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Meta‐analysis: hyperhomocysteinaemia in inflammatory bowel diseases
Author(s) -
Oussalah A.,
Guéant JL.,
PeyrinBiroulet L.
Publication year - 2011
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1111/j.1365-2036.2011.04864.x
Subject(s) - medicine , homocysteine , odds ratio , inflammatory bowel disease , gastroenterology , ulcerative colitis , methylenetetrahydrofolate reductase , hyperhomocysteinemia , disease , genotype , biochemistry , chemistry , gene
Aliment Pharmacol Ther 2011; 34: 1173–1184 Summary Background The magnitude of association between homocysteine metabolism and inflammatory bowel diseases (IBD) remains unknown, whereas the association between hyperhomocysteinaemia and thrombosis remains controversial in IBD. Aim To conduct a systematic review and meta‐analysis to examine these issues. Methods The literature search was conducted using MEDLINE database and international conference abstracts from January 1966 to April 2011 and included all studies that evaluated plasma homocysteine level in IBD. Results Twenty‐eight studies evaluated the plasma homocysteine level and/or hyperhomocysteinaemia risk in IBD patients. Five studies assessed the association of hyperhomocysteinaemia with thrombosis. The mean plasma homocysteine level was significantly higher in IBD patients when compared with controls (weighted mean difference (WMD) = 3.75 μmol/L; 95% CI, 2.23–5.26 μmol/L; P < 0.0001; reference ranges for plasma homocysteine level: 5–12 μmol/L). The mean plasma homocysteine level did not differ between ulcerative colitis (UC) and Crohn’s disease (CD) (WMD = 0.41 μmol/L; 95% CI, −2.45 to 3.06 μmol/L; P = 0.76). The risk of hyperhomocysteinaemia was significantly higher in IBD patients when compared with controls [odds ratio (OR) = 4.65; 95% CI, 3.04–7.09; P < 0.0001]. The risk of hyperhomocysteinaemia was not higher among IBD patients who experienced thromboembolic complications (OR = 1.97; 95% CI, 0.83–4.67; P = 0.12). Plasma folate level was inversely correlated with IBD risk associated with MTHFR C677T polymorphism ( P = 0.006). Conclusions The risk of hyperhomocysteinaemia is significantly higher in IBD patients when compared with controls. The risk assessment of hyperhomocysteinaemia–related thrombosis in IBD requires further investigation. Deficient folate status is associated with a higher impact of MTHFR C677T polymorphism on IBD risk.