title: Prothrombotic inherited abnormalities other than factor V Leiden mutation do not play a role in venous thrombosis in inflammatory bowel disease.
abstract: OBJECTIVE
  Because the incidence of thromboembolism is increased in patients with inflammatory bowel disease, we attempted to assess the role of prothrombotic inherited coagulation abnormalities in the development of thrombosis.
  
  
  METHODS
  Four populations were compared: 15 patients with inflammatory bowel disease and a previous venous thrombosis, 58 control patients with inflammatory bowel disease but without thrombosis, 110 patients without inflammatory bowel disease but with previous deep venous thrombosis, and 84 healthy subjects. Inherited and acquired risk factors of venous thrombosis, e.g., factor V Leiden and prothrombin 20210A mutations, C677T methylenetetrahydrofolate reductase polymorphism, a polymorphism located in exon 13 of factor V gene, inflammatory and hypercoagulability markers were studied in each population.
  
  
  RESULTS
  In the study, 14.3% of thrombotic patients with inflammatory bowel disease had factor V Leiden mutation versus 0% of control patients with inflammatory bowel disease (p = 0.04), 15.5% of thrombotic patients without inflammatory bowel disease (NS) and 3.6% of the healthy controls. A total of 14% of thrombotic patients with inflammatory bowel disease and 11.8% of thrombotic patients without inflammatory bowel disease carried prothrombin 20210A mutation, compared to 1.7% of control patients with inflammatory bowel disease; however, the difference was just below significance. Other inherited coagulation abnormalities were not statistically significantly different among the four populations.
  
  
  CONCLUSIONS
  Our study confirms that factor V Leiden mutation increases the risk for thrombotic events but is not more frequent in patients with inflammatory bowel disease. Our results do not support the role of other thrombotic risk factors.
authors.affiliation: Hepatology and Gastroenterology Unit, Rouen University Hospital-Hospital Charles Nicolle, France.
authors.forename: C
authors.initials: C
authors.lastname: Guédon
authors.forename: V
authors.initials: V
authors.lastname: Le Cam-Duchez
authors.forename: O
authors.initials: O
authors.lastname: Lalaude
authors.forename: J F
authors.initials: JF
authors.lastname: Ménard
authors.forename: E
authors.initials: E
authors.lastname: Lerebours
authors.forename: J Y
authors.initials: JY
authors.lastname: Borg
mesh_terms: D000328:Adult; D000368:Aged; D005165:Factor V; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005787:Gene Frequency; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000097:blood / Q000235:genetics*; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D008875:Middle Aged; D009154:Mutation / Q000502:physiology; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000235:genetics; D017293:Protein S / Q000032:analysis; D011516:Prothrombin / Q000235:genetics; D012016:Reference Values; D020246:Venous Thrombosis / Q000235:genetics*
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D017293:Protein S; C095381:factor V Leiden; D005165:Factor V; D011516:Prothrombin; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2)