Relationship Between Vitamin B12, Homocysteine and Oxidative Stress in Juvenile Idiopathic Arthritis

Abstract

Juvenile idiopathic arthritis (JIA), which is one of the rheumatic diseases, is a systemic inflammatory disease characterized by chronic and erosive synovitis that involves peripheral joints. In patients who had been diagnosed with JIA, increasing proinflammatory cytokines, metabolic abnormalities associated with systemic inflammation, may provoke vascular endothelial damage which can cause atherosclerosis.

Homocysteine is another metabolite among the factors causing endothelial dysfunction. Homocysteine is an intermediate metabolite which is formed during the conversion of methionine to cysteine and high levels of homocysteine in blood can lead to vascular damage. Dietary folate and vitamin B12 deficiency can cause an increase in blood homocysteine levels. Vitamin B12 is essential for the transfer of methyl group and cell division in humans, but it is also important for the proliferation, maturation and regeneration of the nerve cells. In addition, "functional vitamin B12 deficiency" in which blood vitamin B12 level is in the normal range and without severe clinical symptoms like anemia has also been reported. Studies have showed that vitamin B12 deficiency can lead to oxidative stress without causing significant increase in homocysteine levels by its effects on cytokines, growth factors, nitric oxide metabolism, antioxidant enzymes and producing reactive oxygen species.