BACKGROUND/AIM: Homocysteine (2-amino-4-mercaptobutyric acid) is an amino acid that may be found in small quantities in all cells, and is quantitatively the major methionine metabolite. The most prevalent form is protein-bound homocysteine (about 80%), mostly to albumins. If catabolism of homocysteine is impaired either due to enzyme defect or deficiency of required intracellular cofactors, homocysteine accumulates in cells and reaches the circulation. The aim of our study was to determine homocysteine values and factors affecting homocysteine metabolism in patients with liver cirrhosis. METHODS: The prospective study included 35 patients with liver cirrhosis and 30 age and sex matched healthy controls. All the examinations were based on: medical history, physical examination, laboratory tests including serum homocysteine levels and liver biopsy. The degree of liver failure was assessed according to the Child-Pugh classification. RESULTS: The mean plasma homocysteine levels were much higher in the patients with liver cirrhosis than in the healthy controls (t-test, p < 0.001). There was no significant difference between the plasma homocysteine concentration and etiology of liver cirrhosis (ANOVA, p > 0.05). Correlation analysis showed a positive correlation between the homocysteine and creatinine concentrations and between the serum albumin and homocysteine values, (Pearson's correlation, p < 0.01, and p < 0.05 respectively). CONCLUSION: In liver cirrhosis, the genesis of homocysteinemia is multifactorial, influenced significantly by impaired catabolic liver function, renal failure and hypoalbuminemia.
BACKGROUND/AIM: Homocysteine (2-amino-4-mercaptobutyric acid) is an amino acid that may be found in small quantities in all cells, and is quantitatively the major methionine metabolite. The most prevalent form is protein-bound homocysteine (about 80%), mostly to albumins. If catabolism of homocysteine is impaired either due to enzyme defect or deficiency of required intracellular cofactors, homocysteine accumulates in cells and reaches the circulation. The aim of our study was to determine homocysteine values and factors affecting homocysteine metabolism in patients with liver cirrhosis. METHODS: The prospective study included 35 patients with liver cirrhosis and 30 age and sex matched healthy controls. All the examinations were based on: medical history, physical examination, laboratory tests including serum homocysteine levels and liver biopsy. The degree of liver failure was assessed according to the Child-Pugh classification. RESULTS: The mean plasma homocysteine levels were much higher in the patients with liver cirrhosis than in the healthy controls (t-test, p < 0.001). There was no significant difference between the plasma homocysteine concentration and etiology of liver cirrhosis (ANOVA, p > 0.05). Correlation analysis showed a positive correlation between the homocysteine and creatinine concentrations and between the serum albumin and homocysteine values, (Pearson's correlation, p < 0.01, and p < 0.05 respectively). CONCLUSION: In liver cirrhosis, the genesis of homocysteinemia is multifactorial, influenced significantly by impaired catabolic liver function, renal failure and hypoalbuminemia.