Homocysteine is a part of metabolic pathway changes and remethylation of methionine, the important source of methyl groups for all anabolic pathways of an organism. Hyperhomocysteinemia (HHC) is defined as increased plasma level of total homocysteine (tHcy) above reference level. Pathophysiologic effects of elevated Hcy are represented by direct injury of endothel, changes in oxidoregulation balance, oxidative stress, changes in antithrombogenic balance leading to increase of thrombogenic activity, and to increase in atherogenic activity. All those actions result in worsening of clinical and metabolic state of critically ill patient. In our pilot study we sought to detect HHC in critically ill patients, and to evaluate its value on monitoring and treatment outcome. In the set of ninety-eight patients, we found HHC in 32.58 per cent of cases. Mean level of homocysteine in non-survivors was 27.6 mmol/l; in survivors 10.9 mmol/l. Mortality rate was 68.97% in the group of patients with HHC; patients with normal level of homocyxteine had a mortality rate 46.67%. In three patients we revealed a gene mutation for methylenetetrahydrofolate reductase. Hereditary or acquired deficit of this gene is considered to be a cause of HHC. The results of the pilot study need to be confirmed on a larger patient group.

        Key words: homocysteine – hyperhomocysteinemia – critically ill patient