Association between serum aspartate transaminase and homocysteine levels in hemodialysis patients.
BACKGROUND
Hyperhomocysteinemia is a common metabolic abnormality in patients undergoing hemodialysis (HD). An impairment of remethylation of homocysteine (Hcy) is seen in these patients but cannot account completely for hyperhomocysteinemia. Homocysteine is derived from transmethylation of methionine that can be metabolized through transamination pathway alternatively. However, the significance of transamination in the metabolism of Hcy in HD patients is not studied.


METHODS
A total of 145 patients undergoing HD for more than 3 months were enrolled in the study. Vitamins B were not prescribed routinely to these patients. Among them, 49 patients had positive test results for hepatitis B surface antigen or antihepatitis C virus antibody. Serum Hcy, folic acid, vitamin B12, pyridoxal 5' -phosphate, methionine, and transaminase were measured, and parameters of dialysis adequacy were calculated. Multiple linear regression model was used to analyze the factors determining Hcy levels.


RESULTS
All patients had higher Hcy levels (40.3 +/- 28.3 micromol/L) than the upper limit of reference range 15 micromole/L. The levels of vitamin B(12) were all higher than 160 pg/mL (118 pmol/L). Only 9 patients had serum folic acid lower than 3 ng/mL (6.8 nmol/L). The predialysis Hcy levels were correlated with age, HD duration, folic acid, vitamin B12, and aspartate transaminase (AST) levels among all patients or the subgroup of hepatitis noncarriers with linear multiple regression analysis. In hepatitis carriers, AST levels were not associated with Hcy. A cutoff value of AST less than 14 U/L predicted a predialysis Hcy level higher than 27 micromol/L in noncarriers, with a sensitivity of 83.9% and a specificity of 50.2%.


CONCLUSIONS
In addition to vitamin B12 and folic acid, the serum AST levels correlated inversely with predialytic Hcy levels independently in hepatitis noncarrier HD patients. The results suggest that transamination may play an important role in the development of hyperhomocysteinemia when impaired transmethylation is encountered in uremic patients.
Huang
Jenq-Wen
JW
Department of Internal Medicine, National Taiwan University Hospital and Far Eastern Memorial Hospital, Taipei, Taiwan.
Yen
Chung-Jen
CJ
Pai
Mei-Fen
MF
Wu
Kwan-Dun
KD
Tsai
Tun-Jun
TJ
Hsieh
Bor-Shen
BS
D001219:Aspartate Aminotransferases / Q000097:blood* / Q000502:physiology; D005260:Female; D005492:Folic Acid / Q000097:blood; D005544:Forecasting; D006510:Hepatitis B Antibodies / Q000097:blood; D006511:Hepatitis B Antigens / Q000097:blood; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood / Q000209:etiology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000009:adverse effects / Q000379:methods*; D014511:Uremia / Q000097:blood / Q000209:etiology; D014803:Vitamin B Complex / Q000097:blood
D006510:Hepatitis B Antibodies; D006511:Hepatitis B Antigens; D006710:Homocysteine; D014803:Vitamin B Complex; D005492:Folic Acid; D001219:Aspartate Aminotransferases