The role of hypercoagulability in ischemic colitis

Abstract

Objective. The aim of this study is to evaluate the role of thrombophilia-hypercoagulability in ischemic colitis (IC). Material and methods. Thrombophilia and fibrinogen were evaluated in 56 cases of IC and 44 controls with known predisposing factors but no evidence of IC. Thrombophilic factors tested were: protein C (PC), protein S, antithrombin (AT), resistance to activated protein C (APCR), lupus anticoagulant (LA), factor V G1691A mutation (FV Leiden), prothrombin G20210A mutation, methylenetetrahydrofolate reductase (MTHFR) gene C677T and A1298C mutations and plasminogen activator inhibitor-1 (PAI-1) gene 5G/4G and 4G/4G polymorphisms. Results. In IC group were recorded: i) low levels of PC and AT (p = 0.064 and p = 0.022, respectively); ii) low levels of APCR (normal: >2, p = 0.008); iii) high levels of fibrinogen (p = 0.0005); iv) higher number of homozygotes for MTHFR A1298C and C677T mutations (p = 0.061 and p = 0.525 (Pearson chi-square), respectively); v) greater prevalence of 5G/4G and 4G/4G polymorphisms (p = 0.031 (Pearson chi-square)) and vi) higher incidence of LA-positive individuals (p = 0.037, Fischer’s exact test). Multivariate analysis was performed to determine the effects of prothrombotic factors in IC. 5G/4G polymorphism of PAI-1 gene (odds ratio (OR) 12.29; 95% confidence interval (CI) 2.26–67.00), APCR (OR 0.089; 95% CI 0.011–0.699) and fibrinogen (OR 1.013; 95% CI 1.003–1.023) were determined as predictors of IC. Conclusions. This study suggests that hypercoagulability, hereditary or acquired, plays an essential role in the manifestation of IC.

Key Words:

• activated protein C resistance
• antithrombin III deficiency
• fibrinogen
• ischemic colitis
• protein C deficiency
• protein S deficiency
• thrombophilia

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.