Hyperhomocysteinemia in cirrhosis is not a cardiovascular risk

ABSTRACT

The study aimed to evaluate and highlight the relationship between the serum Hcy concertrations in cirrhotic patients and some important risk factors for atherosclerotic cardiovascular disease, and to relate the findings with the severity of liver dysfunction. Subjects and A total of25 male patients with liver cirrhosis [mean age +/- SD= 38.16 +/- 9.89 years] and 10 age and sex matched healthy controle [mean age +/- SD= 34.80 +/- 8.53 years] were included in the study. Biochemical evaluation of serum Hcy, plasma PAI-1 antigen and vWF antigen levels. HOMA-IR as well as serum lipid pattern were performed for patients and controls. A significant increase in mean serum Hcy levels was found in cirrhotic patients compared to controls, [24.12 +/- 17.65 versus 11.62 +/- 2.67 micro mol/L; P=0.002], and the increase was directly related to the severity of liver disease [r=0.887; P=0.001]. The mean plasma levels of PAI-1 and vWF antigens levels were significantly higher in patients than controls [60.24 +/- 43.63 versus 29.50 +/- 9.33 ng/ml; P=0.002 and 4.67 +/- 0.92 versus 2.04 +/- 0.11 IU/ml; P<0.001 respectively] but did not correlate with other parameters. The fasting blood glucose, serum insulin and HOMA-IR were significantly elevated in cirrhotic patients compared to controls [5.29 +/- 1.34 versus 4.27 +/- 0.88 mmol/L; P=0.01, 15.09 +/- 9.59 versus 8.92 +/- 2.94 micro IU/ml; P=0.007 and 3.94 +/- 2.45 versus 1.71 +/- 0.65; P<0.001 respectively]. The serum lipids in patients revealed significant decrease in TC, TG, and HDL-C while the decrease was statistically nonsignificant in LDL-C in patients compared to controls [127.00 +/- 29.89 versus 174.73 +/- 19.00 mg/dl. 68.60 +/- 26.12 versus 101.30 +/- 9.49 mg/dl, 26.40 +/- 11.39 versus 68.41 +/- 3.43 mg/dl; P< 0.001 and 83.53 +/- 26.86 versus 86.06 +/- 18.99 mg/dl; P=0.756 respectively]. Conclusions: Patients with liver cirrhosis have elevted serum Hcy concentrations which correlated with the degree of liver disease. However, they are protected from the adverse effects of hyperhomocysteinemia on the cardiovascular system by many mechanisms; increased serum NO may be one of them. The possible role of hyperhomocysteinemia on liver fibrogenesis is proposed for further study in the future