OBJECTIVE

Advanced oxidation protein products (AOPP) and ischemia-modified albumin (IMA) are forms of oxidatidatively modified albumin and have recently been investigated as indicators of oxidative stress. They are increased in different disorders, including diabetes mellitus, as a result of hyperglycaemia, oxidative stress and hypoxia. The usefulness of the plasma levels of these two parameters in estimating kidney dysfunction in type 2 diabetic patients (T2DM) was compared in this study.

METHODS

Plasma levels of AOPP and IMA were determined spectrophotometrically in 218 individuals, 153 patients with T2DM and 65 healthy people.. The urinary albumin/creatinine ratio (UACR) was used as the reference to define the stage of kidney dysfunction by the assessment of the degree of albuminuria.

RESULTS

Receiver Operating Characteristic (ROC) curve analysis, likelihood ratio (LR), and Youden's index (J) revealed that AOPP and IMA had acceptable sensitivities and specificities in individuals with different degrees of albuminuria; however, AOPP had higher values of the area under the curve (AUC: 0.934) than IMA, as well as 100% sensitivity and 77.01% specificity for distinguishing patients with micro- and macroalbuminuria.

CONCLUSIONS

Both AOPP and IMA may be helpful clinical markers for estimating kidney dysfunction, but AOPP is better able to identify diabetic patients with nephropathy. We suggest that AOPP is almost ideal for discriminating between T2DM patients with micro- and macroalbuminuria.

BACKGROUND

The aim of this study was to retrospectively evaluate the utility of assessing ischemia-modified albumin (IMA) levels for diagnosing acute coronary syndrome (ACS) in patients presenting to the emergency room (ER) with chest pain.

METHODS

The records of patients admitted to the ER with chest pain between August 2006 and December 2008 were examined. Those subsequently diagnosed with ACS were included in the study. Serum IMA and cardiac troponin I (cTnI) concentrations were determined in blood samples obtained from patients within 3h of ER admission and on days 1, 3, 7 and 14. IMA and cTnI cut-off values for diagnosis of ACS were employed and the successful diagnosis rates were compared.

RESULTS

Of the patients diagnosed with ACS following ER presentation with acute chest pain, the correct diagnosis rate was significantly higher as determined by assessment of IMA vs. cTnI concentrations within 3h of ER presentation (81.02% vs. 42.34%, P<0.01). Thereafter there were no between marker differences in rates of successful diagnosis.

CONCLUSIONS

These findings support the notion that IMA may be a useful biochemical marker for the early diagnosis of ACS, particularly in patients presenting to the ER with acute chest pain.

BACKGROUND

Oxygen metabolism has an important role in the pathogenesis of rheumatoid arthritis (RA). Abundant amounts of ROS have been identified in the synovial fluid of RA patients. The accumulation of ROS in cells also serves as an important intracellular signaling of molecules that amplify the synovial inflammatory-proliferative response. Thus, the aim of this study was to assess the IMA levels and other oxidative stress and inflammatory biomarkers in RA subjects.

METHODS

IMA, AOPP, CRP, hemoglobin, Hct, MCV, RF, creatinine, urea levels were assessed in 16 RA subjects and 20 healthy controls.

RESULTS

IMA levels were significantly higher in the RA group than in the control group (0.495 +/- 0.01 vs. 0.433 +/- 0.02 ABSU, p = 0.038). No significant differences were observed for the other markers studied.

CONCLUSIONS

This study demonstrated that RA is related to oxidative stress and inflammation. We also showed for the first time an increase of IMA levels in RA subjects, suggesting that this pathology promotes an increase in the oxidative stress process.

The goal of the present study was to address the various risk factors associated in normolipidemic acute myocardial infarction (AMI) patients admitted to the intensive coronary care unit (ICCU). The study compared serum lipid profiles, lipid peroxidation markers, antioxidants and inflammatory markers in acute myocardial infarction (AMI) patients and age/sex-matched controls. A lipid profile, lipid peroxidation, enzyme antioxidants, endogenous antioxidants, ischemia modified-albumin (IscMA), ceruloplasmin, C-reactive protein (CRP), fibrinogen, lipoprotein (a) and paraoxonase-1 activities were analyzed in 330 subjects, 165 acute myocardial infarction (AMI) patients and 165 age/sex-matched controls. We observed significantly higher (p < 0.0001) total cholesterol and triglyceride levels and lower high-density lipoprotein cholesterol (HDL-C) levels in the AMI patients. The lipoprotein (a), ceruloplasmin, CRP and fibrinogen levels were higher and the bilirubin, ascorbic acid, uric acid, albumin, superoxide dismutase, catalase, glutathione peroxidase and paraoxonase-1 activities were lower in AMI patients than controls. The malondialdehyde (MDA) and conjugated diene (CD) levels were significantly higher (p < 0.0001) in AMI patients.

We previously demonstrated that altering extracellular sodium (Na_o) and calcium (Ca_o) can modulate a form of electrical communication between cardiomyocytes termed "ephaptic coupling" (EpC), especially during loss of gap junction coupling. We hypothesized that altering Na_o and Ca_o modulates conduction velocity (CV) and arrhythmic burden during ischemia. Electrophysiology was quantified by optically mapping Langendorff-perfused guinea pig ventricles with modified Na_o (147 or 155 mM) and Ca_o (1.25 or 2.0 mM) during 30 min of simulated metabolic ischemia (pH 6.5, anoxia, aglycemia). Gap junction-adjacent perinexal width ( W_P), a candidate cardiac ephapse, and connexin (Cx)43 protein expression and Cx43 phosphorylation at S368 were quantified by transmission electron microscopy and Western immunoblot analysis, respectively. Metabolic ischemia slowed CV in hearts perfused with 147 mM Na_o and 2.0 mM Ca_o; however, theoretically increasing EpC with 155 mM Na_o was arrhythmogenic, and CV could not be measured. Reducing Ca_o to 1.25 mM expanded W_P, as expected during ischemia, consistent with reduced EpC, but attenuated CV slowing while delaying arrhythmia onset. These results were further supported by osmotically reducing W_P with albumin, which exacerbated CV slowing and increased early arrhythmias during ischemia, whereas mannitol expanded W_P, permitted conduction, and delayed the onset of arrhythmias. Cx43 expression patterns during the various interventions insufficiently correlated with observed CV changes and arrhythmic burden. In conclusion, decreasing perfusate calcium during metabolic ischemia enhances perinexal expansion, attenuates conduction slowing, and delays arrhythmias. Thus, perinexal expansion may be cardioprotective during metabolic ischemia. NEW & NOTEWORTHY This study demonstrates, for the first time, that modulating perfusate ion composition can alter cardiac electrophysiology during simulated metabolic ischemia.

End-stage renal disease (ESRD) with and/or without treatment by hemodialysis (HD) is associated with accelerated atherosclerosis, leading to cardiovascular disease (CVD) including acute coronary syndromes. Therefore, the regulation of CVD is a crucial issue for ESRD patients. Given the recent reports that paraoxonase-1 (PON-1) and ischemia-modified albumin (IMA) could predict CVD-related mortality in ESRD, the two recent biomarkers may be useful for preventive strategies for CVD. This review paper presents current data on the relationships between PON-1, IMA, and ESRD. Many studies have shown that circulating PON-1 activity is lower in ESRD patients, and we have shown that its levels increase after HD. Although circulating IMA levels can increase before HD in ESRD patients, there remains to be little data. Our pilot study has shown a significant inverse correlation between PON-1 and IMA in ESRD patients. Although the pathogenic link between PON-1 and IMA remains speculative, considering both biomarkers may provide new insights into the prevention of CVD in ESRD patients.

Owing to their higher risk for cardiac death or ischemic complications, patients with acute coronary syndrome (ACS) must be identified from other causes of chest pain. Patients with acute coronary syndrome are divided into categories based on their electrocardiogram; those with new ST-segment elevation and those who present with ST-segment depression. The subgroups of patients with ST-segment elevation are candidates for immediate reperfusion, while fibrinolysis appears harmful for those with non-ST elevation myocardial infarction. There is increasing evidence to encourage appropriate risk stratification before deciding on a management strategy (invasive or conservative) for each patient. The TIMI, GRACE or PURSUIT risk models are recommended as useful for decisions regarding therapeutic options. Cardiac biomarkers are useful additions to these clinical tools to correctly risk stratify ACS patients. Cardiac troponin is the biomarker of choice to detect myocardial necrosis and is central to the universal definition of myocardial infarction. The introduction of troponin assays with a lower limit of detection will allow for earlier diagnosis of patients who present with chest pain. Analytical and clinical validations of these new assays are currently in progress. The question is whether the lower detection limit of the troponin assays will be able to indicate myocardial ischemia in the absence of myocardial necrosis. Previous to the development of ultrasensitive cardiac troponin assays free fatty acids unbound to albumin and ischemia modified albumin were proposed as biochemical markers of ischemia. Advances in our knowledge of the pathogenesis of acute coronary thrombosis have stimulated the development of new biomarkers. Markers of left ventricular performance (N-terminal pro-brain natriuretic peptide) and inflammation (e.g. C-reactive protein) are generally recognized as risk indicators. Studies suggest that using a number of biomarkers clinicians can risk stratify patients over a broad range of short and long term cardiac events. Nevertheless, it is still under debate as to which biomarker combination is best preferred for risk prediction. This review will focus on recent practice guidelines for the management of patients with ACS as well as current advances in cardiac biomarkers, their integration into clinical care and their diagnostic, prognostic and therapeutic utility.

Early and accurate diagnosis of intestinal ischemia is important in order to provide rapid and correct treatment and reduce morbidity and mortality rates. Clinical signs and symptoms are often unspecific. This systemic review sums up literature regarding human plasma biomarkers for acute mesenteric ischemia reported during the last ten years. Classic, general markers, including lactate, white cell count, base excess, show poor diagnostic accuracy for intestinal ischemia. Preliminary results for ischemia-modified albumin are promising, which is also true for the inflammatory marker procalcitonin. Best diagnostic accuracy is described for D-dimer, a-Glutathione S-transferase (a-GST) and Intestinal fatty acid binding protein (I-FABP), reflecting coagulation activity and mucosal damage respectively. Future studies should be directed at phase four questions (Do patients who undergo the diagnostic test fare better (in their ultimate health outcomes) than similar patients who do not?) for these markers and the identification of additional, novel plasma biomarkers signaling various types and stages of intestinal ischemia.

The constriction of vessels due to atherosclerotic lesions causes hypoxia/ischemia and oxidative changes resulting in transformation of free albumin to ischemia-modified albumin (IMA) in the circulation and increased carotid intima-media thickness (cIMT). We investigated the reliability of IMA increase in evaluating atherosclerosis in patients with familial Mediterranean fever (FMF) compared with cIMT. Patients with FMF (n = 58) diagnosed by the Tel-Hashomer criteria in attack-free period and 38 healthy people were included in the study. Patient demographics as well as the clinical and laboratory characteristics of the healthy controls and patients with FMF were noted. The IMA levels and cIMT in patients with FMF were 0.30 ± 0.09 absorbance units (ABSUs) and 1.12 ± 0.27 mm, respectively, and in the control group, IMA levels and cIMT were 0.25 ± 0.07 ABSU and 0.74 ± 0.26 mm, respectively. The IMA levels and cIMT were significantly higher in patients with FMF than in controls (P= .020 andP< .0001, respectively). The IMA values showed positive correlation with cIMT in patients with FMF(r= .302,P= .041). Our results reveal that IMA--an oxidative stress marker--may be an indicator of atherosclerosis in patients with FMF. This finding deserves further investigation.

BACKGROUND

Oxidative stress is characterized by increased production of reactive oxygen species resulting in the generation of lipid peroxides such as malondialdehyde (MDA). The studies have shown that ischemia-modified albumin (IMA), which has widely been studied as a marker of ischemia, also increases as result of oxidative stress. Hence, the current study was done to evaluate the serum MDA, IMA along with serum uric acid, and albumin, which are important metabolic antioxidants.

METHODS

Fifty patients with acute ischemic stroke were taken as cases and compared with 50 age- and sex-matched controls. Serum MDA, IMA, uric acid, and albumin were estimated both in cases and controls. Serum MDA was estimated by the method of Satoh and IMA by Bar-Or et al. The results were analyzed statistically.

RESULTS

Serum MDA and IMA values were significantly increased in cases (P < 0.0001), whereas serum uric acid and albumin values were significantly decreased (P < 0.05) in comparison to controls. There was also highly significant positive correlation between serum IMA and MDA (r = 0.843,P < 0.0001), whereas there were significant negative correlations between serum IMA and uric acid (r = -0.237,P < 0.05), and albumin (r = -0.326,P < 0.05).

CONCLUSIONS

Hence, we conclude the oxidative stress plays a major role in the etiopathogenesis of acute ischemic stroke, and the deranged oxidant-antioxidant balance further contributes to its severity.

OBJECTIVE

Ischaemia-modified albumin (IMA), as measured by the albumin-cobalt binding (ACB) test, has been cleared by the US Food and Drug administration as a biomarker to exclude the presence of myocardial ischaemia in patients. Although there are a number of published studies detailing the clinical utility of IMA, data on the biological variation of IMA are still lacking. In this study we determined the analytical and biological variance components of ischaemia modified albumin, and compared the distribution of IMA values in our patient population to those provided by the kit manufacturer.

METHODS

IMA was determined once a week for five consecutive weeks on a cohort of healthy subjects using a colorimetric method, the A CB test on a Roche modular analyser.

RESULTS

The analytical coefficient of variation (CV(A)) was 5%, and the within-subject (CV(I)) and between-subject (CV(G)) biological variations were 3 and 7%, respectively. Analysis of the repeated measures with gender and race (black and Caucasian) as between-subject factors, and weeks (1-5) as the within-subject factor showed that gender had no significant effect on circulating IMA concentrations (p = 0.3146), whereas race did have a significant effect (p = 0.0062). A significant (p = 0.0185) interaction was observed between gender and race.

CONCLUSIONS

The ACB test could bring a new dimension to the care and management of patients with acute coronary syndrome. Further studies for normal population distributions by gender and ethnicity, and an optimum cut-off value appear to be required.

Human serum albumin (HSA) is the most abundant protein in the human body. HSA injections prepared by fractionating human blood have mainly covered the demand for albumin to treat hypoalbuminemia, the state of low concentration of albumin in blood. HSA in solution may exist in various forms such as monomers, oligomers, polymers, or as mixtures, and its conformational change and/or aggregation may occur easily. Considering these characteristics, there is a great chance of modification and polymer formation during the preparation processes of albumin products, especially injections. The albumin cobalt binding (ACB) test reported by Bar-Or et al. was originally designed to detect ischemia modified albumin (IMA), which contains the modified HSA N-terminal sequence by cleavage of the last two amino acids. In this study, we developed a cobalt albumin binding (CAB) assay to correct the flaws of the ACB test with improving the sensitivity and precision. The newly developed CAB assay easily detects albumin configuration alterations and may be able to be used in developing a quality control method for albumin and its pharmaceutical formulations including albumin injections.

OBJECTIVE

To investigate diagnostic value of ischemia-modified albumin (IMA) levels in patients applying to emergency with symptoms of acute coronary syndrome (ACS) and acute ischemic stroke (AIS).

METHODS

Two patient groups (ACS and AIS) and a control group were constituted. The study was discontinued upon reaching 30 patients in each group. Following patient approval at the initial visit, a total of 10 ml venous blood sample was obtained from all patients with a high clinical suspicion of ACS and AIS. The Troponin I and the IMA levels were determined in the blood samples.

RESULTS

Statistically significant higher IMA values were determined in the patient groups compared to the control group (p<0.001 for both groups). No statistically significant correlation was found between the IMA and the Troponin I values in the ACS and the AIS groups (p>0.05 for both groups). The sensitivity of IMA was 83% and 87% for ACS and AIS, respectively. The specificity of IMA was 90% and 87% for ACS and AIS, respectively.

CONCLUSIONS

The sensitivity and specificity values, determined according to the optimal cut-off values in the groups demonstrated that IMA could be a useful diagnostic marker in ACS and AIS patients.

BACKGROUND

Diagnosis of acute coronary syndrome (ACS) is important, due to the associated very high mortality. Failure to diagnose ACS is a problem both for the patients and the clinicians. Ischemia modified albumin (IMA) has already been licensed by the US Food and Drug Administration for the diagnosis of suspected myocardial ischemia.

METHODS

Patients attending the emergency department (ED) within 6 h after having features of ACS were selected. IMA was done on admission. Blinded to the IMA results patients were fully evaluated and a diagnosis of non-ischemic chest pain (NICP), unstable angina (UA) or myocardial infarction (MI) was made. Later IMA results were correlated in each group.

RESULTS

Mean IMA value was 56.38 ± 23.89 u/ml in NICP group whereas in UA group it was 89.00 ± 7.76 u/ml and MI group was 87.50 ± 9.62 u/ml. This showed a sensitivity of 92% and specificity of 87%. The positive predictive value of the test was 88% and negative predictive value was 94%. In 16 patients an early diagnosis could be made when compared with Trop-T. Of the 89 patients 11 patients died in hospital. The IMA value was compared between this group and the patients who survived. Patients who died had a mean IMA value of 88.5 with a standard deviation of 5.33 whereas in patients who survived the mean value was 78.26 which was not statistically significant.

CONCLUSIONS

In conclusion the benefit of the test would be to rule out ACS in patients who present early to ED with inconclusive diagnosis.

BACKGROUND

Heart-type fatty acid binding protein (hFABP) and ischemia-modified albumin (IMA) have been put forward as novel biomarkers to detect myocardial injury shortly after onset of ischemia. We compared hFABP and IMA with cardiac troponin I (cTnI) for speed and reliability in the diagnosis of perioperative myocardial infarction (PMI) after coronary artery bypass graft surgery (CABG).

METHODS

In all, 210 consecutive patients undergoing isolated CABG with cardiopulmonary bypass were enrolled in a prospective study. Blood samples were taken perioperatively and throughout the first 72 hours after surgery; clinical data and events were recorded. In cohort A, serum concentrations of hFABP and cTnI were measured using a combined quantitative bedside assay. In cohort B, IMA and cTnI serum concentrations were measured using an albumin cobalt binding test. Perioperative myocardial infarction was defined using a cTnI cutoff of greater than 10.5 ng/mL occurring within 24 hours of CABG or new electrocardiographic changes.

RESULTS

In cohort A, 14 patients were identified with PMI (group 1), whereas 94 had no PMI and served as controls (group 2). Both hFABP and cTnI were increased in group 1 as compared with group 2 (p < 0.001). Although cTnI did not differ before 12 hours, hFABP diverged much earlier, at 1 hour postoperatively (p < 0.001). An hFABP concentration of 20 μg/mL at 1 hour detected PMI with an area under the curve of 77.1%. In cohort B, 18 patients were identified with PMI (group 3), and 84 patients served as controls (group 4). No difference in cTnI values could be observed between the groups until 12 hours postoperatively. Ischemia-modified albumin failed to differentiate at any postoperative time point; the low discriminative power of IMA was confirmed with an area under the curve of 53.3% at 1 hour, 48.5% at 6 hours, and 39.3% at 12 hours postoperatively.

CONCLUSIONS

Heart-type fatty acid binding protein is a sensitive and rapid biomarker that detected PMI reliably at 1 hour after CABG, much earlier than cTnI. The diagnostic value of IMA for detection of PMI appears to be very limited in this setting.

UNASSIGNED

Diabetes is a major health problem associated with hyperglycemia and chronically increased oxidative stress and enhanced formation of advanced glycation end-products (AGEs). The aim of this study was to determine whether oxidative plasma biomarkers in diabetic patients could be evidenced and associated with vascular complications.

UNASSIGNED

Oxidative stress biomarkers such as thiols, ischemia-modified albumin (IMA), glycated albumin (GA), fructosamine, and AGEs were measured in 75 patients with poorly controlled type 2 diabetes (HbA1c>> 7.5%) with (44) or without (31) vascular disease and in 31 nondiabetic controls.

UNASSIGNED

Most biomarkers of oxidation and glycation were significantly increased in diabetic patients in comparison with nondiabetics. Fructosamines, GA, IMA, and AGEs were positively correlated and levels of fluorescent AGEs were significantly increased in the plasma from patients presenting vascular complication.

UNASSIGNED

These results bring new evidence for the potential interest of glycated albumin, oxidative stress, and glycoxidation parameters in the monitoring of type 2 diabetic patients. Furthermore, it emphasizes fluorescent AGEs as a putative indicator for vascular event prediction in diabetic patients.

Human serum albumin (HSA), a non-glycosylated protein, is widely employed as carrier for drug delivery systems. A series of recombinant, mannosylated-HSA mutants (Man-rHSAs: D63N, A320T and D494N) and their triple mutant (TM-rHSA: D63N/A320T/D494N) were prepared, that can be selectively delivered to the liver via mannose receptor (MR) on the liver non-parenchymal cells. A pharmacokinetic analysis of (111)In-Man-rHSAs in mice showed that they were rapidly cleared from the blood circulation, and were largely taken up by the liver rapidly in the order: TM-rHSA>D494N>)A320T=D63N, consistent with their degree of mannosylation. In vivo competition experiments with an excess amount of chemically modified Man-BSA or mannan suggested that the hepatic uptake of TM-rHSA was selectively mediated by MR on Kupffer cells. Lastly, a TM-rHSA-NO conjugate, S-nitrosylated TM-rHSA, effectively delivered NO to the liver and then exhibited a significant inhibitory effect against hepatic ischemia/reperfusion injury model rats, accompanied by the induction of heme oxygenase-1.

Diagnosis of cardiac ischemia in patients coming to emergency departments (ED) with symptoms of acute chest pain is often difficult. Many markers are sensitive and specific for the detection of myocardial necrosis but may not rise during reversible myocardial ischemia. Ischemia-modified albumin (IMA) has recently been shown to be a sensitive and early biochemical marker of ischemia. The variation laws were observed by measuring IMA and C-reactive protein (CRP) of 113 patients in ED within 12 hr after onset of chest pain. In the observation, blood was taken for IMA and CRP. Patients underwent standardized triage, diagnostic procedures, and treatment. Results of IMA and CRP were correlated with final diagnoses of nonischemic chest pain (NICP) and acute coronary syndrome (ACS). There were obvious distinction of IMA and CRP levels between the NICP and ACS groups. Receiver operator characteristic (ROC) curve analysis was used to determine the optimal cutoff of this assay for identifying individuals with ACS patients from NICP. The area under the curves of IMA is 0.948. The sensitivity and specificity of albumin cobalt binding (ACB) at a cutoff value of 70.0 units/mL were 94.4% and 82.6%, respectively. The area under the curves of CRP is 0.746. Sensitivity and specificity of CRP at a cutoff value of 3.16 mg/L were 70.0% and 73.9%, respectively. Negative predictive value (NPV) of IMA and CRP for ischemia origin was 79.2% and 38.6%, respectively. IMA may make an early diagnosis of acute coronary ischemia, and will improve the early diagnostic sensitivity and specificity of ACS.

Acute intestinal ischemia is a relative rare abdominal emergency, associated with considerably high morbidity and mortality rates. Although the conventional diagnostic approach to acute intestinal ischemia entails a preliminary evaluation of signs and symptoms, followed by radiological and laboratory investigations, a definitive diagnosis is can usually be made after laparotomy, which still remains the gold standard diagnostic (and therapeutic) procedure. Several potential laboratory biomarkers have been investigated over the past decades, but none of these seems to reach a suitable diagnostic accuracy for an early and reliable diagnosis of intestinal ischemia. The aim of this narrative review is to provide an overview on traditional laboratory tests for diagnosing acute intestinal ischemia (i.e., complete blood count, D-dimer, blood gas analysis, total lactic acid, C-reactive protein and procalcitonin), and summarize current evidence regarding some emerging and potentially useful biomarkers such as D-lactate, intestinal fatty acid-binding protein (I-FABP), ischemia modified albumin (IMA), α-glutathione S-transferase (α-GST), interleukin-6 (IL-6), citrulline and smooth muscle protein of 22 kDa (SM22). Among the various tests, D-lactate, IMA and I-FABP are perhaps the most promising, since they are characterized by optimal sensitivity and relatively good specificity, early kinetics, and can be measured with assays suited for a rapid diagnosis.

It is known that xanthine oxidoreductase contributes significantly to ischemia/reperfusion injury by generating reactive oxygen species. Ischemia-modified albumin (IMA) is a biomarker of acute myocardial ischemia with high sensitivity but moderate specificity. Our study aims to evaluate the xanthine oxidase (XO) system and the IMA level in the serum of patients with ischemic heart disease, and their correlation with traditional cardiac markers. The study was conducted on 60 patients with ischemic heart disease and 22 healthy subjects (control group). Subjects were divided into three groups: group I (30 patients with ST-elevated myocardial infarction), group II (30 patients with chronic stable angina), and the control group (22 subjects). The patients and controls had laboratory tests performed including lipid profile, cardiac enzymes, XO, uric acid, and IMA. The serum levels of XO and IMA were significantly higher in group I (1.65 ± 0.29 U/ml and 0.58 ± 0.15 ABSU, respectively) than in group II (1.11 ± 0.20 U/ml and 0.29 ± 0.10 ABSU, respectively) and the control group (0.95 ± 0.16 U/ml and 0.24 ± 0.08 ABSU, respectively) (P < 0.001). There was a significant positive correlation between XO and IMA in group I. Also, there was significant positive correlation between XO or IMA and other cardiac markers, with the highest level of significance between IMA and creatine kinase (CK-MB). In group II only XO activity was significantly elevated in comparison with controls. These results confirm the role of XO enzyme in ischemic heart disease with involvement of IMA, at a detectable level, during the early necrotic phase.

BACKGROUND

Normal pregnancy is always associated with immense stress in order to accommodate the increasing demands of the developing fetus. Various metabolic changes along with vascular remodeling occur in maternal system. Due to this, pregnancy is always associated with oxidative stress and generation of Reactive Oxygen Species (ROS). Ischemia Modified Albumin (IMA) generated by ROS is found to be sensitive and early biochemical marker of ischemic heart disease and now used as an important marker to distinguish between ischemic and non-ischemic pathologies. Pregnancy being a hypoxic ischemic condition may lead to increase in serum IMA.

OBJECTIVE

The present study was aimed at evaluating maternal serum Ischemia Modified Albumin (IMA) in normal pregnancy and correlate it with serum Malondialdehyde (MDA), a known lipid peroxidation marker. Similarly IMA/Albumin was evaluated for correction of decrease in serum albumin in pregnancy and correlated with serum MDA.

METHODS

Serum IMA, IMA/Albumin and MDA was analysed in 40 healthy normal pregnant women and 41 non-pregnant healthy controls. Serum IMA was estimated by albumin cobalt binding test. Student t-test and Pearson's correlation coefficient was used for statistical analysis.

RESULTS

Serum IMA and IMA/Albumin was significantly higher (p < 0.001) in normal pregnant women (72.54±9.89 U/L, 20.16±3.94) compared to non-pregnant healthy control (48.47±8.30 U/L, 10.51±1.76). Serum MDA was also significantly higher in normal pregnant women. A statistical significant positive correlation was found between serum IMA, IMA/Albumin with MDA in normal pregnant women.

CONCLUSIONS

Maternal serum IMA is also increased in normal pregnancy and its correlation with MDA shows maternal serum IMA, can be considered as the marker of oxidative stress and can be used to monitor the progress of pregnancy, which may be remarkably increased in various complications related to pregnancy.

The objective of this study is to evaluate the possible protective effects of selenium (Se) against cyclophosphamide (CP)-induced acute cardiotoxicity in rats. A total of 42 male Spraque-Dawley rats were divided into six groups (n = 7). Rats in the first group were served as control. Rats in the second group received CP (150 mg/kg) at the sixth day of experiment. Animals in the third and fourth groups were treated with only 0.5 and 1 mg/kg Se respectively for six consecutive days. Rats in the fifth and sixth groups received respective Se doses (0.5 or 1 mg/kg) for 6 days and then a single dose of CP administered on the sixth day. On day 7, the animals were sacrificed; blood samples were collected to measure malondialdehyde (MDA), glutathione (GSH), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and ischemia-modified albumin (IMA) levels. Heart tissues were processed routinely and tissue sections were stained with H + E for light microscopic examination. In the CP-treated rats MDA, LDH, CK-MB, and IMA serum levels increased, while GSH levels decreased. Microscopic evaluation showed that tissue damage was conspicuously lower in CP plus Se groups. Moreover, 1 mg/kg Se was more protective than 0.5 mg/kg Se as indicated by histopathological and biochemical values. In conclusion, Se is suggested to be a potential candidate to ameliorate CP-induced cardiotoxicity which may be related to its antioxidant activity.

The primary study aim was to determine whether ischemia-modified albumin (IMA) predicts adverse outcome in patients attending the emergency department (ED) with acute chest pain. Ischemia-modified albumin is a sensitive marker of myocardial ischemia. However, little is known about its ability to predict outcome in patients presenting to the ED with acute chest pain. We prospectively studied 207 patients who presented to the ED with acute chest pain suggestive of acute coronary syndrome within 3 h of the onset of symptoms. Blood samples for IMA assessment were obtained on admission. We evaluated a 30-day combined end point (cardiac death, myocardial infarction, recurrent angina) and 1-year all-cause mortality. A total of 31 (15%) patients experienced the 30-day composite end point and 16 patients (7.7%) died during the 1-year follow-up. Short-term combined end point (9.6% vs 20.4%, P = 0.03) and 1-year mortality rate (11.7% vs 3.8%, log rank 3.978, P = 0.046) were significantly higher in patients with IMA levels >93.3 U/ml compared to patients with lower IMA. On multivariate analysis, IMA remained an independent predictor of both 30-day combined end point (odds ratio 1.04, 95% confidence interval [CI] 1.01-1.07, P = 0.01) and 1-year mortality (hazard ratio 1.038, 95% CI 1.006-1.070, P = 0.018). Ischemia-modified albumin is an independent predictor of short-and long-term adverse outcomes in patients presenting to the ED with typical acute chest pain.

BACKGROUND

There is little data about the additive effects of ischemia-modified albumin (IMA) on the exercise stress test (EST) used for the screening of ischemic heart disease. The relationship between myocardial ischemic burden and the change in IMA (DeltaIMA) during EST was investigated.

RESULTS

EST was performed using the Bruce protocol to evaluate chest pain or exertional dyspnea in 155 patients (men 89, 53+/-13 years). Blood samples for IMA were obtained before and immediately after EST. According to the EST results and the pattern of DeltaIMA, patients were categorized into 3 groups (none was classified as EST(-)/DeltaIMA(+)): (1) (EST(-); (2) EST(+)/DeltaIMA(-); and (3) EST(+)/DeltaIMA(+). After EST, 60 of 155 (38.7%) patients were EST(+) and 14/60 (23.3%) were EST(+)/DeltaIMA(+). Duke treadmill score was significantly lower in the EST(+)/DeltaIMA(+) group compared with the other groups (-9.0+/-7.9, -1.7+/-4.2, 6.7+/-4.4, respectively, P<0.001); 43/60 (72%) patients with EST(+) underwent coronary angiography and the proportion of patients with a large ischemic burden was higher in the EST(+)/DeltaIMA(+)group compared with the EST(+)/DeltaIMA(-) group (72.7% vs 15.6%, P=0.001).

CONCLUSIONS

Increased IMA after EST suggests a large ischemic burden in coronary artery disease, so the DeltaIMA during EST may be useful for predicting the severity of myocardial ischemia.