Assessment of thrombophilic abnormalities during the active state of inflammatory bowel disease

Abstract

Background/Aims:Thromboembolic disease has been recognized as a complication of inflammatory bowel disease (IBD). The relative contributions of inherited or acquired thrombophilia and the inflammatory response to the mechanism of this tendency are unclear. Thrombotic events are more common in active disease although significant numbers also occur spontaneously. The aim of this study was to investigate common thrombophilic markers in patients with active IBD.Methods:Twenty-six patients with IBD who had active disease, and 40 sex- and age-matched non-IBD patients were recruited into the study. For all the subjects, complete blood counts, C-reactive protein levels, erythrocyte sedimentation rate, International normalized ratio, activated partial thromboplastin time, and levels of lupus anticoagulant, anticardiolipin antibodies (ACA IgG), proteins C and S, antithrombin-III (AT-III), and factor V were measured.Results:The International normalized ratio, activated partial thromboplastin time, and levels of proteins C and S were comparable between the two groups. However, antithrombin-III levels were significantly lower in the IBD group as compared with that in the healthy control group (P < 0.001). ACA IgG was detected in one patient in the IBD group. Factor V Leiden mutation was present in 3.8% of the patients in the IBD group, whereas the prevalence was 2.5% in the control group. Significantly elevated platelet counts were observed in patients with active Crohn's disease compared with that in the control group (P < 0.001), but they were not significantly increased in active ulcerative colitis (P = 0.231).Conclusions:The present study failed to establish a strong association between the common thrombophilic markers and the active clinical course of IBD, with the exception of high platelet counts and lower levels of AT-III in the IBD group as compared with those in the control group. All other parameters of thrombophilia were comparable between the two groups.

Factor V Leiden and Inflammation

“…Numerous studies have been performed in an attempt to detect a relationship with the presence of FVL mutation and the incidence of IBD [ 86 ]. The majority of publications have not found a clear association between FVL and the risk of developing IBD, although FVL continues to be considered a risk factor which may influence the clinical manifestations during IBD [ 84 , 86 – 88 ]. Similarly, Liang et al [ 89 ] revealed that FVL mutation was not significantly associated with the risk of developing IBD.…”

Ulcerative colitis and thrombocytosis: Case report and literature review

“…[ 22 , 23 ] It has been reported that the increased risk of thromboembolism is related to the overexpression of CD40L in PLTs, which may be the only source of CD40L in IBD patients. [ 6 , 24 , 25 ] Patients hospitalized with IBD have a higher risk of VTE and VTE-related mortality compared with hospitalized patients without IBD. [ 26 ] Moderately to severely active UC is an important risk factor for VTE.…”

Factor V Leiden and inflammatory bowel disease: a systematic review and meta-analysis

“…The allele frequency of Factor V Leiden mutation was reported to be 4.4% in Europeans and 0.6% in Asia, and was not reported in Africa [45]. Taking into account the differences of races, data from all European countries were further analyzed, excluding two studies from North America [13,33] and one from Egypt [35]. No significant heterogeneity was found in the results of the remaining 16 studies (I 2 = 29.3%, P = 0.13).…”

“…Some studies then suggested the frequency of Factor V Leiden mutation was higher in IBD patients than that in controls, or higher in IBD patients with thrombosis than in those without [13][14][15][16][17][18][19][20][21]. However, some studies found no association between Factor V Leiden mutation and IBD risk [22][23][24][25][26][27][28][29][30][31][32][33][34][35]. One study showed that the mutation was less frequent in thrombotic IBD patients than in thrombotic non-IBD patients [36].…”