OBJECTIVE

Lower-extremity vascular diseases are important complication of diabetes. In the present study, we investigated the influence of blood glucose fluctuation in type 2 diabetes-associated lower-extremity vascular diseases, and explore the possible mechanism.

METHODS

Patients with type 2 diabetes was assigned to Group B (without lower-extremity vascular disease) and group C (with lower-extremity vascular disease). Healthy subjects (Group A) served as normal controls. All patients received dynamic blood glucose monitoring for 72 h. The mean amplitude of glycemic excursion (MAGE) and the largest amplitude of glycemic excursion (LAGE) were estimated. The levels of von Willebrand factor (vWF), ischemia-modified albumin (IMA), glycosylated hemoglobin (HbA1c), and biochemical indices were examined, and the lower-extremity vascular diseases were scored in patients from group C.

RESULTS

Groups B and C have higher systolic blood pressure (SBP), total cholesterol (TC) level, high-density lipoprotein cholesterol (HDL-C) level, HbA1c level, and vWF level and lower IMA level than those in Group A (p < 0.05). Elevated MAGE and LAGE were observed in groups B and C as compared with Group A. Correlation analysis revealed that the score of lower-extremity vascular diseases was associated with MAGE, LAGE, SBP, LDL-C, vWF, HbA1c, and IMA (p < 0.05). Stepwise multiple-linear regression analysis revealed that lower-extremity vascular diseases were involved with MAGE, IMA, and vWF.

CONCLUSIONS

Enhanced fluctuation in patients with type 2 diabetes may promote the occurrence and development of lower-extremity vascular diseases through aggravating vascular endothelial injury.

During ischaemia, the extracellular level of adenosine increases, which has cytotoxic effects. In endothelium, cell surface adenosine deaminase (ADA) complexing CD26 is coordinately induced during ischaemia as part of an adaptative response by eliminating adenosine. We examined whether a similar mechanism exists for mononuclear cells. We studied mononuclear cell surface ADA (MCADA) and dipeptidyl-peptidase IV activity (DPPIV) of membrane CD26 during percutaneous transluminal coronary angioplasty (PTCA) as a model of ischaemia-reperfusion. Enzymatic activities were compared with levels of ischaemia-modified albumin (IMA), a marker of ischaemia-reperfusion.

RESULTS

Patients (15 men and 5 women) with non-ST segment elevation acute coronary syndrome related to a stenosis of proximal left anterior descending artery were prospectively included before revascularization. MCADA, DPPIV and IMA were measured before PTCA (T0) then 15 (T15) and 120 (T120) minutes after reperfusion. Fifteen healthy control subjects were enrolled. At T0, MCADA and IMA levels were higher in patients than in controls. MCADA decreased at T15 (median, IQR: 8.2 [7.6-9.8] IU) relative to T0 (11.25 [10-13.5] IU, p<0.01) and remained low at T120. DPPIV decreased at T15 (0.9 [0.7-1.1] AU) relative to T0 (1.05 [0.99-1.48] AU; p<0.01) and remained low at T120. IMA level increased only at T120. MCADA and DPPIV were correlated. Our findings are that MCADA and DPPIV decreased rapidly after angioplasty, suggesting that both catalysts are early markers of reperfusion.

CONCLUSIONS

MCADA and DPPIV are sensitive and early markers of ischaemia-reperfusion process during PTCA.

BACKGROUND

The objective of this study was to evaluate the serum levels of ischemia modified albumin and oxidative stress parameters in patients with cardiac syndrome X.

METHODS

A total of 61 patients, composed of 32 consecutive patients (24 female, 8 male, average age: 47.63 +/- 9.49 years) diagnosed with cardiac syndrome X by coronary angiography (initially performed following the identification of ischemia by exercise stress test or myocardial perfusion scintigraphy) and a control group of 29 consecutive patients (15 female, 14 male, average age: 49.59 +/- 11.68 years) with similar features without cardiac syndrome X were included in the study. The levels of the ischemia modified albumin (IMA), ferric reducing antioxidant power (FRAP), prooxidant-antioxidant balance (PAB), and advanced protein oxidation products (AOPP) were determined by colorimetric methods.

RESULTS

Patients have significantly higher PAB, AOPP, and IMA levels in the patient group than in the control group (p < 0.01, p < 0.001, and p < 0.02, respectively). Also, serum triglyceride (p < 0.005) and hs-CRP (p < 0.0001) levels were significantly higher in the patient group (p < 0.01, p < 0.001, and p < 0.02, respectively). We found that there was a significant correlation between hs-CRP, plasma PAB (r: 0.258; p < 0.05), AOPP (r: 0.459; p < 0.001), and triglyceride levels (r: 0.404; p < 0.01). Plasma AOPP levels were also significantly positive correlated with triglyceride levels (r: 0.463; p < 0.001). In addition, during the correlation analysis performed on the patient group, a positive correlation was observed between the levels of IMA with the levels of plasma PAB and plasma AOPP (r: 0,994; p < 0.01 and r: 0.857; p < 0.05, respectively) In a multiple linear regression analysis, AOPP levels were significantly related with hs-CRP and triglyceride (R2: 0.380, p < 0.0001 and p < 0.05). Simple linear regression analysis was performed between plasma PAB (as dependent variable) and hs-CRP levels. Plasma PAB levels were related with hs-CRP (R2: 0.258, p < 0.05). Using the receiver-operator characteristic (ROC) curve, the best cut-off values for predicting cardiac syndrome X of PAD, AOPP, IMA, and hs-CRP levels were 88.1 arbitrary units, 68.5 kloramin T micromol/L, 7.17 U/mL, and 1.09 mg/dL, respectively.

CONCLUSIONS

Based on the results of our study, the increase in oxidative stress during cardiac syndrome X appears to be related to elevated levels of IMA. Treatment modalities that decrease oxidative stress might be beneficial for the treatment of cardiac syndrome X.

OBJECTIVE

To determine the release kinetics of different biomarkers with potential as novel early ischaemic biomarkers in patients with acute coronary syndrome (ACS); it is difficult to establish the detailed release kinetics in patients with acute myocardial infarction (AMI).

METHODS

We analysed the release kinetics of soluble fms-like tyrosine kinase (sFlt-1), ischaemia modified albumin (IMA), and heart-type fatty acid binding protein (hFABP) in patients with hypertrophic obstructive cardiomyopathy who were undergoing transcoronary ablation of septal hypertrophy (TASH), a procedure mimicking AMI. Consecutive patients (n=21) undergoing TASH were included. Blood samples were collected before TASH and 15, 30, 45, 60, 75, 90, and 105 min and 2, 4, 8, and 24 h after TASH. sFlt-1 and hFABP were quantified in serum, and IMA was quantified in plasma using immunoassays.

RESULTS

sFLT-1 and hFABP increased significantly 15 min after induction of AMI vs baseline as follows: sFlt-1, 3657.5 ng/L (IQR 2302.3-4475.0) vs 76.0 ng/L (IQR 71.2-88.8) (p<0.001); hFABP, 9.0 ng/mL (IQR 7.0-15.4) vs 4.6 ng/mL (IQR 3.4-7.1) (p<0.001). sFlt-1 demonstrated a continuous decrease after the 15th min. hFABP showed a continuous increase until the 8th hour with a decline afterwards. The IMA concentrations increased significantly 30 min after induction of AMI vs baseline, with values of 26.0 U/mL (IQR 21.8-38.6) vs 15.6 U/mL (IQR 10.1-24.7) (p=0.02), and then decreased after 75 min.

CONCLUSIONS

sFlt-1 and hFABP increased very early after induction of myocardial ischaemia, showing different release kinetics. The additional information provided by these findings is helpful for developing their potential combined use with cardiac troponins in patients with suspected AMI.

BACKGROUND

Ischemia-modified albumin (IMA) is an altered type of serum albumin that forms under conditions of oxidative stress and an independent predictor of major adverse cardiovascular events.

OBJECTIVE

To measure the levels of IMA in 45 children and adolescents with β-thalassemia major (β-TM) compared with 30 healthy controls and assess its relation to lipid peroxidation, vascular complications and subclinical atherosclerosis.

METHODS

β-TM patients without symptoms of heart disease were studied focusing on transfusion history, chelation therapy, serum ferritin, malondialdehyde (MDA) and IMA levels. Echocardiography was performed and carotid intima media thickness (CIMT) was assessed.

RESULTS

IMA and MDA levels were significantly higher in β-TM patients compared with controls (p < 0.001). IMA was higher among patients with heart disease, pulmonary hypertension risk and serum ferritin ≥2500 µg/l than those without. TM patients compliant to chelation had significantly lower IMA levels. IMA levels were positively correlated to MDA and CIMT while negatively correlated to ejection fraction and fractional shortening.

CONCLUSIONS

Our results highlight the role of oxidative stress in the pathophysiology of vascular complications in thalassemia. IMA could be useful for screening of β-TM patients at risk of cardiopulmonary complications and atherosclerosis because its alteration occurs in early subclinical disease.

BACKGROUND

The early prediction of gangrenous/perforated appendicitis is of great importance for the surgical planning, further treatments, and predicting the course of disease. Ischemia-modified albumin (IMA) was previously reported as a biomarker of various ischemia-based diseases. Our aim is to determine the predictive value of serum IMA in the severity of acute appendicitis.

METHODS

Sixty-two patients who underwent urgent appendectomy were included in the study. Plasma level of IMA was measured after diagnosis and before treatment. All patients were classified as noncomplicated (acute) appendicitis and complicated (gangrenous/perforated) appendicitis according to histopathological findings, and comparisons were made between the groups.

RESULTS

The data of 62 patients with a mean age of 30.1 years were statistically evaluated. The pathological diagnoses were acute appendicitis in 33 (53.2%), and gangrenous/perforated appendicitis in 29 (46.8%) patients. There were significant differences in computed tomography (CT) findings (P = .031) and IMA (P = .012) levels between the groups. A strong positive correlation between IMA levels and CT findings was also found (Spearman ρ = +0.688, P = .003).

CONCLUSIONS

The IMA can be considered as a novel and useful marker to distinguish gangrenous/perforated appendicitis from noncomplicated appendicitis. The correlation of IMA with CT findings also enhances the predictive value of IMA.

OBJECTIVE

The aim of this cross-sectional study was to determine the oxidant and antioxidant status and a novel ischemia marker - ischemia modified albumin - in the cord blood of smoker and non-smoker pregnants.

METHODS

This study was performed on 30 smoker and 60 non-smoker pregnant women. Malondialdehyde (MDA), vitamin A and E, total antioxidant capacity (TAC) and ischemia modified albumin (IMA) levels and superoxide dismutase activities (SOD) were determined in the cord blood of the contributors.

RESULTS

In the cord blood of the smoker women compared to the non-smokers; MDA (µmol/L) levels increased (5.17 ± 0.25, 3.60 ± 0.06, p = 0.000), IMA (ABSU) levels increased (0.913 ± 0.02, 0.830 ± 0.01, p = 0.050), SOD (U/ml) activities decreased (8.22 ± 0.14, 8.63 ± 0.14, p = 0.045), Vit A(µg/L) (339.06 ± 17.52, 454.91 ± 16.56, p = 0.000) and Vit E (mg/L) levels decreased (2.8 ± 0.15, 7.58 ± 0.38, p = 0.000) and TAC (Mm Trolox) levels decreased (3.25 ± 0.15, 4.08 ± 0.09, p = 0.000), and these differences were statistically significant. We found moderate and strong positive correlations between smoking status and IMA (r = 0.325, p = 0.002) and smoking status and MDA levels (r = 0.636, p = 0.000). Smoking status presented weak, moderate and strong negative correlations with SOD activities, TAC, Vit A and Vit E levels, respectively (r = -0.237, p = 0.024), (r = -0.420, p = 0.000), (r = -0.443, p=0.000), (r = -0.795, p = 0.000).

CONCLUSIONS

It was determined that smoking cigarette during gestation disturbed the balance between the oxidant and antioxidant system and caused oxidative stress. Increased IMA levels in cord blood of smoker pregnants suggests that smoking during pregnancy causes fetal ischemia.

This study sought to clarify the role and underlying mechanisms of human serum albumin (HSA) therapy in global cerebral ischemia/reperfusion (GCI/R)-induced brain damage in rats. Five groups of adult male Wistar rats (n = 12 per group) were created as follows: sham operation (Sham), global cerebral ischemia/reperfusion (GCI/R), HSA treatment (GCI/R + HSA), Dickkopf-1 (DDK1) treatment (GCI/R + DDK1), and DDK1 plus HSA treatment (GCI/R + DKK1 + HSA). The GCI/R injury model was created using the modified Pusinelli four-vessel occlusion method. After 24 h, rats were evaluated using neurological scoring, Nissl staining, and brain tissue water content. The mRNA expression of Wnt, GSK3β, and β-Catenin in the brain were detected by quantitative real time polymerase chain reaction. The protein expression of β-Catenin and GSK-3β were investigated by western blot and immunohistochemical analysis in the presence and absence of the Wnt/β-Catenin antagonist, DKK-1. Complex I activity and ROS content were also measured. After 24 h of reperfusion, the behavior score and brain tissue water content in the GCI/R + HSA group were lower than that in the GCI/R group. In addition, the degree of neuronal injury was significantly reduced in the GCI/R + HSA group (P < 0.05). The ROS content was significantly decreased and Complex I activity was markedly raised in the GCI/R + HSA group compared to the GCI/R group (P < 0.05). Further, GSK-3β expression in the GCI/R + HSA group was lower than that in the GCI/R group, while the Wnt and β-catenin expression were increased. These effects were reversed by DKK1. Taken together, we showed that HSA attenuates GCI/R-induced brain damage and may be neuroprotective via regulation of the Wnt/β-catenin/ROS signaling pathway.

The objective of the present study was to determine whether preischemic administration of syringic acid (SA) would attenuate renal ischemia-reperfusion injury (IRI). Rats were divided into three groups: Sham group; IR group; and IR + SA group. The effects of SA were examined using biochemical parameters including serum ischemia-modified albumin (IMA), total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), tissue superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and malondialdehyde (MDA). The apoptosis status and histopathological changes were evaluated. After calculating the score for each histopathological change, the total score was obtained by summing all the scores. In the SA group, MDA, IMA, TOS, and OSI decreased significantly compared to the IR group. After SA administration, the increase in GPx activity was found to be significant. Apoptosis decreased significantly in the SA group compared with the IR group. The total score significantly decreased after administration of SA. Taken together, our findings suggest that SA preconditioning is effective in reducing tissue damage induced in kidney IRI. Renal histology also showed convincing evidence regarding the protective nature of SA.

Cisplatin (CP) is a chemotherapeutic agent used to treat various types of cancer; nephrotoxicity is the most common adverse effect of the drug. We investigated the protective effects of propolis against CP induced kidney injury. Thirty-six male rats were divided into six equal groups: untreated control group, 50 mg/kg/day propolis group, 100 mg/kg/day propolis group, single-dose 7 mg/kg CP group, 7 mg/kg CP + 50 mg/kg/day propolis and 7 mg/kg CP + 100 mg/kg propolis. Rats were sacrificed after 14 days and kidneys were removed for histopathological and biochemical analyses. We used hematoxylin & eosin and periodic acid-Schiff staining to evaluate kidney histopathology and we used the TUNEL technique to assess apoptosis. We also measured total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), ischemia-modified albumin (IMA) and malondialdehyde (MDA) levels in tissue and blood specimens. Normal morphology was observed in the control, 50 mg/kg/day propolis and 100 mg/kg/day propolis groups by light microscopy. Degeneration of tubule cells, edema and tubule dilation were increased in the CP group compared to the control group. Degeneration of tubule cells and dilation of Bowman's spaces were decreased in the CP + 50 mg/kg/day propolis and CP + 100 mg/kg/day propolis groups compared to the CP group. Tubule dilation decreased significantly in the CP + 100 mg/kg propolis group compared to the CP group. Also, the 7 mg/kg CP group exhibited altered proximal tubule epithelial cells, loss of brush border and thickening of the parietal layer of Bowman's capsule in glomeruli and basal laminae of tubules. A normal brush border was observed in the CP + 50 mg/kg/day propolis and CP + 100 mg/kg/day groups. Serum OSI and MDA levels were increased in the CP group compared to the control group. Serum MDA levels decreased significantly in the CP + 50 mg/kg/day propolis and 100 mg/kg CP + propolis groups compared to the CP group. CP caused significant damage to kidney tissue; propolis exhibited dose-dependent prevention of tissue damage.

BACKGROUND

Cardiovascular morbidity is high among patients with peripheral arterial occlusive disease (PAOD). The aim of this study was to evaluate the ability of ischemia-modified albumin (IMA), N-terminal proBNP (NT-proBNP), and high-sensitive cardiac Troponin T (hs-cTnT) to predict cardiovascular complications in male patients with Fontaine stage II PAOD.

METHODS

68 men with stage II PAOD underwent treadmill testing. NT-proBNP, IMA and hs-cTnT were measured before and after exercise. Patients were followed up prospectively and complete follow-up data were available for 66 individuals.

RESULTS

Median follow-up time was 43.0months. 12 (18.2%) patients had suffered from a major adverse cardiac event (MACE). IMA and NT-proBNP baseline concentrations were significantly higher in patients who developed MACE during follow-up: IMA: 110.6±2.4kU/L vs. 102.5±0.9kU/L (p<0.001); NT-proBNP: 270.5±295.9ng/L vs. 84.6±15.4ng/L (p=0.007). In multivariable regression models only IMA was significantly associated with the primary endpoint (HR=1.07, CI 1.01-1.13; p=0.029).

CONCLUSIONS

In the present study, a serum concentration of >103.9kU/L of IMA was a better independent predictor of MACE than NT-proBNP or hs-cTnT. IMA might be a valuable tool for risk stratification in PAOD patients.

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.

Preeclampsia is a multisystem disorder involves altered homeostasis of oxidants-antioxidants, inflammatory process and endothelial dysfunction. The present study aim was to determine the levels of oxidative stress parameters (malondialdehyde, protein carbonyl, ischemia modified albumin and xanthine oxidase), nutrient antioxidants (vitamin C and vitamin E), enzyme antioxidants (catalase, superoxide dismutase, glutathione peroxidase glutathione reductase), total antioxidant status (TAS) and its association with nitric oxide. The study population consists of three groups, non pregnants (Group 1, n = 57), normotensive pregnants (Group 2, n = 57) and Preeclampsia (Group 3, n = 57). Group 2 and 3 were followed after delivery within 48 h. In preeclampsia xanthine oxidase, malondialdehyde and uric acid levels were significantly increased (p < 0.001), while TAS decreased (p < 0.05) when compared to normotensive pregnant and non pregnant. Catalase, glutathione reductase levels were increased (p < 0.005) and vitamin E, super oxide dismutase levels were decreased (p < 0.001) in preeclampsia when compared to normal pregnants. Receiver operating characteristics curve analysis showed area under curve for xanthine oxidase (0.8), malondialdehyde (0.804), Uric acid (0.84), ischemia modified albumin (0.92) and catalase (0.88) which indicated as good markers in preeclampsia. Amongst, ischemia modified albumin is a better marker of intrauterine hypoxic reperfusion risk with sensitivity 87.7 % and specificity 91.2 %. The increased hydrogen peroxide from xanthine oxidase adds to oxidative stress and increased catalase activity in preeclampsia represents combating action. Increased oxidative stress, decreased TAS and its apparent reversible changes evinced within 48 h after delivery in preeclampsia illustrated that placental abnormality is the contributing factor in the pathogenesis.

BACKGROUND

Hypoxia plays an important role in the development and progression of hematologic malignancies.

OBJECTIVE

This study was intended to investigate the effectiveness of ischemia-modified albumin (IMA) for demonstrating hypoxia in patients with acute leukemia.

METHODS

Blood specimens were collected from 132 subjects (44 acute leukemia patients, 40 iron deficiency anemia (IDA) patients and 48 healthy controls). Serum levels of IMA and malondialdehyde (MDA) were analyzed using conventional methods.

RESULTS

Serum levels of IMA were higher in patients with acute leukemia than in those with IDA and healthy controls (acute leukemia patients; 0.69 ± 0.14 ABSUs, IDA patients; 0.61 ± 0.09 ABSUs, controls; 0.50 ± 0.09 ABSUs, respectively). There was a negative correlation between serum IMA levels and hemoglobin (Hb) values (r = - 0.312) and between serum IMA levels and hematocrit (Hct) values, (r = - 0.305) in patients with acute leukemia. Serum levels of MDA were higher in patients with acute leukemia than in those with IDA. But there was no difference in patients with acute leukemia and IDA compared to healthy controls (acute leukemia patients; 2.23 ± 1.82 nmol/mL, IDA patients; 1.36 ± 0.94 nmol/mL, healthy controls; 1.79 ± 0.78 nmol/mL, respectively).

CONCLUSIONS

IMA can be effective for demonstrating hypoxia in patients with acute leukemia.

BACKGROUND

Amnestic mild cognitive impairment (aMCI) is considered to be a prodromal stage of Alzheimer's disease. The clinical role of ischaemia-modified albumin (IMA) and the association between IMA and oxidative stress in aMCI have not been investigated. The aim of the study was to explore this relationship and to generate new ideas for controlling Alzheimer's disease.

METHODS

This community-based case-control study included 113 patients with aMCI and 832 cognitively normal controls. Serum levels of albumin and IMA, diacron-reactive oxygen metabolite, and biological anti-oxidant potential, were measured. The IMA/albumin ratio and the biological anti-oxidant potential/diacron-reactive oxygen metabolite ratio were calculated.

RESULTS

In univariate analysis, the serum IMA level and the IMA/albumin ratio were higher in the aMCI patients than in the controls (P < 0.001, P < 0.001, respectively). In multivariate analysis, a serum IMA level ≥476.4 ng/mL and an IMA/albumin ratio ≥9.4 were separately associated with the development of aMCI (odds ratio = 3.56, 95% confidence interval: 2.33-5.46; odds ratio = 3.43, 95% confidence interval: 2.25-5.27, respectively). There was a linear correlation between serum IMA level and several oxidative stress markers (biological anti-oxidant potential/diacron-reactive oxygen metabolite ratio: r = -0.585, P < 0.001; diacron-reactive oxygen metabolite: r = 0.549, P < 0.001; biological anti-oxidant potential: r = -0.293, P < 0.001).

CONCLUSIONS

Serum IMA might be a potential biomarker for oxidative stress in aMCI.

OBJECTIVE

To investigate the role of protein oxidative damage and antioxidant defense in relationship to hyperglycemia measured as fasting plasma glucose (FPG), glycated hemoglobin (A1C), and duration of disease in type 2 diabetes mellitus (DM) and diabetic retinopathy (DR).

METHODS

This study recruited 23 non-diabetic subjects, 16 DM patients without any complications and 18 DR patients. The serum ischemia modified albumin (IMA) and glutathione (GSH) levels were measured. The IMA results were corrected for serum albumin. Between-group differences were studied by analysis of variance and between-variable associations were studied by Spearman's and partial correlations.

RESULTS

IMA and cIMA values were elevated, whereas GSH was decreased in both patient groups vs controls (P<0.05), and the increase in IMA formation is not related to serum albumin changes. DR patients have much severe oxidative stress (OS) status with high IMA and cIMA, and low GSH than in the DM group (P<0.05). Both FPG and A1C levels were positively associated with IMA in DM group, while in the DR group, duration of disease too had a positive association with IMA. The antioxidant GSH had negative correlations with FPG (r=-0.52, P=0.02) and IMA (r=-0.49, P=0.03) in the DR group. Partial correlation analyses predicted mutual or independent associations among parameters.

CONCLUSIONS

Severe OS in DR has been associated with increased FPG, A1C, and disease duration. Both hyperglycemia and elevated oxidative damage detected as IMA are collectively associated with depleted GSH status. Our study unravels the need for monitoring of OS in addition to standard glycemic management in DR.

OBJECTIVE

The finding that ischemia-modified albumin (IMA) is increased in pre-eclamptic pregnancy suggests a role for IMA as a potential biomarker for abnormal placental development related to miscarriage. This study was undertaken to evaluate IMA levels in women with recurrent pregnancy loss (RPL).

METHODS

This case-control study was performed between March 2008 and September 2009, at the Department of Obstetrics and Gynecology of Meram School of Medicine. Serum IMA and albumin concentrations were assessed in 43 women with a history of two or more unexplained first trimester miscarriages (group 1), and 42 healthy pregnant women (group 2) in the first trimester. IMA, adjusted IMA and albumin concentrations were compared between the groups. Statistical analysis was performed using Student's t-test and Mann-Whitney U test.

RESULTS

IMA and adjusted IMA levels were significantly higher in women with RPL (1.11+0.08 and 1.09+0.09, respectively) compared to women in group 2 (0.88+0.10 and 0.88+0.11, respectively). Albumin levels in group 1 were significantly lower compared with group 2. There was a negative correlation between IMAand albumin levels in each group.

CONCLUSIONS

Maternal IMA levels appear to be elevated in women with early RPL. This finding may suggest that an abnormally high hypoxic intrauterine environment may be associated with abnormal placental development that contributes to early miscarriage.

OBJECTIVE

Ischemia-modified albumin (IMA) is a sensitive biomarker of myocardial ischemia. However, data on IMA levels in acute heart failure (HF) are still lacking. In this study, we aimed to evaluate serum IMA levels in acute decompensated HF and the effects of dobutamine and levosimendan treatments on IMA levels.

METHODS

This was a prospective, multicenter study that included 70 patients hospitalized with acute decompensated HF and left ventricular ejection fraction < 35%. Blood samples for IMA measurements were obtained on admission and 24-48 h after the initiation of HF therapy. Twenty-nine patients were treated with standard HF therapy, 18 received levosimendan, and 23 received dobutamine in addition to standard of care. A single serum specimen was also collected from 32 healthy individuals each. IMA concentrations were measured by the albumin cobalt binding colorimetric assay, and the results were given in absorbance units (AU). Independent and paired sample t-tests, Mann-Whitney U test, and Wilcoxon signed-rank test were used for the analysis.

RESULTS

In patients with acute decompensated HF, the serum concentration of IMA was significantly higher than those of healthy subjects (0.894 ± 0.23 AU vs. 0.379 ± 0.08 AU, p < 0.001). Overall, the IMA levels significantly decreased after 24-48 h of HF therapy (0.894 ± 0.23 AU and 0.832 ± 0.18 AU, p = 0.013). Furthermore, the IMA levels were also found to significantly decrease with standard HF therapy (1.041 ± 0.28 vs. 0.884 ± 0.15 AU, p = 0.041), with levosimendan (0.771 ± 0.18 vs. 0.728 ± 0.18 AU, p = 0.046) and also with dobutamine (0.892 ± 0.18 vs. 0.820 ± 0.13 AU, p = 0.035).

CONCLUSIONS

Patients with acute decompensated HF had elevated IMA levels, and appropriate HF therapy significantly reduced the serum IMA levels. Dobutamine or levosimendan did not increase the IMA levels, suggesting a lower potential in inducing myocardial ischemia when used in recommended doses.

BACKGROUND

Ischemia-modified albumin (IMA) has been shown to be a rapidly rising and sensitive biochemical marker especially for the diagnosis of myocardial ischemia. The aim of this study was to evaluate the influence of temperature on the capacity of cobalt binding to human albumin and the influence of this variable on IMA measurement.

METHODS

The following temperatures of incubation were tested for human albumin standard 25 degrees C, 28 degrees C, 31 degrees C, 34 degrees C, and 37 degrees C and for patients with suspected acute coronary syndrome, room temperature and 37 degrees C. IMA was measured by cobalt-albumin binding assay.

RESULTS

There was a strong positive correlation (r = 0.98, p < 0.001) between IMA and the assay temperatures. IMA levels were 0.68 +/- 0.25 absorbance units (ABSU) at room temperature and 0.92 +/- 0.33 ABSU (p < 0.001) at 37 degrees C in the study participants.

CONCLUSIONS

IMA values were influenced by the assay temperature.

BACKGROUND

The aim of this study was to describe a method to measure ischaemia-induced alterations of the binding capacity of serum albumin to exogenous nickel.

METHODS

We measured the levels of cardiac troponin I (cTnI), serum albumin, ischaemia-modified albumin (IMA) measured by a cobalt-albumin binding assay (CABA), and a nickel-albumin binding assay (NABA) in the following groups: myocardial infarction (n = 32) and non-ischaemic chest pain (n = 64).

RESULTS

IMA, cTnI and NABA levels were higher in the myocardial infarction group. NABA presented a higher ability to discriminate myocardial ischaemia than CABA.

CONCLUSIONS

Patients with myocardial infarction have reduced nickel binding to human serum albumin, and NABA may have an important role as an early marker of myocardial ischaemia.

OBJECTIVE

Oxidative stress (OXS) plays critical role in the development of diabetic retinopathy (DRP). Increased concentrations of serum ischemia-modified albumin (IMA) have been demonstrated as a novel and inexpensive measure of oxidative stress. Although few pilot studies have reported increased IMA in DRP, the available literature is limited to comprehensively describe the potential significance of IMA in predicting DRP.

METHODS

The authors performed a meta-analysis to investigate IMA in DRP compared with control and diabetes mellitus subjects. The authors also performed a meta-analysis of area under curve for IMA. PubMed (Medline), Embase, Scopus, Web of Science, Science Direct, Springer Link, and Google Scholar databases were searched for relevant studies in serum IMA in DRP. The authors obtained five observational studies. Meta-analysis was performed using Review Manager 5.3 and MEDCALC 15.8 software to present the pooled-overall effect size as standardized mean difference and overall area under curve value of IMA.

RESULTS

Random-effects meta-analysis indicated a significant increase in serum IMA in patients with DRP compared with control (standardized mean difference = 2.48, P < 0.0001) and diabetes mellitus groups (standardized mean difference = 1.43, P < 0.0001). Our results also show that IMA can significantly predict the development of DRP (area under curve = 0.86, P < 0.001).

CONCLUSIONS

Serum IMA may be useful as a simple marker in monitoring of oxidative stress status in DRP and showed significant discriminatory ability in DRP. Future comparative studies in large are needed to further investigate IMA in different types of DRP; proliferative and nonproliferative.

BACKGROUND

Ectopic pregnancies constitute about 2% of all pregnancies which are the leading cause of pregnancy-related deaths and a considerable cause of maternal morbidity. Oxidative stress can lead to a number of pregnancy related diseases including miscarriage, eclampsia and preterm labor. Ischemia modified albumin (IMA) which reflects the oxidative stress may be used as a marker for ectopic pregnancy. Our aim was to compare the levels of IMA and total antioxidant status (TAS) in ectopic and normal pregnancies and to understand if IMA can be used as a marker to diagnose ectopic pregnancy.

METHODS

Our case-control study consisted of 38 women with ectopic and 42 women with normal pregnancy. IMA and TAS levels were determined in serum samples with an albumin-cobalt binding test and by commercially available kits, respectively. IMA levels were adjusted according to serum albumin levels. Index of oxidation (IOS) was calculated by dividing adjusted IMA (A-IMA) levels with TAS. A receiver operating characteristics (ROC) curve analysis was made and cut-off values for the biomarkers were investigated in SPSS 21.0 program (SPSS, Chicago, IL). Data were presented as mean ± standard deviation and a p value < .05 was accepted as statistically significant.

RESULTS

There was a statistically significant difference in IMA, A-IMA, and IOS levels between ectopic and normal pregnancies. Although TAS level was not different statistically, it was lower in ectopic pregnancy. According to ROC curve analysis, IOS had the largest area under curve. A cut-off value of 0.545 for IOS had 81.6% sensitivity and 59.5% specificity.

CONCLUSIONS

According to our study, oxidative stress plays an important role in ectopic pregnancy and either A-IMA or IOS can be evaluated as a marker of ectopic pregnancy after further studies.