THROMBOPHILIA AND INFLAMMATORY BOWEL-DISEASE - DOES FACTOR-V MUTATIONHAVE A ROLE

Background An increased tendency for thromboembolism is a well known p roblem of inflammatory bowel disease (IBD). Microvascular thrombosis h as also been claimed as a pathogenic factor in IBD. Recently a point m utation in the gene coding factor V (FV Leiden) has been identified in various thromboembolic diseases, but the role in IBD is unknown. Obje ctive To determine the frequency of FV Leiden in IBD patients and comp are with a group of controls. Methods Sixty-three IBD patients [43 ulc erative colitis (UC) patients and 20 Crohn's disease (CD) patients] an d 36 healthy controls were included in the study. Only one of the UC p atients had a history of cerebral thromboembolism. The extracted DNA f rom frozen blood was subjected to polymerase chain reaction for the am plification of FV gene. The amplicons were hybridized both with the mu tant and wild-type probes to detect FV mutation. Readings of optical d ensity above 0.3 were considered as positive results. According to the patterns of ELISA, heterozygosity and homozygosity for normal and mut ant alleles were determined. Results Eight (18%) of UC patients were h eterozygous normal and one (2%) patient had homozygous mutation. Eight (45%) of the 20 CD patients had a heterozygous pattern and one (5%) h ad a homozygous pattern. In the control group four (11%) subjects show ed a heterozygous genotype. FV Leiden was found to be statistically mo re frequent in CD patients (P < 0.005) (odds ratio 6.5, 95% confidence interval 1.3-18.), but not in the UC patients as compared with contro ls (P > 0.05). There was no significant correlation between FV Leiden presence and disease activity, gender or disease duration for both UC and CD. Conclusion The results suggest that FV Leiden is more frequent in CD patients, but not in the UC patients as compared with controls. The high rate of factor V mutation in our CD patients suggests the ne ed for further studies to confirm a relationship between this mutation and aetiology of the disease. fur J Gastroenterol Hepatol 10:827-829 (C) 1998 Lippincott Williams & Wilkins.