BACKGROUND

Among various reactive oxygen species, hydroxyl radicals have the strongest chemical activity, which can damage a wide range of essential biomolecules such as lipids, proteins, and DNA.

OBJECTIVE

The objective of this study was to investigate the beneficial effects of curcumin on prevention of oxidative damage of biomolecules by hydroxyl radicals generated in in vitro by a Fenton like reaction.

METHODS

We have incubated the serum, plasma and whole blood with H2O2/Cu2+/ Ascorbic acid system for 4 hours at 37 0C and observed the oxidation of biomolecules like albumin, lipids, proteins and DNA.

RESULTS

Curcumin at the concentrations of 50,100 and 200 μmoles, prevented the formation of ischemia modified albumin, MDA, protein carbonyls, oxidized DNA and increased the total antioxidant levels and GSH significantly.

CONCLUSIONS

These observations suggest the hydroxyl radical scavenging potentials of curcumin and protective actions to prevent the oxidation of biomolecules by hydroxyl radicals.

Aflatoxin B1 (AFB1) is the most potent of the mycotoxins and is widely observed in nutrition abnormalities. There are some studies suggesting oxidative stress-induced toxic changes on liver related to AFB1 toxicity. The aim of the present study was to evaluate whether antioxidant caffeic acid phenethyl ester (CAPE) relieves oxidative stress in AFB1-induced liver injury in rat. Twenty-four male rats were equally divided into three groups. The first group was used as a control. The second group received three doses of AFB1. The three doses of CAPE were given to constitute the third group with doses of AFB1. After 10 days of experiment, liver and serum samples were taken from all animals. Serum gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), glutathione s-transferase (GST), nitric oxide (NO) and sulfhydryl values were higher in the AFB1 group than in control, whereas serum GGT, ALP, GST and NO values were decreased by in the AFB1 + CAPE group than in AFB1 group. Liver GST, total oxidant capacity, sulfhydryl, apoptosis index and ischemia-modified albumin values were higher in the AFB1 group than in control, whereas the GST activity and apoptosis index were lower in the AFB1 + CAPE group than in the AFB1 group. There were histopathological degeneration and apoptosis in hepatocytes of AFB1 group. The findings were totally recovered by CAPE administration. In conclusion, we observed that AFB1 caused oxidative and nitrosative hepatoxicity to hepatocytes in the rat. However, CAPE induced protective effects on the AFB1-induced hepatoxicity by modulating free radical production, biochemical values and histopathological alterations.

Complex regional pain syndrome type 1 (CRPS1) may be evoked by ischemia/reperfusion, eliciting acute and chronic pain that is difficult to treat. Despite this, the underlying mechanism of CRPS1 has not been fully elucidated. Therefore, the goal of this study is to evaluate the involvement of inflammation, oxidative stress, and the transient receptor potential ankyrin 1 (TRPA1) channel, a chemosensor of inflammation and oxidative substances, in an animal model of chronic post-ischemia pain (CPIP). Male Wistar rats were subjected to 3 h hind paw ischemia/reperfusion (CPIP model). Different parameters of nociception, inflammation, ischemia, and oxidative stress were evaluated at 1 (acute) and 14 (chronic) days after CPIP. The effect of a TRPA1 antagonist and the TRPA1 immunoreactivity were also observed after CPIP. In the CPIP acute phase, we observed mechanical and cold allodynia; increased levels of tumor necrosis factor-α (hind paw), ischemia-modified albumin (IMA) (serum), protein carbonyl (hind paw and spinal cord), lactate (serum), and 4-hydroxy-2-nonenal (4-HNE, hind paw and spinal cord); and higher myeloperoxidase (MPO) and N-acetyl-β-D-glucosaminidase (NAGase) activities (hind paw). In the CPIP chronic phase, we detected mechanical and cold allodynia and increased levels of IMA (serum), protein carbonyl (hind paw and spinal cord), and 4-HNE (hind paw and spinal cord). TRPA1 antagonism reduced mechanical and cold allodynia 1 and 14 days after CPIP, but no change in TRPA1 immunoreactivity was observed. Different mechanisms underlie acute (inflammation and oxidative stress) and chronic (oxidative stress) phases of CPIP. TRPA1 activation may be relevant for CRPS1/CPIP-induced acute and chronic pain.

BACKGROUND

Albumin and α1-acid glycoprotein (AGP) are two of the most abundant proteins found in plasma. Their effect on the pharmacokinetic profile of exogenous compounds has major implications to clinical practice. Recent exploration into their possible role as diagnostic markers underlines their significance, and provides highlights their potential in medicinal applications.

METHODS

This review summarizes the current understanding behind albumin and AGP. Specifically, the review focuses on their structure, physiological function, and their potential use in diagnostics as biomarkers. The article lists and describes the most common methods, with a specific focus on their use in drug design and clinical practice.

CONCLUSIONS

Human serum albumin and AGP play a significant role in clinical practice. Research on human serum albumin and AGP, as potential diagnostic biomarkers, has been so far successful, with the development of novel diagnostic methods for detecting ischemia-modified albumin in cardiac ischemia patients. While research into this particular aspect is still in its infancy, future research should make things somewhat clearer and provide a better insight into the true potential of plasma proteins as a whole.

OBJECTIVE

To determine the prevalence of elevated troponin levels after a marathon, and test for an association with reduced renal clearance.

METHODS

Prospective observational study of entrants running the full (42 km) 2007 Perth Marathon, Western Australia.

METHODS

Elevated troponin levels >> or = 0.1 microg/L) after the race; pre- and post-race survey data, and biochemical parameters.

RESULTS

27% of runners (92/346) enrolled in the study, of whom 88 (96%) completed it. Most were men (71%; 65/92); mean age was 43.1 years (SD, 9.8 years; range, 25-64 years) and mean body mass index (BMI) was 24.1 kg/m(2). Raised troponin levels were seen in 32% of participants (28/88), the highest being 1.4 microg/L. The strongest predictor for developing elevated troponin levels was a decrease in weight (odds ratio [OR], 2.15; 95% CI, 1.27-3.65). Creatinine increase was also associated with elevated troponin levels (OR, 1.03; 95% CI, 1.01-1.06), but pre-race estimated glomerular filtration rate, age, sex, BMI, training factors, marathon experience and race time were not. Most runners (99%; 87/88) had elevated levels of ischaemia-modified albumin after the race.

CONCLUSIONS

Troponin level increases were common among marathon finishers. The strongest predictors were weight loss and an increase in creatinine levels, suggesting that reduced renal clearance is an associated factor. Further study is needed to determine the clinical significance of these findings, and to understand the mechanism.

BACKGROUND

Metabolic syndrome (MetS) is a complex metabolic disease connected especially with lipid and carbohydrate disturbances. It is postulated that oxidative stress (OS) is linked to metabolic syndrome, constituting a novel component of its pathogenesis.

OBJECTIVE

We aimed to examine the plasma level of oxidatively modified proteins--advanced oxidation protein products (AOPP) and ischemia modified albumin (IMA)--as well as thiol (SH) groups and evaluate their connection with metabolic agents in relation to MetS prevalence.

METHODS

The levels of AOPP, IMA and SH groups were measured spectrophotometrically in 106 patients with MetS risk factors and in 32 control subjects.

RESULTS

The levels of examined parameters differed significantly between patients with MetS risk factors and the control group. AOPP significantly correlated with glucose (r = 0.30, p = 0.008), HDL-Ch (r = -0.34, p = 0.005), TG (r = 0.48, p < 0.001) and fibrinogen (r = 0.37, p < 0.001). The levels of AOPP and IMA increased progressively with the number of MetS risk factors, being the most significant for AOPP. The highest values of AOPP were associated with the presence of at least three risk factors. Only AOPP were an independent determinant for MetS occurrence in the studied population (OR = 2.72, p = 0.04). Mutual dependence between metabolic, oxidative stress and inflammatory parameters was revealed.

CONCLUSIONS

Oxidative modifications of proteins are increased in MetS and accumulation of MetS risk factors enhances manifestation of OS. AOPP is the most appropriate parameter for determination of OS, with potential diagnostic value in MetS patients.

The aim of this study was to evaluate ischemia-modified albumin levels (IMA) in polycystic ovary syndrome (PCOS) cases with and without insulin resistance and the correlation of IMA with carotid intima media thickness, homocysteine, and high-sensitivity C-reactive protein levels. Significantly higher levels of IMA in young lean PCOS cases, more relevant in insulin resistant cases, indicates chronic hypoxia and oxidative stress which might play a role in the metabolic consequences in PCOS.

OBJECTIVE

To investigate the protective effect of quercetin (QE), an anti-inflammatory and anti-oxidant agent, on torsion-detorsion induced histopathological changes and blood IMA levels in experimental ovarian ischemia-reperfusion (IR) injury.

METHODS

Twenty-four female Wistar rats were randomly divided into four groups in this study (n=6). Group I, (sham operation); Group II, torsion-detorsion plus saline (IR); Group III, torsion-detorsion plus solvent (dimethylsulfoxide: DMSO, IR+DMSO); Group IV, torsion-detorsion plus 15 mg/kg/bw quercetin (IR+QE) injected intraperitoneally 30 min prior to detorsion. After 3h of reperfusion, the right ovaries were removed surgically. The ovary tissue samples were fixed in 10% formalin solution for histopathological and immunohistochemical examination. Blood samples were obtained at the end of the procedures for each group of animals.

RESULTS

Ovarian sections in Groups II and III showed higher follicular cell degeneration, hemorrhage, vascular congestion and edema when compared with Group I. Administration of quercetin in rats significantly prevented degenerative changes in the ovary. Significantly less histopathological changes were found in Group IV compared with Groups II and III. Caspase-3 and TUNEL positive cells were detected in the ovarian surface, follicle epithelium, and stromal cells in all experimental groups, and there was a significant increase in Groups II and III compared with Group I (P<0.05). Treatment with quercetin decreased the number of caspase-3 and TUNEL positive cells. IR increased the ischemia modified albumin (IMA) levels in comparison to the sham group (1.06 ± 0.10 ABSU and 0.92 ± 0.08 ABSU, P<0.05). Quercetin administration before IR reduced the levels of IMA (0.93 ± 0.08 ABSU, P<0.05).

CONCLUSIONS

Administration of quercetin is effective in preventing tissue damage induced by IR injury in ovaries.

The primary objective of this prospective dose-finding pilot study is to demonstrate the tolerability and safety of four dosages of 25% human albumin in patients with subarachnoid hemorrhage (SAH). For each dosage group, the study will enroll 20 patients who meet the eligibility criteria. The enrolled patients will undergo follow-up for 90 days post-treatment. The primary tolerability hypothesis is that intravenous 25% human albumin can be given without precipitating treatment related serious adverse events beyond expectations. The study will determine the maximum tolerated dosage of 25% human albumin therapy based on the rate of treatment related serious adverse events during treatment: severe or life-threatening heart failure. The secondary objectives are to obtain preliminary estimates of the albumin treatment effect using the incidence of neurological deterioration within 15 days after symptom onset. In addition, the incidence of rebleeding, hydrocephalus, seizures, delayed cerebral ischemia and the incidence of vasospasm (both symptomatic and by transcranial Doppler ultrasound criteria) within 15 days after symptom onset will be evaluated. Furthermore, the serum osmolality and serum albumin concentrations, serum magnesium concentration, blood pressure and heart rate within 15 days of symptom onset will also be observed. The Glasgow Outcome Scale, Barthel Index, modified Rankin Scale, NIH Stroke Scale, and Stroke Impact Scale will be performed 3 months after the onset of symptoms to assess residual neurological deficits.

BACKGROUND

Diagnosis of cardiac ischemia in patients attending emergency department with symptoms of acute coronary syndrome (ACS) is often difficult. Biochemical tests like cardiac troponin (cTnI/T) and CK-MB may not rise during reversible myocardial ischemia. Previous reports suggest that oxidative damage due to ischemic conditions rapidly modifies human serum albumin and reduce its capacity to bind exogenous cobalt. Ischemia modified albumin (IMA) has shown to be a sensitive and early biochemical marker.

OBJECTIVE

To validate the use of IMA albumin as a diagnostic test for ischemic heart disease and compare its efficacy with CK-MB and cTnI.

METHODS

Four sequential samples from 25 patients admitted to MICU, TASH were tested for IMA. Thirty addiional samples from healthy volunteers were assayed to establish the reference range of IMA. Patients were classified as AMI and non-AMI groups based on the clinical presentation, ECG and echocardiography findings. Colorimetrically assayed parameters included: total protein, albumin, urea, creatinine, CKT and IMA.

RESULTS

High number of male patients with old age were diagnosed as having AMI. Mean IMA levels were increased in patients with ACS compared to the control group and patients with Non-AMI. The mean +/- SEM value of IMA for the patient group was 83.0 +/- 6.6, which is significantly higher (p = 0.0001) than the control group with mean IMA 26.0 +/- 1.2. IMA has demonstrated a sensitivity and specificity of 100% and 85.3% respectively, and an area under the receiver operator characteristics (ROC) curve as 0.948 (95% confidence interval (CI): 0.914-0.983. The overall efficacy of IMA in differentiating AMI from Non-AMI cases appears to be comparable to that of CK-MB and cTnI.

CONCLUSIONS

The IMA Test can be assayed by simple and quick method, which may serve as a useful diagnostic tool for the assessment of myocardial ischemia/infarct.

The measurement of cardiac troponins has emerged as the biochemical "gold standard" for the diagnosis and management of patients with acute chest pain. However, earlier markers should support investigation strategies, as several patients with acute coronary syndrome might present with non-diagnostic concentrations. Ischemia-modified albumin (IMA), measured by the albumin cobalt binding (ACB) assay, was recently proposed for early detection of myocardial ischemia. To establish the potential influence of endurance training on the diagnostic approach to patients with suspected myocardial injury, cardiac troponin T (cTnT), creatine kinase isoenzyme MB (CK-MB), myoglobin and IMA were evaluated in healthy individuals subjected to different aerobic workloads. The concentrations of both IMA and CK-MB were significantly increased in athletes subjected to high-workload endurance training, whereas the concentration of cTnT and myoglobin was not influenced by physical exercise in the medium term. Taken together, our results demonstrate that demanding aerobic physical activity might influence the generation of IMA, which might be increased in the medium term following high-workload endurance training, while the concentration of other conventional markers of myocardial injury remains non-diagnostic.

OBJECTIVE

This experimental study aimed to assess the changes in the levels of serum ischemia-modified albumin (IMA) and interleukin-6 (IL-6) by time in cases of acute mesenteric ischemia due to superior mesenteric artery occlusion.

METHODS

Twenty-one New Zealand rabbits were randomly divided into three groups. Blood samples were collected at hours 0, 1, 3, and 6 from animals in a control group; a sham group following a simple laparotomy; and in an ischemia group following superior mesenteric artery ligation. All blood samples were analyzed for serum IMA and IL-6 levels, and then the time-dependent changes of biomarkers were investigated.

RESULTS

The serum IMA levels of the ischemia group at hours 3 and 6 were significantly higher than those of the control and sham groups (hour 3, p = 0.017; hour 6, p = 0.001). The increase in serum IL-6 levels in the ischemia group at hours 1, 3, and 6 compared to the control and sham groups was also significant (hour 1, p = 0.002; hour 3, p = 0.003; hour 6, p = 0.003).

CONCLUSIONS

IMA may be helpful as a marker in the diagnosis of acute mesenteric ischemia; however, its diagnostic value and use as a routine biochemical test should be assessed in further studies.

BACKGROUND

Ischemia-modified albumin (IMA) has been shown to be a rapidly rising and sensitive biochemical marker for the diagnosis of myocardial ischemia. In this study, we evaluated the levels of IMA in myocardial infarction and prostate diseases, as well as the influence of HDL cholesterol levels on C-reactive protein (CRP) and IMA levels.

METHODS

A total of 27 patients with myocardial infarction (MI), 102 patients with benign prostatic hyperplasia (BPH), 84 patients with prostate cancer (PCA), and 21 healthy subjects were enrolled in this study. IMA levels were measured in whole studied patients. Cardiac troponin I (cTnI), cholesterol, HDL cholesterol, and CRP were measured in MI and control groups.

RESULTS

IMA values were significantly higher in patients with MI (0.5215+/-0.0241 ABSU) and BPH (0.4150+/-0.0156 ABSU) in comparison to control subjects (0.3381+/-0.0194 ABSU). IMA and CRP were higher in MI group, especially in patients with HDL cholesterol levels lower than 38 mg/dL. The ability of IMA to discriminate myocardial infarction was higher than CRP. Significant correlations between CRP and HDL, CRP and IMA, and HDL and IMA were reported.

CONCLUSIONS

IMA and CRP increase in myocardial damage, and the decrease of HDL cholesterol appears to enhance the inflammatory response. IMA also increase in benign prostate hyperplasia and this finding suggests that the diagnosis of prostate diseases must be considered on evaluation of IMA as a marker of cardiac ischemia.

BACKGROUND

Ischaemia is a common phenomenon in the pathogenesis of a wide range of medical and surgical conditions, including myocardial infarction, mesenteric vascular occlusion and compartment syndrome. Ischaemia modified albumin has been suggested as an aid to clinical decision making in various clinical settings. This study examines the usefulness of IMA in the diagnosis of limb ischaemia (LI).

METHODS

This case-controlled study was performed in the emergency department of Karadeniz Technical University Hospital, Turkey. 22 patients presenting to the emergency departments and definitively diagnosed with LI were enrolled in the study. A control group of 22 healthy volunteers served as a reference for biochemical parameters.

RESULTS

The mean serum IMA level for LI patients was 0.295 (SD 0.062) ABSU. The mean serum IMA level for control patients was 0.174 (SD 0.061) ABSU. There was a statistically significant difference between the mean LI patient and mean control patient IMA levels (p<0.0005). A ROC curve analysis reveals the relationship between sensitivity and specificity for IMA in limb ischaemia.

CONCLUSIONS

There is a significant increase in serum IMA in limb ischaemia. Furthermore, using a cutoff of 0.22 ABSU, ROC curve analysis shows that IMA is 81.8% sensitive and 81.8% specific 81.8% in patients with clinically severe lower limb ischaemia. Future studies would be needed to determine if IMA would be clinically useful in the diagnosis of subtle limb ischaemia.

The aim of this study was to clarify how collagen deposition or medial hypertrophy of the vascular wall affects the coronary dilator reserve in pressure-overloaded hearts and whether inhibition of collagen deposition reverses the abnormalities after relief of pressure overload. We used ascending aortic banding and debanding methods and superimposed beta-aminopropionitrile in some of the banded rats (50 mg/kg i.p., twice a day). Ten weeks of banding increased in vivo peak systolic left ventricular pressure and produced medial hypertrophy, an increase in collagen deposition in the myocardial and perivascular tissues, and myocardial hypertrophy in the banded group without beta-aminopropionitrile treatment. Superimposition of beta-aminopropionitrile treatment on banding inhibited the increase in collagen deposition. In the groups debanded after the 10-week banding period, both with and without beta-amino-propionitrile treatment, medial and myocardial hypertrophy regressed 4 weeks after debanding. We estimated coronary dilator reserve in Langendorff preparations perfused with modified Tyrode's solution containing oxygenated bovine red blood cells and serum albumin. The ratio of reactive peak flow after brief ischemia-to-resting flow decreased in both of the banded groups. After debanding, the ratio remained lower in the banded group without beta-aminopropionitrile treatment than in the control group. However, debanding in the group with beta-aminopropionitrile treatment increased the ratio to a level similar to that of the control group. Thus, in pressure-overloaded cardiac hypertrophy with coronary hypertension, coronary reserve seems to be determined by medial hypertrophy independently of collagen deposition, but collagen deposition plays an important role in the reversal of vasodilator reserve after relief of the overload.

Overt hypothyroidism and subclinical hypothyroidism are thought to be associated with atherosclerosis and a chronic ischemic process. Ischemic modified albumin (IMA) is a novel marker of ischemia. We examined serum IMA levels in patients with subclinical and overt hypothyroidism. We recruited patients who presented to our clinic for thyroid disease control. We compared demographic data, fasting blood sugar, serum lipid levels, and the prevalence of metabolic syndrome by the presence of overt, subclinical, and no hypothyroidism. Cobalt binding to albumin capacity was analyzed using a rapid colorimetric technique and compared among the groups. We assessed 11 men and 74 women with a mean age of 39.9 ± 12 years. Of these, 48 (56.5 %) were euthyroid, 24 (28.2 %) had subclinical hypothyroidism, and 13 (15.3 %) had overt hypothyroidism. The groups did not differ significantly in terms of age; body mass index; waist circumference; systolic and diastolic blood pressures; levels of fasting and nonfasting blood sugar, high- and low-density lipoproteins, and triglycerides; and the presence of metabolic syndrome. Mean serum IMA level also did not differ significantly among the groups: 0.20 ± 0.08 absorbance units (ABSU) in the euthyroid participants, 0.18 ± 0.08 ABSU in those with subclinical hypothyroidism, and 0.20 ± 0.09 ABSU in those with overt hypothyroidism (P = 0.754). Mean IMA values did not differ significantly by sex, cigarette use, the presence of metabolic syndrome, or the presence of thyroid autoantibodies. Serum IMA levels did not differ among patients with overt or subclinical hypothyroidism in this case-control study.

OBJECTIVE

The primary aim of this study was to investigate whether IMA levels are helpful in the diagnosis of pulmonary embolism (PE). The secondary aim was to determine whether IMA was more effective alone or in combination with clinical probability scores in the diagnosis of PE. Thirdly, the sensitivity and specificity of IMA is compared with D-dimer both with and without clinical probability scores in patients with suspected PE.

METHODS

Consecutive patients presenting to the emergency department with suspected PE were prospectively recruited, and healthy volunteers were also enrolled as controls. D-dimer and IMA levels were measured for the entire study group. Wells and Geneva scores were calculated and s-CTPA was performed on all suspected PE patients.

RESULTS

The study population consisted of 130 patients with suspected PE and 59 healthy controls. Mean IMA levels were 0.362 +/- 0.11 ABSU for Group A, the PE group (n = 75); 0.265 +/- 0.07 ABSU for Group B, the non-PE group (n = 55); and 0.175 +/- 0.05 ABSU for Group C, the healthy control group (p < 0.0001). At a cut-off point of 0.25 ABSU, IMA was 93% sensitive and 75% specific in the diagnosis of PE. PPV was 79.4% and NPV was 78.6%. Mean D-dimer levels were 12.48 +/- 10.88 microg/ml for Group A; 5.36 +/- 7.80 microg/ml for Group B and 0.36 +/- 0.16 microg/ml for Group C (p < 0.0001). The D-dimer cut-off point was 0.81 microg/ml with a sensitivity of 98.9% and a specificity of 62.7%, PPV of 69.4% and NPV of 83.3%. The use of IMA in combination with Wells and Geneva clinical probability scores was determined to have a positive impact on these scores' sensitivity and negative predictive values.

CONCLUSIONS

IMA is a good alternative to D-dimer in PE diagnosis in terms of both cost and efficiency. Used in combination with clinical probability scores, it has a similar positive effect on NPV and sensitivity to that of D-dimer. The PPV of IMA is better than D-dimer, but it is still unable to confirm a diagnosis of PE without additional investigation.

Cardiovascular disease is the leading cause of mortality and morbidity in Western countries. Despite its remarkable medical and social consequences, the prevalence of peripheral arterial disease (PAD) is often underestimated among atherosclerotic disorders. So far, little is known about the behavior of traditional and emerging markers of ischemic heart disease that should allow the reliable identification of PAD patients at increased risk of developing myocardial ischemia and heart failure or dysfunction. To investigate this topic, we measured cardiac troponin T (cTnT), ischemia-modified albumin (IMA) and NT-prohormone-brain natriuretic peptide (NT-proBNP) in 35 consecutive patients with clinically ascertained PAD (stage 2-4, according to Lériche-Fontaine) asymptomatic for chest pain and current heart failure, and 20 controls displaying moderate to high cardiovascular risk factors (hypertension, diabetes, hyperlipidemia), but with no clinical evidence of PAD. Although the concentrations of cTnT and IMA were not statistically increased in PAD patients, NT-pro-BNP values were substantially higher in PAD patients than in controls (62.6 vs. 7.4 pmol/L, p<0.0001). The percentage of subjects displaying values exceeding the specific NT-proBNP diagnostic threshold (>14.8 pmol/L) was also significantly different between PAD patients and controls (74% vs. 10%, p<0.001). After excluding PAD patients exceeding the 0.01 ng/mL cTnT cutoff value indicative of current ischemic cardiac involvement, the median concentration of NT-proBNP remained statistically increased (28.0 vs. 5.8 pmol/L, p<0.0001). Taken together, these results indicate that NT-proBNP, but not IMA, is substantially increased in PAD patients. This finding suggests that such patients, even though asymptomatic, might develop myocardial dysfunction, and thus warrant further investigation.

OBJECTIVE

Ischemia-modified albumin (IMA) is a novel marker for diagnosis of myocardial ischemia and it is considered as a serum marker. The aim of the study was to evaluate salivary IMA levels in patients with acute myocardial infarction (AMI) and to determine the relation between serum and salivary IMA levels.

METHODS

A total of 60 patients with AMI and 40 control subjects who are age and sex matched with AMI group were included in our study. The diagnosis of AMI was based on the WHO classification criteria. All patients underwent the clinical assessment, consisting of electrocardiography, and serum cardiac markers. Serum and salivary IMA levels were measured at the first and second days of AMI by using a colorimetric method.

RESULTS

Serum IMA levels were significantly higher in the first and second day of AMI patients, however, salivary IMA levels were significantly higher in the first day of AMI patients compared to the control (P < 0.05). There was a positive correlation between salivary IMA levels and serum IMA levels both in the first and second day of AMI patients (r = 0.298, P < 0.05; r = 0.319, P < 0.05, respectively).

CONCLUSIONS

We concluded that salivary IMA levels at the first day of AMI could be used as an alternative marker to serum IMA levels for diagnosis of AMI.

OBJECTIVE

We designed this experimental study to determine the value of ischemia-modified albumin in the diagnosis of pulmonary embolism.

METHODS

Twenty-four mature female New Zealand rabbits were divided into 4 groups, each consisting of 6 animals. These were classified into group 1 ,the control group; group 2, the deep venous thrombosis group; group 3, the deep venous thrombosis with pulmonary embolism group; and group 4, the pulmonary embolism-alone group. Deep venous thrombosis was produced by ligation of the iliac vein. To establish pulmonary embolism, 2 clots were administered from the iliac vein. Blood samples were taken from all the groups at hours 0, 1, 3, and 6 for ischemia-modified albumin measurement.

RESULTS

Pulmonary embolism was established in all the rabbits in groups 3 and 4, and this was confirmed by tomographic and histologic findings. Measurement of mean ischemia-modified albumin levels for all rabbits at hours 0, 1, 3, and 6 revealed that mean ischemia-modified albumin levels in groups 3 and 4 were statistically significantly higher than those in groups 1 and 2. There was no difference between the mean ischemia-modified albumin levels in groups 1 and 2 nor between groups 3 and 4. The alteration in ischemia-modified albumin levels over time was statistically significant.

CONCLUSIONS

The results of our experimental study demonstrate that ischemia-modified albumin levels may be useful in the diagnosis of pulmonary embolism.

BACKGROUND

To investigate whether serum ischemia-modified albumin or C-reactive protein is reliable for predicting type 2 diabetic patients with ketosis.

METHODS

One hundred and four diabetic patients, 48 with diabetic ketosis, and 33 controls were enrolled in the study. Serum ischemia-modified albumin and C-reactive protein were measured and evaluated for their ability to distinguish diabetic ketosis.

RESULTS

Compared to the controls, the ischemia-modified albumin and C-reactive protein levels were higher in patients with diabetic ketosis and type 2 diabetes at the baseline. The levels of ischemia-modified albumin were higher in patients with type 2 diabetes than in the controls. C-reactive protein and ischemia-modified albumin levels were reduced after insulin treatment. The level of ischemia-modified albumin was an independent risk marker for diabetic ketosis (OR = 1.085, P = 0.008, 95% CI: 1.022-1.152). Receiver operating characteristic curves revealed that the areas under the curve were 0.917 for the modified albumin and 0.357 for C-reactive protein.

CONCLUSIONS

This study indicates that ischemia-modified albumin was significantly associated with diabetic ketosis and was more sensitive than C-reactive protein in reflecting diabetic ketosis.

BACKGROUND

Ischemia-modified albumin (IMA) has been proposed as a useful rule-out marker for the diagnosis of acute coronary syndrome (ACS) in the emergency department. This study evaluated the ability of IMA to predict the acute myocardial infarction (AMI) diagnosis in a population of chest pain patients.

METHODS

The study population comprised 107 subjects (men, 62%; women, 38%) admitted with suspected ACS. None of the patients had ST-segment elevations that qualified for immediate revascularization. Ischemia-modified albumin was determined from serum with albumin cobalt binding test (Inverness Medical Innovations Inc, Stirling, UK). Furthermore, cardiac troponin T, creatinine kinase MB mass, myoglobin, and heart-type fatty acid binding protein (H-FABP) were determined on arrival, after 6 to 9 hours, and after 12 to 24 hours. All patients had at least 2 blood samples taken to exclude/verify the AMI. AMI was defined by a cardiac troponin T level greater than 0.03 microg/L.

RESULTS

Thirty-three percent of the patients (n = 35) had a final diagnosis of AMI. The sensitivity of admission IMA for a final diagnosis of ACS was 0.86 (95% confidence interval [95% CI], 0.69-0.95). Specificity was 0.49 (95% CI, 0.36-0.60). Negative predictive value was 0.88 (95% CI, 0.72-0.95). The optimal cutoff threshold derived from the receiver operating characteristics (ROC) curve (ROC analysis) was determined as 91 U/mL. The area under the ROC curve was 0.73. Ischemia-modified albumin did not, at any time, provide superior sensitivity or specificity compared with other biomarkers. We do not find the data supportive of IMA as a standard marker in the emergency department.

Ischemia-modified albumin is the first biomarker for myocardial ischemia to be approved by the FDA. Other markers are being evaluated such as free fatty acids, pregnancy-associated plasma protein-A, glycogen phosphorylase isoenzyme BB, sphingosine-1-phosphate and whole blood choline. This area of clinical research will continue to grow, given the importance of detecting myocardial ischemia. Which marker or combination of markers will, ultimately, be the best approach awaits further research.