Serum fetuin-A in metabolic and inflammatory pathways in patients with myocardial infarction


Krisztián Vörös M.D., Semmelweis University, Department of Family Medicine, Kútvölgyi út 4., Budapest H-1125, Hungary. Tel.: +36 1 355 8530; fax: +36 1 214 0841; e-mail:


Eur J Clin Invest 2011; 41 (7): 703–709


Background  Although multifunctional glycoprotein α2HS-glycoprotein/human fetuin-A (AHSG) is involved in atherosclerosis, it is not clear whether high or low concentrations are more important. We studied the correlation of serum AHSG with adiponectin, leptin, resistin, C-reactive protein (CRP) and tumour necrosis factor-α (TNF-α) to see whether its metabolic effects or its involvement in subclinical inflammation are dominant in patients with established coronary disease.

Materials and methods  In this cross-sectional study, AHSG concentration was determined in sera of 171 patients (age: 62 ± 6 years, mean ± SD) with previous myocardial STEMI infarction and normal renal function and 81 age-matched healthy controls by radial immunodiffusion.

Results  Patients had increased AHSG levels (673 ± 103 vs. 619 ± 96 mg L−1, < 0·001) compared to controls. Obese and diabetic patients had higher AHSG concentration than those with normal BMI or without diabetes but even the latter group had elevated AHSG levels (667 ± 101 mg L−1, n = 88) compared to controls (P = 0·002). Serum AHSG correlated negatively with adiponectin (r = −0·236, P = 0·006) even after adjusting for BMI (r = −0·177, P = 0·043). AHSG determined adiponectin levels independently from BMI, age and other adipocytokines (P = 0·014). The correlation between leptin and AHSG (r = 0·321, P = 0·021) weakened following adjustment for BMI (r = 0·209, P = 0·072). Serum AHSG did not correlate significantly with CRP, resistin and TNF-α concentrations. BMI and resistin but not AHSG determined TNF-α levels independently.

Conclusions  AHSG is elevated in sera of patients with previous myocardial infarction. Association with adipokines favours the concept that AHSG is involved in atherosclerosis more likely through metabolic pathways (insulin resistance, obesity and adipocyte dysfunction) than by inflammation in patients with post-myocardial infarction.