Coeliac disease is a typical example of a malabsorption syndrome conferring increased risk for various deficiency states, including folate and vitamin B12. Hyperhomocysteinemia is significantly more frequent in patients with newly diagnosed coeliac disease than healthy controls.
A research team led by Dr. Muhammed Hadithi from Netherlands investigated the effect of vitamin B6, folate, and vitamin B12 daily supplements on homocysteine levels in patients with coeliac disease.
In the study, vitamin B6, folate, vitamin B12, and fasting plasma homocysteine levels were investigated in 51 consecutive adults with coeliac disease and 50 healthy control individuals matched for age and sex.
They found that patients with celiac disease and using vitamin supplements had higher serum vitamin B6 (P = 0.003), folate (P < 0.001), and vitamin B12 (P = 0.012) levels than patients who did not or healthy controls (P = 0.035, P < 0.001, P = 0.007, for vitamin B6, folate, and vitamin B12, respectively). Lower plasma homocysteine levels were found in patients using vitamin supplements than in patients who did not (P = 0.001) or healthy controls (P = 0.003). However, vitamin B6 and folate, not vitamin B12, were significantly and independently associated with homocysteine levels. Twenty-four (48%) of 50 controls and 23 (50%) of 46 patients with celiac disease carried the MTHFR thermolabile variant T-allele (P = 0.89).
They concluded that Homocysteine levels are dependent on Marsh classification and the regular use of B-vitamin supplements is effective in reduction of homocysteine levels in patients with celiac disease.
The study demonstrates in agreement with earlier findings, that both the presence and the severity of coeliac disease were determinants of homocysteine levels. The regular use of B vitamin supplements was associated with higher serum vitamin B6, folate, and vitamin B12 and lower plasma homocysteine levels in patients with coeliac disease. Furthermore, B vitamin supplements seem to have a protective role against the effect of villous atrophy on homocysteine levels, irrespective to the genetic susceptibility status as manifested by carrying the C677T polymorphism of 5,10-methylenetetrahydrofolate reductase.
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