Anti-AHSG monoclonal antibody, clone 308543 [Biotin]

Background Although multifunctional glycoprotein alpha 2HS-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-a (TNF-alpha) 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, P < 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-alpha concentrations. BMI and resistin but not AHSG determined TNF-alpha 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.

OBJECTIVES To evaluate the association of fetuin-A polymorphisms with calcium oxalate nephrolithiasis. Fetuin-A is a circulating calcium-regulatory glycoprotein that inhibits extraosseous calcification. METHODS Fetuin-A c. 742C > T and c. 766C > G polymorphisms were investigated in 103 patients with calcium oxalate nephrolithiasis and 73 age- and gender-matched healthy volunteers, using polymerase chain reaction-restriction fragment length polymorphism techniques. Additionally, we compared serum fetuin-A levels in the 2 groups. RESULTS A statistically significant difference was observed between the control and patient groups (chi(2) test, P = .003) for the genotype of fetuin-A c. 766C > G polymorphism. The odds ratio (95% confidence interval) for the CG genotype in those at risk of stone disease was 4.2 (1.73-10.28). The frequency distribution for fetuin-A c. 742C > T polymorphism was not statistically different in stone patients and controls (P = .77). Serum mean fetuin-A concentration was significantly lower in the patients (710.38 +/- 156.42 mu g/mL) than in the controls (810.89 +/- 173.43 mu g/mL, P = .0001). In the patient group (but not in the control group), subjects carrying fetuin-A genotype 1 had significantly higher serum fetuin-A concentrations than the group carrying fetuin-A genotype 2-1 (P = .001). CONCLUSIONS These results reveal that the patients with fetuin-A c. 766C > G gene polymorphism may be at higher risk for renal calcium oxalate stone formation. UROLOGY 75: 928-932, 2010. (C) 2010 Elsevier Inc.