Only 2 samples out of 157 tribals showed presence of FVL in heterozygous state (1.27%). None of the 59 subjects belonging to Oraon tribe from Madhya Pradesh showed FVL. The incidence in the general caste group was 2.39%. Surprisingly, 2 non-tribal groups: Vatalia Prajapatis (10.25%) and Parsis (10.57%) showed very high incidence. Fifteen-year-old Parsi male showed FVL homozygosity but no history of thrombotic event till that time. In our patients series we have found the frequency of FVL similar to that in the control group (Table 1). Only 3.39% of the patients with DVT showed FVL heterozygosity as against 20-40% of them reported to carry this genetic defect in western population (1). The other striking feature of our study is very high incidence (21%) in Budd-Chiari cases. The association of FVL with BCS has been reported by us and others (5, 6). One billion Indian population includes 450 tribes (little less than 10%). Tribals are aboriginal, isolated in the interiors and hilly regions of India. They are genetically different from non-tribals. Some extremely primitive strains have Negrito element. The main stream population is divided into various subgroups called “caste”. They are a mixture of several races like Caucasoid, Mongoloid and Proto-Austral- oid over thousand of years. Our study included Parsis, a population migrated from Iran at the end of 7th century (7). The other population of Vatalia Prajapatis is from western India. Both these groups are highly endogamous and showed very high incidence of FVL (Table 1). It could be due to a founder effect. The Great Andamanese of Andaman and Nicobar islands is the smallest tribal community with a strength of only 35. It is an endangered tribe of Negrito race. Till recently, they were a typical hunting and food gathering tribe leading a seminomadic existence. The tribals studied from western Indian region (Table 1) were once hunters, fishermen and food gatherers but later acquired primitive cultivation. FVL was found in both these tribal groups. Thus, FVL was found in primitive, nomadic tribes and different non-tribal groups in Indian population. The limited racial and geographical distribution of FVL earlier suggested a single origin of the mutation possibly in the original Europeans or the migrating Neolithic farmers (8). During the neolithic age, starting 10,000 years ago, farming emerged from the Middle East spread towards the northwest of Europe. Also, mitochondrial DNA analysis suggested that many of the original Europeans survived, possibly with some Middle Eastern admixture (9). The haplotype study suggested a single origin in Indo-Europeans (10). A common origin of the mutation was shown in Ashkenazi Jews and Iraqi and Moroccan Ar- abs (11). The FVL distribution has been attributed to its spread by the neolithic migration of farmers from the Middle East (11). The people of Indian subcontinent seem to have had gene exchange with Iranian population (7). It was also suggested that the invading armies of Alexander the Great spread the mutation throughout Europe and North India (8). In conclusion, our data suggests that origin of FVL solely in proto-Europeans is unlikely since the mutation is detected in isolated, primitive tribals of Andaman and Nicobar islands in India who are believed to have Negrito element. Acknowledgements We are grateful to Hematology unit, K. E. M. Hospital for their support towards access to the patients studied here. We thank Dr. Roshan Colah, Shankarkumar U., Dr. Mukherjee M. for providing samples of Parsis, Oraons, Vatalia Prajapatis and Great Andamanese. We also thank Dr. A. C. Goraksha- kar for his valid suggestions in anthropological point of view. A. R. Pawar, Shrimati Shetty, K. Ghosh, Dipika Mohanty Institute of Immunohaematology, New Multistoreyed Building, K. E. M. Hospital Campus, Mumbai, India How Old Is Factor V Leiden Mutation? Thromb Haemost 2001; 86: 1591 – 2 Correspondence to: Dr. (Miss) Dipika Mohanty, Director, Institute of Im- munohaematology, 13 th Floor, New Multistoreyed Building, K. E. M. Hospital Campus, Mumbai, 400 012, India – Phone: 91-22-4 13 85 18-19; Fax: 91-22- 4 13 85 21; E-mail: mohanty@bom5.vsnl.net.in Table 1 The prevalence % [n] of FVL in India Downloaded by: University of Nottingham. Copyrighted material.