## Background: The pathogenesis of inflammatory bowel disease (ibd) involves the interaction between genetic susceptibility, mucosal immunity, and intestinal bacteria. bacterial translocation is a common event in these patients and plays an important role in the perpetuation of chronic intestinal i
Association of hyperhomocysteinemia and folate deficiency with colon tumors in patients with inflammatory bowel disease
β Scribed by Jean Marc Phelip; Veronique Ducros; Jean Luc Faucheron; Bernard Flourie; Xavier Roblin
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 104 KB
- Volume
- 14
- Category
- Article
- ISSN
- 1078-0998
No coin nor oath required. For personal study only.
β¦ Synopsis
Background:
Folate deficiency associated with hyperhomocysteinemia might increase the risk of developing colorectal cancer. the aim of this study was to evaluate factors associated with colonic carcinogenesis, in particular, folate and homocysteinemia levels, in a cross-sectional study of patients with inflammatory bowel disease (ibd).
Methods:
Ibd patients with carcinogenic lesions discovered during colonoscopy [dysplasia-associated lesion or masses (dalm), colorectal cancer] were included and compared with the whole population of ibd patients with a normal colonoscopy performed during the same period. the following parameters were collected at the time of colonoscopy: age, sex, type, duration, activity, and extent of the disease, treatment, smoking status, and vitamin b12, folate, and homocysteinemia levels. univariate and multivariate analyses were performed after adjusting for the main parameters.
Results:
One hundred and fourteen patients [41 with ulcerative colitis (uc), 73 with crohn's disease (cd)] were included. twenty-six carcinogenic lesions were isolated: 18 dalm (7 high-grade and 11 low-grade dysplasia) and 8 colorectal cancers. in univariate analysis, the factors associated with carcinogenesis were: active smoking (p = 0.03), folate level < 145 pmol/l (p = 0.02), hyperhomocysteinemia > 15 micromol/l (p = 0.003), duration of disease > 10 years (p = 0.006), and uc (p = 0.02). in multivariate analysis, patients with hyperhomocysteinemia associated with folate deficiency had 17 times as many carcinogenic lesions as patients with normal homocysteinemia whatever the folate status and duration of the disease (p = 0.01). patients with hyperhomocysteinemia without folate deficiency had 2.5 times as many carcinogenic lesions as patients with normal homocysteinemia (p = 0.08).
Conclusions:
Our data suggest that in ibd patients with normal homocysteinemia, the increase in carcinogenic risk is negligible. conversely, in patients with hyperhomocysteinemia, folate deficiency may be associated with increased colorectal carcinogenesis in ibd patients.
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