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Hypercoagulable state in idiopathic ulcerative colitis: role of hyperhomocysteinemia and hyperfibrinogenemia
Vaibhav S Banait1, M S Sandeep, Shrimati Shetty
1Department of Gastroenterology, King Edward Memorial Hospital, Mumbai 400 012, India.
Insights
Vascular thrombosis is uncommon in ulcerative colitis (UC). Hyperhomocysteinemia, linked to folate levels, and hyperfibrinogenemia were observed and potentially reversible with folate supplementation.
Area of Science:
- Gastroenterology
- Hematology
- Genetics
Background:
- Previous studies on hypercoagulable factors in inflammatory bowel diseases (IBD) used heterogeneous patient groups and varied medication regimens.
- Understanding specific hypercoagulable factor prevalence in ulcerative colitis (UC) is crucial for risk assessment.
Purpose of the Study:
- To determine the frequency of thrombotic complications in UC patients.
- To evaluate for hyperhomocysteinemia, its relation to vitamin B12, folate levels, and MTHFR C677T mutation.
- To assess hyperfibrinogenemia and factor V Leiden mutation prevalence in UC.
Main Methods:
- Eighty-six adult UC patients were identified; 28 were included in the study after excluding those on medications affecting coagulation factors.
- Blood tests were performed at baseline and after 2 months of remission, with patients receiving folic acid supplementation.
- Evaluated parameters included homocysteine, vitamin B12, folate, MTHFR C677T genotype, fibrinogen, and factor V Leiden mutation.
Main Results:
- Vascular thrombotic events occurred in 4 patients during follow-up.
- Hyperhomocysteinemia was found in 39.3% of UC patients, significantly higher than controls (p=0.007).
- Hyperfibrinogenemia was detected in 3 patients, with no significant association with disease characteristics. Folate supplementation reduced homocysteine levels in affected patients.
Conclusions:
- Vascular thrombosis is infrequent in this UC cohort.
- Hyperhomocysteinemia, responsive to folate, and hyperfibrinogenemia were observed.
- The contribution of hyperhomocysteinemia, hyperfibrinogenemia, and factor V Leiden mutation to thrombosis in UC appears limited.
Background:
Previous reports on hypercoagulable factors in inflammatory bowel diseases involve heterogeneous populations and patients on various medications.
Aims:
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.
Conclusion:
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.
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