title: Hypercoagulable state in idiopathic ulcerative colitis: role of hyperhomocysteinemia and hyperfibrinogenemia.
abstract: BACKGROUND
  Previous reports on hypercoagulable factors in inflammatory bowel diseases involve heterogeneous populations and patients on various medications.
  
  
  OBJECTIVE
  To determine the frequency of thrombotic complications in ulcerative colitis (UC); to evaluate for hyperhomocysteinemia and its relationship to vitamin B12 and folate levels and methylene tetrahydrofolate reductase (MTHFR) mutation; and to evaluate for hyperfibrinogenemia and factor V Leiden mutation.
  
  
  METHODS
  Eighty-six adult patients with UC were seen during the study period; 28 of them underwent blood tests and constituted the study population. Patients who received medications that affect these factors were among the 58 excluded. Tests were obtained at baseline and after 2 months during remission. Patients received folic acid in addition to treatment for UC.
  
  
  RESULTS
  Vascular thrombotic events were noted in 4 patients during follow up. Hyperhomocysteinemia was detected in 11 (39.3%) patients (controls 15/100, p=0.007). Heterozygous state for MTHFR C677T mutation was found in 5 (17.9%) patients (controls: 0.2% homozygous, 13.6% heterozygous, p>0.05). Plasma homocysteine did not correlate with extent, severity or duration of disease, or with MTHFR C677T heterozygous state, but correlated with serum folic acid level (p=0.003) and BMI (p=0.03). With folate supplementation, homocysteine decreased significantly in patients who had hyperhomocysteinemia at baseline. Hyperfibrinogenemia was detected in 3 patients (none in 100 controls). Plasma fibrinogen was not affected by duration, extent or severity of UC and did not decrease with remission of disease. Only one patient had heterozygous factor V Leiden mutation.
  
  
  CONCLUSIONS
  Vascular thrombosis occurred in less than a fifth of the UC population studied. Hyperhomocysteinemia reversible by folate supplementation and hyperfibrinogenemia were observed, but their contribution and that of factor V Leiden mutation appear to be insignificant.
authors.affiliation: Department of Gastroenterology, King Edward Memorial Hospital, Mumbai 400 012, India.
authors.forename: Vaibhav S
authors.initials: VS
authors.lastname: Banait
authors.forename: M S
authors.initials: MS
authors.lastname: Sandeep
authors.forename: Shrimati
authors.initials: S
authors.lastname: Shetty
authors.forename: Mukta R
authors.initials: MR
authors.lastname: Bapat
authors.forename: Pravin M
authors.initials: PM
authors.lastname: Rathi
authors.forename: Kanjaksha
authors.initials: K
authors.lastname: Ghosh
authors.forename: Dipika
authors.initials: D
authors.lastname: Mohanty
authors.forename: Philip
authors.initials: P
authors.lastname: Abraham
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D003093:Colitis, Ulcerative / Q000150:complications* / Q000235:genetics / Q000378:metabolism*; D005165:Factor V / Q000235:genetics; D005260:Female; D005340:Fibrinogen / Q000378:metabolism*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000453:epidemiology*; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D008875:Middle Aged; D009154:Mutation; D019851:Thrombophilia / Q000453:epidemiology*
chemical_list: C095381:factor V Leiden; D005165:Factor V; D005340:Fibrinogen; D042965:Methylenetetrahydrofolate Reductase (NADPH2)