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.
Abstract

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