Diagnostic accuracy of heart fatty acid binding protein (H-FABP) and glycogen phosphorylase isoenzyme BB (GPBB) in diagnosis of acute myocardial infarction in patients with acute coronary syndrome

Introduction:

This study aimed to assess whether heart fatty acid-binding protein (H-FABP) and glycogen phosphorylase isoenzyme BB (GPBB) could be used for the accurate diagnosis of acute myocardial infarction (AMI) in acute coronary syndrome (ACS) patients.

Materials and methods:

The study included 108 ACS patients admitted to a coronary unit within 3 h after chest pain onset. AMI was distinguished from unstable angina (UA) using a classical cardiac troponin I (cTnI) assay. H-FABP and GPBB were measured by ELISA on admission (0 h) and at 3, 6, 12, and 24 h after admission; their accuracy to diagnose AMI was assessed using statistical methods.

Results:

From 92 patients with ACS; 71 had AMI. H-FABP and GPBB had higher peak value after 3 h from admission than cTnI (P = 0.001). Both markers normalized at 24 h. The area under the receiver operating characteristic curves was significantly greater for both markers in AMI patients than in UA patients at all time points tested, including admission (P < 0.001). At admission, the H-FABP (37%) and GPBB (40%) sensitivities were relatively low. They increased at 3 and 6 h after admission for both markers and decreased again after 24 h. It was 40% for H-FABP and approximately 2-times lower for GPBB (P < 0.01). In AMI patients, both biomarkers had similar specificities, positive- and negative-predictive values, positive and negative likelihood ratios, and risk ratios for AIM.

Conclusion:

H-FABP and GPBB can contribute to early AMI diagnosis and can distinguish AMI from UA.     

Evaluation of clinical utility of serum enzymes and troponin—T in the early stages of acute myocardial infarction

Laboratory infarction diagnostics are based on the detection of elevated serum activities of total Creatine Kinase (CK), Creatine Kinase isoensyme MB, (CKMB), Lactate dehydrogenase (LDH), isoenzyme forms of LDH and transaminases. Determination of these cardiac marker enzymes permits a highly sensitive diagnosis of transmural myocardial infarction. In such patients the diagnosis of acute myocardial infarction can be confirmed by the clinical, symptoms, and changes in the ECG in addition to the enzyme assays. The 50 AMI patients selected in the present study were those admitted to the ICCU of Shri Krishna Hospital, Karamsad. The blood samples were taken at the time of admission (ie. within four hours of the start of chest pain). The samples were analyzed for CK, CKMB, SGOT, (Serum glutamate oxaloactate transaminase) αHBDH α-hydroxybutyrate dehydrogenase and troponin T. The serum CKMB activity in AMI showed an increase only 5–6 hours after the commencement of chest pain. The elevation in SGOT and αHBDH was still delayed. At the same time we could observe that the cardiac Troponin T (cTnT) was elevated at the time of admission of the patient itself. This increase of cTnT in AMI patients was 20 times higher than the normal blood donors. The controls included 25 normal blood donors and 25 patients with polytraumatic injuries with no chest contusion. The study shows that cTnT estimation could serve in the early diagnosis of AMI. The increase of cardiac troponin T in AMI patients was 20 times higher than the normal blood donors in AMI patients at the time of admission. Cardiac troponin T in serum appears to be a more sensitive indicator of myocardial cell injury than CKMB activity and its detection in the circulation may be a useful prognostic indicator in patients with unstable angina as well. When the blood of normal blood donors or that of patients with polytraumatic injury was analysed the troponin T values were well within the normal range in both the above categories showing that cardiac troponin T is highly specific for heart tissue. Although CKMB and cardiac troponin T are released soon after the myocardial injury, the release of cardiac troponin T is much earlier than CKMB thereby invalidating the important role of cardiac troponin T in diagnosing AMI. Cardiac troponin T has been shown to be highly sensitive for cardiac injury and not elevated in any other trauma, heavy exercise or skeletal muscle injury. Cardiac troponin T is ordinarily undetectable in healthy individuals, and so its measurement can serve as a powerful tool in the diagnosis of AMI.     

Heart-Type Fatty Acid-Binding Protein,in Early Detection of Acute Myocardial Infarction: Comparison with CK-MB,Troponin I and Myoglobin

The study aimed to investigate whether heart-type fatty acid binding protein (H-FABP) measurement provides additional diagnostic value to that of conventional cardiac markers in acute myocardial infarction (AMI) within first 6 h after the onset of symptoms. The study included 120 subjects: 60 AMI cases and 60 age and sex matched controls. The cases and controls were further divided into 2 subgroups depending on the time since onset of chest pain as (1) subjects within 3 h and (2) between 3 and 6 h of onset of chest pain. In all the cases and controls, serum H-FABP concentration was measured by Immunoturbidimetric method, serum Troponin I and myoglobin concentrations by Chemiluminescence immunoassay and serum CK-MB concentration by Immuno-inhibition method. The sensitivity, specificity, positive and negative predictive values of H-FABP were significantly greater than CK-MB and myoglobin but were lesser than Troponin I in patients with suspected AMI in both within 3 h and 3–6 h groups. Receiver operating characteristic curves demonstrated greatest diagnostic ability for Troponin I (AUC = 0.99, p < 0.001) followed by H-FABP (AUC = 0.906, p < 0.001) within 3 h and 3–6 h after the onset of chest pain. In conclusion, the diagnostic value of H-FABP is greater than CK-MB and myoglobin but slightly lesser than troponin I for the early diagnosis of AMI within first 6 h of chest pain. H-FABP can be used as an additional diagnostic tool for the early diagnosis of AMI along with troponin I.     

β-Adrenoreceptor Agonist Isoproterenol Alters Oxidative Status,Inflammatory Signaling,Injury Markers and Apoptotic Cell Death in Myocardium of Rats

Sustained high levels of circulating catecholamines are reported to induce cardiotoxicity. Isoproterenol (ISP), a synthetic catecholamine has been widely employed to induce myocardial injury, though the role of inflammation and apoptosis is not well established. This study was designed to investigate the underlying mechanism of oxidative damage, inflammatory signaling, cell death in ISP induced myocardial infarction in rats. Wistar albino rats were divided in two groups: group I (sham control) and group II (ischemic control). ISP (85 mg/kg, s.c.) was administered at an interval of 24 h to group II for two consecutive days. On day third, after 48 h of the first injection of ISP, blood was collected from retro orbital plexus of rat eyes to estimate the biochemical parameters. Glutathione (GSH) and superoxide dismutase (SOD) were measured for antioxidant status. Similarly, malondialdehyde (MDA) was measured as an index of lipid peroxidation. Cardiac markers (SGOT, CK-MB, TropI and LDH) and pro-inflammatory cytokines (IL-6, CRP and TNF-α) were also estimated in ISP-induced rats. At the end of experiments animals were sacrificed for histopathological studies. GSH and SOD showed significant decrease after ISP challenge as compared to sham (control) group (p < 0.01) while MDA level, increased significantly (p < 0.01). ISP, also increased the level of cardiac markers and markers of inflammation significantly (p < 0.01), which was further verified by histopathological studies of the heart tissues. The study confirmed that ISP causes detrimental changes in the myocardium by altering cardiac and inflammatory markers, which leads to severe necrosis. The deleterious effects produced by ISP substantiate its suitability as a novel animal model for evaluation of cardioprotective agents/drugs.     

Genetic Polymorphism of Angiotensin II Type 1 Receptors and Their Effect on the Clinical Outcome of Captopril Treatment in Arab Iraqi Patients with Acute Coronary Syndrome (Mid Euphrates)

Genetic variation in the angiotensin II type 1 receptor (AT1R) has an important effect on the outcome of acute coronary syndrome (ACS) initiated treatment with captopril. This study aims to investigate the impact of genetic polymorphism of AT1R (rs5186 and rs275651) on the ACS outcome in Iraqi patients treated with captopril. A total of 250 Iraqi individuals with ACS were included in this case—control study and they were divided into two study groups; Study group 1 included 125 participants who were prescribed captopril, 25 mg twice daily and study group 2 included 125 participants who received no captopril as part of their ACS treatment (control study). The AT1R gene (rs5186) CC genotype was found to be associated with ST-elevation myocardial infarction (STEMI) (Odd’s ratio (O.R) = 1.2, P = 0.7), while AC was associated with Non-ST-elevation myocardial infarction (NSTEMI) and unstable angina (UA) (O.R = 1.2, P = 0.8). AC genotype is more prone to have Percutaneous coronary intervention (PCI) after ACS attack (O.R = 1.2, P = 0.6). CC genotype had a risk to get less improvement (O.R = 1.6, P = 0.5), so might require higher doses of captopril during acute coronary insult. The AT1R gene (rs275651) AA genotype was associated with UA (O.R = 1.3, P = 0.9). AA and AT genotypes were more prone to have PCI after ACS attack (O.R = 3.9 P = 0.2, O.R = 3.5, P = 0.3 respectively) and thus requiring higher doses of captopril. We conclude that the AT1R rs5186, rs275651 genetic polymorphisms might partially affect the clinical outcome of ACS patients treated with captopril and might have captopril resistance which requires higher doses.     

Association of Elevated Serum Uric Acid with the Components of Metabolic Syndrome and Oxidative Stress in Abdominal Obesity Subjects

Abdominal obesity (AO) and metabolic syndrome (MetS) are associated with the cardiovascular disease and type 2 diabetes. Serum uric acid (SUA) is often elevated in subjects with the AO. We aimed to investigate the association of elevated SUA with the components of MetS, oxidative stress and TG/HDL-C ratio in AO subjects. This cross-sectional study used data from a Health Survey for Prevention of Hypertension and Type 2 Diabetes Mellitus in residents of two districts in Phitsanulok province, including 443 subjects. Anthropometric, blood pressure (BP) and biochemical variables were measured. We categorized the participants to two-group as 248 AO subjects (median age = 58, interquartile range 50.0–65.0 years) and 195 non-AO subjects (median age = 53, interquartile range 47.0–62.0 years). Waist circumference was significantly correlated with SystBP, DiastBP, Glu and SUA (P < 0.05) and SUA was significantly correlated with Glu, TG, HDL-C and TG/HDL-C ratio (P < 0.05). By using multiple logistic regression, we found the association of elevated SUA with abdominal obesity, hyperglycemia, hypertriglyceridemia, reduced HDL-C, elevated TG/HDL-C ratio, MetS and increased oxidative stress after adjusting for their covariates. Our study demonstrated that circulating UA is a major antioxidant and might help protect against free-radical oxidative damage. However, elevated SUA concentrations associated with oxidative stress, MetS, insulin resistance, and components of MetS. Then, SUA may be a marker of increased oxidative stress, insulin resistance and MetS, implying an increased risk of vascular disease and T2DM.     

Anomalous Activity Measurements of Creatine (Phospho) Kinase,CK-MB Isoenzyme in Indian Patients in the Diagnosis of Acute Coronary Syndrome

In the present study, the cause of suspected false-positive (anomalous) values for CK-MB activity, in Indian patients investigated for ACS. Total serum CK and CK-MB activity, serum Troponin I were measured and CK-MB as a percentage of the total CK activity (%CK-MB) calculated. CK-MB was also estimated using densitometry and CK-MB mass assay. Anomalous specimens were tested for the presence of CK isoenzymes. In 22 healthy subjects, 11 male and female, the %CK-MB ranged from 3.6 to 30.2. In 11 male patients, with proven ACS, the %CK-MB was from 4.0 to 17.5. The cut off for anomalous CK-MB activity values was set as >33.0%. In 35 patients with anomalies, total CK values ranged from 39 to 231 U/L, CK-MB from 30 to 161 U/L. Investigation of CK isoenzymes, showed 10 patients had a CK-BB band, 14 an intermediate band between CK-MM and CK-MB (macro-CK type 1), 7 had a cathodal band (macro-CK type 2), and 3 had a band intermediate between CK-MB and CK-BB. This later band does not seem to have been previously reported. Against the CK-MB mass assay, the activity assay showed no correlation, in 43 patients (19 M, 24 F), Pearson coefficient (R²) was 0.006. The CK-MB immunoinhibition assay is better described as measuring “non-CK-MM activity.” A %CK-MB activity >6% as a marker of ACS is not valid in our patient population. Laboratories should not use only CK-MB activity as a biochemical marker of ACS.     

Evaluation of Oxidative Stress and hsCRP in Polycystic Ovarian Syndrome in a Tertiary Care Hospital

PCOS is a heterogeneous endocrine disorder with diverse clinical presentation. Oxidative stress plays a key role in the pathophysiology of this disease. Serumhigh sensitive C-reactive protein (hsCRP), a marker of chronic low grade inflammation, is indicative of future development of cardiovascular disease. Our aim is to evaluate the oxidant status and hsCRP levels in PCOS. The study involved 61 cases and 61 controls in the age group of 18–40 years diagnosed with PCOS. Erythrocyte malondialdehyde (MDA), superoxide dismutase (SOD), serum hsCRP, gonadotrophins, thyroid stimulating hormone, prolactin, glycemic status and lipid profile were estimated. Erythrocyte MDA (p < 0.001), SOD (p = 0.007) and serum hsCRP (p < 0.001) were significantly elevated in PCOS patients than controls. Oxidative stress is present in women with PCOS along with elevated hsCRP.     

Diagnosis of acute myocardial infarction: CK-MB versus cTn-T in Indian patients

The comparative diagnostic efficacy of two cardiac markers: CK-MB and cTn-T, has scarcely been investigated in Indian patients of acute myocardial infarction. The present study was conducted for the same objective. The present study comprised of 59 patients. Males were 44 (75%) and females were 15 (25 %). The age of patients ranged from 32–84 years with mean age of 62.8 yrs. The mean age of males and females were 60 and 63 yrs respectively. All patients presented with history of chest pain with a 12 leads ECG proven MI (ST Elevation, discordant T-waves). CK-MB was estimated in peripheral blood samples at 0,24,48 and 72 hours by an autoanalyzer. Following 12 hours of admission bed side Troponin-T test was done employing cTn-T marker kit. Initially (0 hr), in 50% patients CK-MB was elevated. By end of 24 hours all the patients were CKMB positive and peak level was attained at 24 hrs. Then it tended to decline over next 48 hrs. There were no false positive or negative results. The cTn-T test was positive only in 22 % of ECG positive infarctions. However, the cTn-T positive cases were always accompanied by a higher CK-MB levels. A significantly lower cTn-T positive cases in Indian patients can only be attributed to some difference in amino acid sequence of Indian cTn-T and occidental cTn-T. A larger study from other Indian cardiac centers can either substantiate or contradict our results.     

Glycogen Phosphorylase BB: A more Sensitive and Specific Marker than Other Cardiac Markers for Early Diagnosis of Acute Myocardial Infarction

Cardiac markers are used to evaluate functions of heart. However, there are no satisfactory cardiac biomarkers for the diagnosis of acute myocardial infarction (AMI) within 4 h of onset of chest pain. Among novel cardiac markers, glycogen phosphorylase BB (GPBB) is of particular interest as it is increased in the early hours after AMI. The present study was conducted with the objective to find out the sensitivity and specificity of GPBB over other cardiac markers i.e. myoglobin and CKMB in patients of AMI within 4 h after the onset of chest pain. The study includes 100 AMI patients and 100 normal healthy individuals as controls. In all the cases and controls, serum GPBB and myoglobin concentrations were measured by ELISA where as CK-MB was measured by diagnostic kit supplied by ERBA. The sensitivity and specificity of glycogen phosphorylase BB (GPBB) were greater than CK-MB and myoglobin in patients of AMI within 4 h after the onset of chest pain. Hence, glycogen phosphorylase BB (GPBB) can be used as additional biomarker for the early diagnosis of AMI.     

Association of Resistin with Insulin Resistance and Factors of Metabolic Syndrome in North Indians

Metabolic syndrome (MetS) is a cluster of interrelated common clinical disorders. The role of resistin in insulin sensitivity and MetS is controversial till date. So, the aim of the present study was to investigate the relationship of plasma resistin levels with markers of the MetS in Indian subjects. In a case control study, total 528 subjects were selected for the study. 265 (194 male and 71 female) were cases (with MetS) and 263 (164 male and 99 female) were controls (without MetS). Required anthropometric measurements and calculations were carried out accordingly. All the Biochemical estimations were carried out according to standard protocol. Resistin level was measured by the standard protocol (By ELISA i.e. enzyme linked immunosorbent assay) as illustrated in the kit. Insulin level was also measured by the standard protocol as illustrated in the kit and insulin resistance was calculated by the standard procedures. Plasma resistin levels were significantly higher in cases compared with controls (male = 13.05 ± 4.31 vs. 7.04 ± 2.09 ng/ml; p ≤ 0.001 and female = 13.53 ± 4.14 vs. 7.42 ± 2.30 ng/ml; p ≤ 0.001). Plasma resistin levels were well correlated with waist circumference, glucose, triglycerides, waist/hip ratio, systolic and diastolic blood pressure, high density lipoprotein, total cholesterol, serum low density lipoprotein, serum very low density lipoprotein, insulin and insulin resistance. Plasma resistin levels were elevated in presence of the MetS and were associated with increased metabolic risk factors.     

Ischemia modified albumin: A novel marker for acute coronary syndrome

Early identification of patients with acute myocardial infarction is of prime importance due to the associated very high mortality. Only 22% of the patients presenting at emergency cardiology care with chest pain have coronary disease. A number of biochemical tests like CKMB and Troponin-T/I have been introduced for early detection of the coronary syndrome (ACS). Ischemia modified albumin (IMA) has been recently introduced as a marker of myocardial ischemia. We estimated serum IMA in four sequential samples from 25 patients admitted to ICCU. Twenty five healthy volunteers formed the control group from which the normal range was derived. IMA was significantly raised in ischemia patients than in controls as well as compared to the patients who did not have cardiac ischemia. IMA demonstrated good discrimination between the ischemic and the non-ischemic patients with an Odds Ratio of 16.9 (6.29–46.87) than CKMB which showed an Odds Ratio of 2.07 (1.18–6.08). Sensitivity and specificity of IMA for the detection of ACS was 78.0% and 82.7% compared to 58.0% and 60.0%, respectively for the CK-MB assay. The area under the ROC curve of IMA for ischemic v/s non-ischemic patients was 0.834. IMA appears to be developing into a new and very potent marker, of cardiac ischemia.     

Glycogen phosphorylase isoenzyme BB in the diagnosis of acute myocardial infarction: a meta-analysis

Background

Early diagnosis is crucial for management of patients with suspected acute myocardial infarction (AMI). Among innovative and promising biomarkers, the recent interest raised on glycogen phosphorylase isoenzyme BB (GPBB) has prompted us to perform a meta-analysis of published studies.

Materials and methods:

A systematic electronic search was carried out on PubMed, Web of Science and Google Scholar, with no date restriction, to retrieve all articles that have investigated the early diagnostic performance of GPBB in patients with suspected AMI, and directly reported or allowed calculation of sensitivity and specificity. A meta-analysis of the reported sensitivity and specificity of each study and pooled area under the curve (AUC) was then performed by random effect approach. Heterogeneity was assessed by I-square statistics.

Results:

Eight studies were finally selected for analysis (941 subjects; 506 cases and 435 controls), with a high heterogeneity (I-squared, 86.3%). The resulting pooled estimates and 95% confidence interval were 0.854 (0.801–0.891) for sensitivity, 0.767 (0.713–0.815) for specificity, 0.826 (0.774–0.870) for negative predictive value, 0.802 (0.754–0.844) for positive predictive value, and 0.754 (0.602–0.907) for AUC. In those studies that have simultaneously assessed GPBB and a troponin immunoassay, the combination of these biomarkers did not significantly improve the performance of troponin alone.

Conclusion:

GPBB does not meet the current requirements for an efficient diagnosis of AMI when used as a stand-alone test, whereas its combination with troponin merits further investigation in larger trials.     

Serum Testosterone, 17β-Estradiol and PSA Levels in Subjects with Prostate Disorders

Prostate carcinoma is the most frequently diagnosed malignancy and the second leading cause of death as a result of cancer in men in the US and other parts of the world. There are conflicting reports on the serum levels of testosterone and 17β-estradiol (E₂) in benign prostatic hyperplasia (BPH) and prostate cancer. This study was designed to evaluate the serum concentrations of these hormones in patients with these disorders. Serum levels of prostate specific antigen (PSA), total testosterone and estradiol were determined in 228 subjects comprising of 116 subjects with BPH, 62 subjects with prostate cancer (CaP) and 50 age-matched apparently healthy controls, using ELISA methods. PSA levels were significantly elevated (p < 0.05) in BPH subjects than controls, while there was no significant difference (p > 0.05) in testosterone and estradiol levels of these subjects. PSA and estradiol levels were significantly higher (p < 0.05) in CaP subjects than in controls, while there was no observed significant difference (p > 0.05) in testosterone levels. CaP subjects had significantly raised PSA, testosterone, and estradiol levels than BPH subjects. The mean molar ratio of testosterone: E₂ was lowest among CaP patients (134:1) and highest among controls (166:1). Significant positive correlation between PSA and 17β-estradiol was observed in prostate disorders (BPH and CaP patients: r = 0.347; p = 0.000). Significant negative correlations between testosterone and PSA were also observed among BPH patients (r = −0.221, p = 0.049) and control subjects (r = −0.490, p = 0.000). No significant correlation existed between testosterone and PSA in CaP patients (r = 0.051, p = 0.693). Correlations between age and estradiol in both BPH and CaP were not significant (p > 0.05). This study has shown that, there was a significant increase in serum estradiol in CaP subjects, while the testosterone levels in both BPH and CaP subjects were not different from those of controls.     

Estimation of Ischemia Modified Albumin (IMA) Levels in Patients with Acute Coronary Syndrome

Myocardial ischemia produces free radicals that catalyze a series of oxidative reactions that damage healthy tissues. The N-terminal sequence of albumin is one of the proteins modified by these highly reactive oxygen species and forms the ischemia modified albumin (IMA). This study involves investigations undertaken in different study groups to assess the levels of IMA. Mean serum IMA levels (U/mL) in patients with ST-segment elevated myocardial infarction (92.1 ± 10.6), non-ST-segment elevated myocardial infarction (87.3 ± 5.95) and unstable angina (UA) (88.9 ± 6.16) were significantly higher than non-cardiac chest pain (77.9 ± 6.69) and also healthy subjects (54.7 ± 17.2) (p < 0.001). IMA is a highly sensitive marker and has a high predictive value, which might prove the usefulness of this biomarker for early detection of myocardial ischemia. These data indicate a possible role of the IMA test in the early triage of patients with chest pain.     

Association of Aberrations in One Carbon Metabolism with Intimal Medial Thickening in Patients with Type 2 Diabetes Mellitus

The present work was aimed to study the association of one carbon genetic variants, hyperhomocysteinemia and oxidative stress markers, i.e., serum nitrite, plasma malondialdehyde (MDA) and glutathione (GSH) on intimal medial thickening (IMT) in patients with type 2 diabetes mellitus (T2D). A total number of 76 subjects from ACS Medical College and Hospital, Chennai, India were included in the study, i.e., Group I (n = 42) of T2D and Group II (n = 34) of age- and sex matched healthy controls. The glycated haemoglobin was measured by ion-exchange resin method; plasma homocysteine by Enzyme Linked Immunosorbant Assay method; serum nitrite (nitric oxide, NO), plasma MDA and GSH by spectrophotometric methods; the IMT by high frequency ultrasound. The polymorphisms of one carbon genetic variants were genotyped using polymerase chain reaction-restriction fragment length polymorphism and amplified fragment length polymorphism methods. Results indicate that methyltetrahydrofolate homocysteine methyl transferase (MTR) A2756G allele was found to be protective in T2D and the other variants were not significantly associated with T2D. Glutamate carboxypeptidase II (GCP II) C1561T (r = 0.34; p = 0.05) and methylene tetrahydrofolate reductase (MTHFR) C677T (r = 0.35; 0.04) showed positive correlation with plasma homocysteine in T2D cases. In this study, MTR A2756G allele was found to be protective in T2D; GCP II C1561T and MTHFR C677T showed positive association with plasma homocysteine in T2D cases. Among all the genetic variants, MTR A2756G was found influence IMT. RFC 1 G80A and TYMS 5′-UTR 2R3R showed synergistically interact with MTR A2756G in influencing increase in IMT.     

Abdominal Obesity Associated with Elevated Serum Butyrylcholinesterase Activity,Insulin Resistance and Reduced High Density Lipoprotein-Cholesterol Levels

Abdominal obesity (AO) has a strong correlation with cardiovascular disease and has been linked to Alzheimer’s disease and type 2 diabetes. We investigated the association between AO and elevated serum butyrylcholinesterase (BChE) activity, insulin resistance and the serum lipid profile, including triglyceride (TG), HDL-cholesterol (HDL-C) and LDL-cholesterol (LDL-C) levels in AO and non-AO women subjects. A total of 500 AO subjects (age 49.1 ± 10.5 years), and 142 non-AO women subjects (age 49.9 ± 11.9 years) were enrolled for the general biochemistry tests, serum BChE, fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR). Body mass index, waist circumference, Blood pressure (BP), plasma glucose (Glu), triglyceride (TG), BChE, insulin, HOMA-IR were significantly higher and HDL-C levels were significantly lower in AO subjects (p < 0.05). Waist circumference was significantly correlated with BP, Glu, TG, BChE, insulin and HOMA-IR in AO subjects. Multiple logistic regression demonstrated that AO was associated with elevated BChE, HOMA-IR, hypertension and reduced HDL-C after adjusting for these variables. AO is associated with elevated BChE, insulin resistance, HT and reduced HDL-C. These may predict the development of type 2 diabetes mellitus and may be associated with cognitive disorder in the future, both are mediated through insulin resistance.     

Detection of Bone Metastases in Breast Cancer (BC) Patients by Serum Tartrate-Resistant Acid Phosphatase 5b (TRACP 5b), a Bone Resorption Marker and Serum Alkaline Phosphatase (ALP), a Bone Formation Marker,in Lieu of Whole Body Skeletal Scintigraphy with Technetium99m MDP

Bone metastases are a serious problem in patients with advanced cancer disease and their presence usually signifies serious morbidity prior to the patient’s death. In breast cancer patients the incidence of bone metastasis is observed to be very high at 70 %, as seen during post-mortem examination. Bone metastasis is difficult to diagnose, treat or follow clinically without radiological tools. This study was designed to evaluate the utility of a novel bone resorption marker–serum tartrate-resistant acid phosphatase 5b (TRACP5b) and the bone formation marker such as serum total alkaline phosphatase (ALP), in comparison with whole body skeletal scintigraphy with Technetium99m MDP for the diagnosis of bone metastases (BM) in breast cancer (BC) patients. This study is intended to help the clinician to diagnose bone metastasis without resorting to radiological tools, as they are not cost effective and carry the risk of radiation. Experimental design: Four groups of samples were analysed. 1st group consists 52 normal female (cancer free women), 2nd group consists 38 BC patients without bone metastasis, 3rd group consists 27 breast cancer patients with limited bone metastasis (3 or less than 3 skeletal lesions) and 4th group consists 35 breast cancer patients with extensive bone metastasis (4 or more than 4 skeletal lesions), conformed by whole body skeletal scintigraphy with Technetium99m MDP. One way ANOVA was used to compare serum TRACP5b and serum ALP among these groups. Both serum TRACP5b and serum ALP are not markedly elevated in limited bone metastasis but are strongly elevated in extensive bone metastasis (p < 0.0001). As seen in this study the biochemical bone resorption marker, serum TRACP5b, abnormally increased in extensive bone metastasis of breast cancer patients and can be used as a specific marker for bone metastasis in lieu of radiological tools.     

Influence of Altered Hormonal Status on Platelet 5-HT and MAO-B Activity in Cigarette Smokers

The present study was designed to understand the cigarette smoking-induced alterations in hormones and the resulting changes in platelet serotonin (5-hydroxytryptamine, 5-HT) and monoamine oxidase (MAO-B) activity in chronic smokers. Human male volunteers aged 35 ± 8 years, were divided into two groups, namely controls and smokers (12 ± 2 cigarettes per day for 7–10 years). Results showed that cigarette smoking significantly (p < 0.05) elevated plasma triiodothyronine (T₃), cortisol and testosterone levels with significant (p < 0.05) reduction in plasma tryptophan and thyroxin (T₄). Moreover, smokers showed reduced platelet 5-HT levels and MAO-B activity. In smokers, plasma cortisol was negatively correlated with tryptophan (r = −0.386), platelet MAO-B (r = −0.264), and 5-HT (r = −0.671), and positively correlated with testosterone (r = 0.428). However, testosterone was negatively correlated with platelet MAO-B (r = −0.315), and 5-HT (r = −.419) in smokers. Further, smokers plasma T₃ levels were negatively correlated with platelet MAO-B (r = −0.398), and 5-HT (r = −0.541), whereas T₄ levels were positively correlated with platelet MAO-B (r = 0.369), and 5-HT (r = 0.454). In conclusion, our study showed that altered testosterone and cortisol levels may aggravate behavior, mood disturbances and symptoms of depression by decreasing platelet 5-HT and MAO-B activity in smokers.