Laboratory of Clinical Chemistry

San Giovanni Rotondo, Italy

Laboratory of Clinical Chemistry

San Giovanni Rotondo, Italy
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Kok M.B.,Medical Center Alkmaar | Tegelaers F.P.W.,Medical Center Alkmaar | van Rijn J.L.M.L.,Laboratory of Clinical Chemistry | van Pelt J.,Medical Center Alkmaar
Clinica Chimica Acta | Year: 2014

Background: Several investigators have reported discrepancies between the bromocresol-purple (BCP), bromocresol-green (BCG) and immunonephelometric (INP) assays in dialysis patients. This study compared the abovementioned assays and investigated whether hemodialysis itself or carbamylation of albumin is the cause for this discrepancy. Methods: Samples obtained from hemodialysis patients were analyzed by BCP, BCG and INP. Furthermore, albumin was carbamylated in vitro using isocyanate. Isocyanate converts lysine to homocitrulline. Results: No differences were observed between samples of the pre- and post-hemodialysis groups for BCP. In the control group, BCG averaged 6. g/L higher than INP. BCP did not statistically deviate from INP. In the dialysis group BCG averaged 5. g/L higher when compared to INP, whereas BCP averaged 2. g/L lower. BCP was affected by carbamylation of albumin. BCG and INP measurements were affected to a much lesser extent. Homocitrulline content of hydrolysates was increased in both the carbamylated albumin as well as in the dialysis population. Conclusion: In a hemodialysis population albumin concentrations are not consistently estimated by both BCG and BCP methods. Relative to INP measurements BCG overestimates the albumin concentration (4-10. g/L), whereas BCP leads to an underestimation (0-4. g/L). Carbamylation of albumin is the main attributor to the discrepancy found with BCP. © 2014 Elsevier B.V.

PubMed | Biostatistics Unit, University of Foggia, Geriatric Unit and Gerontology Geriatrics Research Laboratory, Laboratory of Clinical Chemistry and 2 more.
Type: Clinical Trial | Journal: Pain medicine (Malden, Mass.) | Year: 2015

To investigate the role of CYP2D6 phenotype in the outcome of postoperative (PO) pain (POP) treatment.Longitudinal cohort study. Open-label trial with post hoc analysis.General Hospital Surgery and Recovery Units.Ninety unrelated Caucasians submitted to abdominal/thoracic surgery.Standard multimodal POP treatment including opioids (tramadol) and nonsteroidal anti-inflammatory drugs (ketoprofen) at different dosages and infusion rates according to the predicted mild, moderate, or severe POP.Pain (Numeric Rating Scale-NRS) and sedation (Ramsay Sedation Scale-RSS) up to 24 hours after surgery. By genotyping 16 CYP2D6 alleles, the four CYP2D6 phenotypes poor metabolizer (PM), intermediate metabolizers (IM), extensive metabolizers (EM) and ultrarapid metabolizers (UM) were predicted.As compared with the CYP2D6-EM phenotype, in the early PO time (30 min) a higher RSS mean score in IM was observed (P=0.035). A suggestion towards higher mean score in PM (P=0.091) and a minor mean score in UM (P=0.091) was also detected. No difference in the outcome of pain across the CYP2D6 phenotypes was observed.In respect to the normal CYP2D6 phenotype, our results suggested that slowly metabolizers (IMs and PMs) might have a major sedation, whereas more rapid metabolizers (UM) a minor sedation, in the early time after surgery. A minor role of CYP2D6 phenotype in PO analgesia may be suggested.

Barbui T.,Ospedali Riuniti di Bergamo | Carobbio A.,Ospedali Riuniti di Bergamo | Finazzi G.,Ospedali Riuniti di Bergamo | Vannucchi A.M.,University of Florence | And 12 more authors.
Haematologica | Year: 2011

We tested the hypothesis that levels of pentraxin high sensitivity C-reactive protein and pentraxin 3 might be correlated with cardiovascular complications in patients with essential thrombocythemia and polycythemia vera. High sensitivity C-reactive protein and pentraxin 3 were measured in 244 consecutive essential thrombocythemia and polycythemia vera patients in whom, after a median follow up of 5.3 years (range 0-24), 68 cardiovascular events were diagnosed. The highest C-reactive protein tertile was compared with the lowest (>3 vs. <1 mg/L) and correlated with age (P=0.001), phenotype (polycythemia vera vs. essential thrombocythemia, P=0.006), cardiovascular risk factors (P=0.012) and JAK2V617F allele burden greater than 50% (P=0.003). Major thrombosis rate was higher in the highest C-reactive protein tertile (P=0.01) and lower at the highest pentraxin 3 levels (P=0.045). These associations remained significant in multivariate analyses and indicate that blood levels of high sensitivity C-reactive protein and petraxin 3 independently and in opposite ways modulate the intrinsic risk of cardiovascular events in patients with myeloproliferative disorders & copy 2011 Ferrata Storti Foundation.

Mare L.,University of Insubria | Caretti A.,University of Milan | Albertini R.,Laboratory of Clinical Chemistry | Trinchera M.,University of Insubria
International Journal of Biochemistry and Cell Biology | Year: 2013

CA19.9 antigen is a glycoprotein present in human serum and found elevated in various diseases. It is intensively studied since long time as a potential marker for managing cancers of the gastrointestinal tract, but its reliability is widely accepted only for pancreatic cancers. Here, we focused on the tetrasaccharide epitope (NeuAcα2-3Galβ1-3[Fucα1-4]GlcNAc) sialyl-Lewis a studying the biosynthesis, expression, and secretion in colon cancers and related cancer cell lines. We found that the β1,3 galactosyltransferase β3Gal-T5, responsible for sialyl-Lewis a synthesis, is dramatically reduced in colon adenocarcinomas, in terms of both transcript and enzyme activity levels. Moreover, no or very faint antigen is detectable in colon cancer homogenates, by dot-blot or enzyme immunoassay, while it is commonly evident in sera from different patients. In cancer cell lines synthesizing CA19.9, the amount of antigen secreted is proportional to that expressed on the cell surface, and depends on appreciable levels of β3Gal-T5, which appear much higher than those measured in colon cancer specimens. Since colon cancers appear unable to synthesize relevant amount of CA19.9, we suggest that the antigen circulating in the serum of colon cancer patients may have a different and more complex origin than expected so far. © 2013 Elsevier Ltd.

Pinelli A.,University of Milan | Trivulzio S.,University of Milan | Rossoni G.,University of Milan | Redaelli R.,Laboratory of Haemostasis and Thrombosis | Brenna S.,Laboratory of Clinical Chemistry
In Vivo | Year: 2012

Coronary artery diseases (CAD) evolving into acute myocardial infarction (AMI) is associated with coagulation and thrombotic occlusion of coronary vessels in the presence of unstable atheroma. The atheromatous plaque becomes unstable when it is infiltrated by monocytes, macrophages and neutrophils capable of secreting proteases that induce plaque erosion, rupture and initialize the coagulation process. The aim of this study was (a) to analyse the plasma of patients with AMI for the presence of proteases that may activate rapid coagulation, (b) to evaluate coagulation markers as prothrombin fragment (F1+2) and antithrombin III and (c) to find an interrelation between proteases and coagulation markers. The examined plasma showed high values of prothrombin fragment (F1+2) and low levels of antithrombin III. These markers showed a highly significant negative-correlation. The plasma also exhibited increased levels of matrix metalloproteinase-9 (MMP-9) which were positively-correlated with the prothrombin fragment (F1+2). MMP-9 seems to cause the coagulation activity by increasing the level of prothrombin fragment (F1+2) and the consumption of antithrombin III. The examined plasma also exhibited high levels of neutrophil gelatinase-associated lipocalin (NGAL), which is known to modulate MMP-9 activity. The high plasma levels of MMP-9 and NGAL can be attributed to plaque instability and appear to activate sudden coagulation. MMP-9 and NGAL, in the presence of altered values of prothrombin fragment (F1+2) and antithrombin III in AMI patients, seem to be suitable markers to be studied in unstable plaque patients, for the prediction and prevention of acute coronary syndrome.

Calcaterra V.,University of Pavia | Muratori T.,University of Pavia | Klersy C.,IRCCS Policlinico San Matteo Foundation | Albertini R.,Laboratory of Clinical Chemistry | And 3 more authors.
Annals of Nutrition and Metabolism | Year: 2011

Introduction: Obesity is often associated with increased serum alanine aminotransferase (ALT), and elevation of ALT is a marker of non-alcoholic fatty liver disease which is caused in part by insulin resistance, the essential characteristic of metabolic syndrome (MS). We evaluated the prevalence of MS in prepubertal obese children and the usefulness of ALT as an MS marker. Patients: 120 obese children (6.3 ± 1.6 years old) and 50 normal-weight controls (5.3 ± 2.0 years old) were included. Patients were classified as having MS if they met ≥3 of the following criteria: body mass index >97th percentile, triglycerides >95th percentile, high-density lipoprotein cholesterol <5th percentile, systolic (SBP) and/or diastolic (DBP) blood pressure >95th percentile, fasting blood glucose 100 mg/dl and/or impaired insulin sensitivity with homeostasis model assessment for insulin resistance >97.5th percentile. ALT levels were also evaluated. Results: MS occurred in 16.6% of obese patients. Significant differences were present in body mass index (p < 0.001), SBP (p = 0.002) and DBP (p < 0.001) between non-MS and MS obese patients; laboratory data, except total cholesterol, were significantly different in the two groups. The strongest association with MS (as evaluated by the c-statistic) was found for insulin and homeostasis model assessment for insulin resistance (c = 0.92 and 0.91, respectively); also, DBP and SBP showed good discrimination ability (c = 0.73 and 0.72, respectively). ALT levels in the MS group were higher than in the non-MS group (p = 0.02) and associated with MS (p = 0.001; c = 0.69). Conclusion: MS is a consequence of obesity already in very young children. Also, pathological serum ALT levels were significantly correlated with MS and might be considered a marker for defining MS, though confirmation in a longitudinal study is called for. © 2011 S. Karger AG, Basel.

Tsiafoulis C.G.,University of Ioannina | Exarchou V.,University of Ioannina | Tziova P.P.,University of Ioannina | Bairaktari E.,Laboratory of Clinical Chemistry | And 2 more authors.
Analytical and Bioanalytical Chemistry | Year: 2011

The rapid and accurate determination of specific metabolites present in biofluids is a very demanding task which is essential in both medicine and chemistry. l-carnitine (3-hydroxy-4-N-trimethylammonium butyrate) is an important metabolite which participates in a series of biological paths and therefore its determination is of diagnostic importance. A single quantum coherence filtering 1H NMR methodology was used for the accurate and rapid determination of l-carnitine in human serum samples. The methodology is based on spectral simplification, and specifically on the distinction of the N-methyl proton signal of l-carnitine that is greatly overlapped in the 1H-NMR spectrum of serum. The quantitative results provided by the proposed method are in excellent agreement with those obtained by the enzymatic method, which is widely used. The proposed method is rapid (~20 min of experimental time), selective, sensitive, and has good analytical characteristics (accuracy, reproducibility). Selected protein precipitation methods were also investigated and sample pretreatment with EtOH is suggested. © Springer-Verlag 2011.

Leoni V.,Laboratory of Clinical Chemistry | Leoni V.,Foundation IRCCS Institute of Neurology Carlo Besta | Caccia C.,Foundation IRCCS Institute of Neurology Carlo Besta
Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids | Year: 2015

Huntington disease (HD), an autosomal dominant neurodegenerative disorder caused by an abnormal expansion of CAG trinucleotide repeat in the Huntingtin (HTT) gene, is characterized by extensive neurodegeneration of striatum and cortex and severe diffuse atrophy at MRI. The expression of genes involved in the cholesterol biosynthetic pathway and the amount of cholesterol, lanosterol, lathosterol and 24S-hydroxycholesterol were reduced in murine models of HD. In case of HD-patients, the decrease of plasma 24OHC follows disease progression proportionally to motor and neuropsychiatric dysfunction and MRI brain atrophy, together with lanosterol and lathosterol (markers of cholesterol synthesis), and 27-hydroxycholesterol. A significant reduction of total plasma cholesterol was observed only in advanced stages. It is likely that mutant HTT decreases the maturation of SREBP and the up-regulation LXR and LXR-targeted genes (SREBP, ABCG1 and ABCG4, HMGCoA reductase, ApoE) resulting into a lower synthesis and transport of cholesterol from astrocytes to neurons via ApoE. In primary oligodendrocytes, mutant HTT inhibited the regulatory effect of PGC1α on cholesterol metabolism and on the expression of MBP. HTT seems to play a regulatory role in lipid metabolism. The impairment of the cholesterol metabolism was found to be proportional to the CAG repeat length and to the load of mutant HTT. A dysregulation on PGC1α and mitochondria dysfunction may be involved in an overall reduction of acetyl-CoA and ATP synthesis, contributing to the cerebral and whole body cholesterol impairment. This article is part of a Special Issue entitled Brain Lipids. © 2015 Elsevier B.V.All rights reserved.

Cotton F.,Free University of Colombia | Wolff F.,Laboratory of Clinical Chemistry | Gulbis B.,Free University of Colombia
Methods in Molecular Biology | Year: 2013

Hemoglobinopathies are genetic disorders of globin chains characterized by the decreased expression of α - or β -globin chains (thalassemias) or by the synthesis of an abnormal protein (hemoglobin variants in, e.g., sickle cell disease). The screening of most hemoglobinopathies relies, together with hematological results and clinical elements, on the separation and quantification of normal and abnormal hemoglobin fractions. Gel electrophoresis, isoelectric focusing, and HPLC have been the methods of choice for many years. For about 20 years, capillary electrophoresis has appeared as a strong alternative method. Since the early 2000s, automated instruments are commercially available for the analysis of Hb fractions in adult patients but also for neonatal screening. © Springer Science+Business Media, LLC 2013.

Feiereisen P.,Center Hospitalier Of Luxembourg | Vaillant M.,Center Hospitalier Of Luxembourg | Vaillant M.,CRP Sante | Gilson G.,Laboratory of Clinical Chemistry | Delagardelle C.,Center Hospitalier Of Luxembourg
Journal of Cardiopulmonary Rehabilitation and Prevention | Year: 2013

BACKGROUND:: Muscle wasting in chronic heart failure (CHF) is a result of increased catabolism induced by proinflammatory cytokines like tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), and decreased anabolism due to alterations in the insulin-like growth factor 1 (IGF-1)/growth hormone (GH) axis. The goal of this study was to analyze the effects of 3 different training modalities (endurance training, strength training, and combined strength and endurance training [CT]) on circulating cytokines, IGF-1, and GH levels. METHODS:: Patients with CHF (N = 45), NYHA class II-III, left ventricular ejection fraction < 35%, were randomly assigned to 1 of 3 training modalities. They trained for 40 sessions, 3 times weekly. Fifteen CHF patients served as a control group. Blood samples were collected at baseline and 48 hours after the last training session. RESULTS:: There was a significant decrease in circulating IL-6 with all 3 training modalities. Tumor necrosis factor α levels decreased in the training groups and reached statistical significance for the CT group. No change was observed in the control group. There was no difference between the 4 groups. When comparing all trained patients with the control group, the decrease in IL-6 was significant. Concerning IGF-1 and GH, there was no change with training and no change in the control group. CONCLUSION:: Exercise training has no effects on circulating IGF-1 and GH. The decreases in cytokines are evident only when all trained patients are compared with the control group, independently of the modality of training intervention. © 2013 Wolters Kluwer Health Lippincott Williams and Wilkins.

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