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Objective: Menopause is associated with weight gain and an increase of cardiovascular risk. The aim of the present study was to estimate serum ischemia-modified albumin (IMA) levels in postmenopausal women and evaluate their association with body mass index (BMI) and coronary artery disease (CAD). Methods: The study included 130 non-smoker postmenopausal women aged 43-80: 40 with BMI 26-32 kg/m 2 (Group A), 60 with BMI 21-25 kg/m 2 (Group B), and 30 with documented CAD and BMI 23-29 kg/m 2 (Group C). Serum IMA, albumin, hsCRP and NT-proBNP, glucose and insulin were measured. Homeostasis assessment model score (HOMA) and Quantitative insulin sensitivity index (QUICKI) were co-estimated. Results: Serum IMA and IMA to albumin ratio were significantly elevated in Group A as compared to Group B (p < 0.001) and similar to those of Group C. hsCRP and NT-proBNP did not differ between Groups A and B while they were lower in comparison to Group C (p < 0.001). Glucose, insulin and HOMA were elevated in Group A compared to Group B (p < 0.001) while QUICKI was lower (p < 0.001). In Group A, IMA was positively correlated with BMI, hsCRP, insulin, HOMA and negatively with QUICKI. In postmenopausal women, multivariable regression analysis revealed that obesity was the strongest significant determinant of circulating IMA levels (p < 0.001) contributing, therefore, to the elevated serum IMA concentration. Conclusions: Postmenopausal obesity is associated with elevated serum IMA possibly due to obesity associated oxidative stress. IMA measurement could provide an assessment of atherosclerotic burden in postmenopausal women. Further clinical evaluation is under investigation. © 2011 Elsevier Ireland Ltd. All rights reserved.

Background: Ischemia modified albumin (IMA), is a new biomarker of oxidative processes involved with coronary artery disease (CAD). We determined serum IMA, high-sensitivity C-reactive protein (hsCRP), and natriuretic peptide (NT-proBNP), and evaluated their correlation with severity of coronary atherosclerosis in patients undergoing coronary angiography (CA). Cardiac troponin T (cTnT), CK-MB mass, albumin and Total Antioxidant Status (TAS) were also evaluated. Methods: The study included 114 patients (88 men and 30 women) aged 43-80 years with documented CAD without evidence of acute coronary syndrome undergoing CA and 163 controls (131 men and 32 women) similarly aged. Results: IMA, hsCRP and NT-proBNP were higher (p < 0.001 and p = 0.008 for NT-proBNP) while TAS was lower (p < 0.001) in patients than in controls. IMA and TAS were negatively correlated in all subjects (p < 0.01). Among patients, there was no correlation between IMA and the number of diseased vessels. For CAD diagnosis the best cut-off point for IMA was 101.5 KU/L with a sensitivity and a specificity of 87.7% and a negative predictive value of 83.3%. IMA was associated with an increased risk for CAD (OR = 1.23, 95% CI: 1.16-1.31; p < 0.001). Conclusions: IMA determination may provide earlier information of CAD presence before hsCRP or NT-proBNP elevation, contributing to early assessment of overall patient risk. © 2009 Elsevier B.V. All rights reserved.

Objective: To analyze the time course of serum protein S-100b in patients with traumatic brain injury deteriorating to brain death and to investigate the predictive value of initial S-100b levels in relation to clinical and radiologic measures of injury severity with regard to brain death. Methods: Forty-seven patients who sustained severe head injury were studied. Blood samples for measurement of S-100b were drawn on admission in the intensive care unit and every 24 hours thereafter for a maximum of 6 consecutive days or until brain death occurred. Variables related to outcome were recorded, including age, sex, Glasgow Coma Scale (GCS), and brain CT findings on admission. Outcome was defined as deterioration to brain death or not. Results: Of the 47 patients studied, 17 deteriorated to brain death and 30 did not. On admission, patients who became brain dead had higher median serum S-100b levels compared with those who did not (2.32 mug/L vs 1.04 mug/L, p = 0.0028). Logistic regression analysis showed that initial S-100b was an independent predictor of brain death (p = 0.041), in the presence of advanced age (p = 0.043) and low GCS score (p = 0.013). The odds ratio of 2.09 (95% CI, 1.03 to 4.25) indicates a more than doubling of the probability of deteriorating to brain death per 1-mug/L increase in S-100b on admission. At clinical brain death, median S-100b was higher in patients with brain death compared with the peak S-100b value obtained over a 6-day period in those who did not become brain dead (6.58 mug/L vs 1.49 mug/L, p < 0.0001). Conclusions: Prediction of brain death after severe head injury can be improved by combining clinical and S-100b data; thus, serum S-100b determination deserves to be included in the neuromonitoring of patients with severe traumatic brain injury.