Abstract—A range of foreign studies have shown that, in schizophrenia, hyperhomocysteinemia occurs more frequently than in the general population. Hyperhomocysteinemia may be an integrated marker of folate metabolism disorders (as a result of vitamin deficiency and/or genetic predisposition) or involved in the pathogenesis of the disease through several possible molecular mechanisms. In Russia, similar studies have not been conducted. In addition, there are conflicting results of studies on genetic factors involved in folate and homocysteine metabolism in schizophrenia. The aim of this study was to evaluate an association of serum homocysteine, folate, and cobalamin levels with schizophrenia in the Central part of Russia (Nizhny Novgorod region). For this purpose, 50 patients with schizophrenia and 36 healthy volunteers were randomly selected. The levels of homocysteine, folates and cobalamin (B12) were measured in blood serum. The concentration of homocysteine was measured using the Сobas analyzer (Roche Diagnostics) with an enzymatic assay. The content of folate and vitamin B12 was determined by chemiluminescent microparticle immunoassay (Architect, Abbott lab. S.A). It was found that the level of homocysteine was significantly higher in the patients than in the control group (p = 0.0041), and folate levels were significantly lower (p = 0.0072). The level of homocysteine in the patients had a weak negative statistically significant correlation with both folate level (ρ = –0.38; p = 0.0063) and with B12 level (ρ = –0.36; p = 0.0082). Homocysteine level was significantly higher in men than in women in the entire studied population (Z = –2.1068, p = 0.0351), as well as in subgroups of patients (Z = –2.11; p = 0.035) and healthy controls (z = 3.4; p = 0.00067). The data suggest the need for further investigation of hyperhomocysteinemia and other biochemical markers of folate metabolism disorders in schizophrenia in the Russian population and the development of ways to correct them to optimize the treatment of this mental disorder.

摘要—大量国外研究表明，在精神分裂症中，高同型半胱氨酸血症的发生率比普通人群高。高同型半胱氨酸血症可能是叶酸代谢紊乱的综合标志物（由于缺乏维生素和/或遗传易感性）或通过多种可能的分子机制参与了疾病的发病机制。在俄罗斯，尚未进行类似的研究。此外，关于精神分裂症中叶酸和同型半胱氨酸代谢的遗传因素的研究结果相矛盾。这项研究的目的是评估俄罗斯中部（下诺夫哥罗德地区）的血清高半胱氨酸，叶酸和钴胺素水平与精神分裂症的相关性。为此，随机选择了50名精神分裂症患者和36名健康志愿者。在血清中测量同型半胱氨酸，叶酸和钴胺素（B12）的水平。使用Сobas分析仪（Roche Diagnostics）通过酶法测定高半胱氨酸的浓度。叶酸和维生素B12的含量通过化学发光微粒免疫分析法（Architect，Abbott实验室，SA）确定。结果发现，患者的同型半胱氨酸水平明显高于对照组（p = 0.0041），而叶酸水平显着降低（p = 0.0072）。患者的同型半胱氨酸水平与叶酸水平（ρ= –0.38; p = 0.0063）和B12水平（ρ= –0.36; p = 0.0082）均具有弱的负统计学意义。在整个研究人群中，同型半胱氨酸水平显着高于女性（Z = –2.1068，p = 0.0351），以及患者亚组（Z = –2.11；p = 0.035）和健康对照组（z = 3.4） ；p= 0.00067）。数据表明有必要进一步调查俄罗斯人群精神分裂症中的高同型半胱氨酸血症和叶酸代谢异常的其他生化指标，并开发纠正这些异常的方法以优化对这种精神障碍的治疗。