HHcy is the result of increased production and/or decreased disposal of Hcy ( Figure 1). In third pathway, Hcy is metabolized to form cysteine via trans-sulphuration, sequentially catalyzed by vitamin B6-dependent enzymes cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE). In second pathway, Hcy is resynthesized into SAH through the reversal of SAH hydrolase activity. In the folate/vitamin B12‐dependent mechanism, folate in the form of 5‐methyl tetrahydrofolate, derived from 5,10‐methylene tetrahydrofolate reductase catalyzed tetrahydrofolate modification, donates a methyl group to Hcy catalyzed by the vitamin B12‐dependent enzyme methionine synthase to form methionine. In first pathway, approximately 50% of Hcy is re‐methylated to form methionine via two distinct mechanisms: folate/vitamin B12‐dependent re-methylation and folate/vitamin B12‐independent re‐methylation. The disposal of Hcy involves many pathways. Finally, SAH is rapidly metabolized by SAH hydrolase to adenosine and Hcy. SAM is converted into S-adenosyl-L-homocysteine (SAH) via a methyltransferase-catalyzed methyl transfer reaction, donating the methyl group to acceptor molecules (DNA, RNA, amino acids, proteins, phospholipids etc.). S-adenosyl-L-methionine (SAM) synthase catalyzes the reaction of methionine with ATP to form SAM. Hcy is produced in all human tissues through the transmethylation of methionine with three steps. Systemic folinate calcium, a folic acid derivative, and topical vitamin B12 have found to be effective in treating psoriasis. As the role of Hcy in the pathogenesis of psoriasis is most likely established, Hcy can be a potential therapeutic target for the treatment of psoriasis. Hydrogen sulfide (H 2S) may play a protective role in the pathogenesis of psoriasis and the deficiency of H 2S in psoriasis may be caused by HHcy. There may be a link between the oxidative stress state in psoriasis and the effect of HHcy. Hcy can induce nuclear factor kappa B activation, which is critical in the immunopathogenesis of psoriasis.

Moreover, Hcy can drive the immuno-inflammatory process by enhancing the production of the pro-inflammatory cytokines in related to psoriasis. Hcy may promote the immuno-inflammatory process in the pathogenesis of psoriasis by activating Th1 and Th17 cells and neutrophils, while suppressing regulatory T cells. Insufficiency of folic acid and vitamin B 12 can be a cause of HHcy in psoriasis. Recent studies have demonstrated that patients with psoriasis have a significantly higher serum homocysteine (Hcy) level and a higher prevalence of hyperhomocysteinaemia (HHcy).

Psoriasis is caused by a complex interplay among the immune system, genetic background, autoantigens, and environmental factors.

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