Laboratory of Clinical Chemistry and Hematology

Laboratory of, Italy

Laboratory of Clinical Chemistry and Hematology

Laboratory of, Italy

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Van Der Laan S.W.,Laboratory of Experimental Cardiology | Foroughi Asl H.,Karolinska Institutet | van den Borne P.,Laboratory of Experimental Cardiology | van Setten J.,Laboratory of Experimental Cardiology | And 13 more authors.
Atherosclerosis | Year: 2015

Background: The eicosanoid genes ALOX5, ALOX5AP and LTA4H have been implicated in atherosclerosis. We assessed the impact of common variants in these genes on gene expression, circulating protein levels, and atherosclerotic plaque phenotypes. Methods: We included patients from the Stockholm Atherosclerosis Gene Expression study (STAGE, N=109), and the Athero-Express Biobank Study (AE, N=1443). We tested 1453 single-nucleotide variants (SNVs) in ALOX5, ALOX5AP and LTA4H for association with gene expression in STAGE. We also tested these SNVs for association with seven histologically defined plaque phenotypes in the AE (which included calcification, collagen, cellular content, atheroma size, and intraplaque vessel density and hemorrhage). Results: We replicate a known cis-eQTL (rs6538697, p=1.96×10-6) for LTA4H expression in whole blood of patients from STAGE. We found no significant association for any of the SNVs tested with serum levels of ALOX5 or ALOX5AP (p>5.79×10-4). For atherosclerotic plaque phenotypes the strongest associations were found for intraplaque vessel density and smooth muscle cells in the ALOX5AP locus (p>1.67×10-4). Conclusions: We replicate a known eQTL for LTA4H expression in whole blood using STAGE data. We found no associations of variants in and around ALOX5, ALOX5AP and LTA4H with serum ALOX5 or ALOX5AP levels, or plaque phenotypes. On the supposition that these genes play a causal role in atherosclerosis, these results suggest that common variants in these loci play a limited role (if any) in influencing advanced atherosclerotic plaque morphology to the extent that it impacts atherosclerotic disease. © 2015 Elsevier Ireland Ltd.


Lippi G.,Laboratory of Clinical Chemistry and Hematology | Avanzini P.,Laboratory of Clinical Chemistry and Hematology | Aloe R.,Laboratory of Clinical Chemistry and Hematology | Cervellin G.,Academic Hospital of Parma
Laboratory Medicine | Year: 2014

Objective: Establish whether hemolysis in samples collected from intravenous lines is influenced by catheterization site. Methods: Blood was collected from all patients (67 total) admitted to the emergency department the same morning, through a 20-gauge catheter placed in a vein of the upper limb directly into an evacuated blood tube. Serum was tested for hemolysis index by multi-wavelength photometric readings. Results: The frequency of hemolyzed specimens was 30% (20/67). Hemolysis rate in median cephalic and basilic veins (17%) was comparable to that of median anterobrachial vein but lower than cephalic vein (29%; P =0.01), basilic vein (33%; P <0.01), and metacarpal plexus veins (75%; P <0.01). Compared with median basilic and cephalic veins, the relative risk of hemolysis was 1.4 from median anterobrachial vein, 1.6 from cephalic vein, 1.9 from basilic vein, and 4.3 from metacarpal plexus veins. Conclusion: Drawing blood frocm catheters placed distally from median veins carries higher hemolysis risk.


Caroli B.,University of Parma | Pasin F.,University of Parma | Aloe R.,Laboratory of Clinical Chemistry and Hematology | Gnocchi C.,Laboratory of Clinical Chemistry and Hematology | And 3 more authors.
Journal of Endocrinological Investigation | Year: 2014

Background: Vitamin D deficiency is common in the general population and may impair skeletal muscle function. Very few data are available regarding this condition in professional athletes. Aim: To evaluate some skeletal parameters and in particular serum 25-hydroxyvitamin D status in professional rugby players during two different sunlight exposure times (October and early April) and to assess its impact on bone metabolism. Materials and methods: Twenty-one male healthy professional rugby players living in northern Italy at latitude of 44°55′N (age 24.6 ± 4.3 years; height 182.0 ± 0.05 cm; mass 96.3 ± 14.6 kg; BMI 28.9 ± 3.7 kg/m2) participated in this observational study. During 2012/2013 Italian rugby season, 25-hydroxyvitamin D, PTH and other related biochemical parameters were monitored. Dietary calcium intake and body composition by DXA were also evaluated. Results: Significant changes were observed between October and April data for 25-hydroxyvitamin D concentration (22.8 ± 5.8 vs. 19.1 ± 5.3 ng/ml; p = 0.001) whereas serum PTH, calcium and phosphorus plasma levels did not change. They presented with an appropriate daily intake of calcium (1,304.8 ± 477.9 mg; max 1,939 mg; min 228 mg). Conclusions: Professional rugby athletes practicing a sport characterized by intense outdoor training and with good calcium intake are at higher risk of hypovitaminosis D that worsens significantly during times of low cutaneous vitamin D production. Further studies are warranted to evaluate whether an appropriate supplementation with cholecalciferol in professional athletes is needed. © 2014 Italian Society of Endocrinology (SIE).


Russcher H.,Erasmus Medical Center | Van Deursen N.,Erasmus Medical Center | Ermens T.,Laboratory of Clinical Chemistry and Hematology | De Jonge R.,Erasmus Medical Center
Nederlands Tijdschrift voor Klinische Chemie en Laboratoriumgeneeskunde | Year: 2013

Point of Care Testing (POCT) accelerates the availability of critical labtest information that clinicians require to make rapid treatment decisions and monitor a patient's response. Especially, in pediatric environments, the ability to perform multiple tests with just a few drops of blood is precious. Total white blood cell (WBC) count and differentiation is an important tool in diagnosing infections. In an emergency care setting, both lymphocytopenia and the neutrophil to lymphocyte count ratio (NLCR) may serve as simple markers for discrimination between severe bacterial and viral infections and are better predictors of bacteremia than routine parameters like CRP level, total WBC and neutrophil count (1, 2). Recently, HemoCue launched a POCT analyser (HemoCue WBC DIFF system), able to count and differentiate white blood cells, including differentiation (DIFF, absolute and percentage) in neutrophil, lymphocyte, monocyte, eosinophil and basophil counts in capillary or venous whole blood (3). The Hemocue WBC DIFF technique is based on cell counting using a microcuvette with a small volume of only 10 μl of blood. The blood sample is drawn into the cavity of the microcuvette by capillary force. A cell-lysing agent will hemolyse the red blood cells and a staining agent will stain the white blood cells. The microcuvette is placed in the analyser and the numbers of white blood cells are counted by image analysis (4). This study was undertaken to assess the reliability of the HemoCue WBC DIFF system fulfilling the medical and clinical requirements regarding to accuracy and precision according to CLSI EP9-A2 (5) of measurement for total white blood cell and 5-parts differential count in capillary pediatric samples.


Tersteeg C.,Catholic University of Leuven | Fijnheer R.,Laboratory of Clinical Chemistry and Hematology | Pasterkamp G.,Laboratory of Clinical Chemistry and Hematology | De Groot P.G.,Laboratory of Clinical Chemistry and Hematology | And 3 more authors.
Seminars in Thrombosis and Hemostasis | Year: 2015

Von Willebrand factor (VWF) is one of the most important proteins of the hemostatic system. Its multimeric state is essential for its natural function to guide platelets to sites of injury. ADAMTS13 is the key protease that regulates the multimeric state of VWF. Without ADAMTS13, VWF multimers can grow to pathologically large sizes. This is a risk factor for the life-threatening condition thrombotic thrombocytopenic purpura (TTP). In this condition, VWF-rich thrombi occlude the microvasculature of various tissues. Intriguingly, a complete ADAMTS13 deficiency does not cause continuous TTP, either in patients or genetically targeted mice. Instead, TTP occurs in episodes of disease, separated by extended periods of remission. This indicates that regulating factors beyond ADAMTS13 are likely involved in this pathologic cascade of events. This raises the question of what really happens when ADAMTS13 is (temporarily) unavailable. In this review, we explore the possible role of complementary mechanisms that are capable of modifying the thrombogenic potential of VWF. Copyright © 2016 by Thieme Medical Publishers, Inc.


PubMed | Laboratory of Clinical Chemistry and Hematology and Catholic University of Leuven
Type: Journal Article | Journal: Seminars in thrombosis and hemostasis | Year: 2016

Von Willebrand factor (VWF) is one of the most important proteins of the hemostatic system. Its multimeric state is essential for its natural function to guide platelets to sites of injury. ADAMTS13 is the key protease that regulates the multimeric state of VWF. Without ADAMTS13, VWF multimers can grow to pathologically large sizes. This is a risk factor for the life-threatening condition thrombotic thrombocytopenic purpura (TTP). In this condition, VWF-rich thrombi occlude the microvasculature of various tissues. Intriguingly, a complete ADAMTS13 deficiency does not cause continuous TTP, either in patients or genetically targeted mice. Instead, TTP occurs in episodes of disease, separated by extended periods of remission. This indicates that regulating factors beyond ADAMTS13 are likely involved in this pathologic cascade of events. This raises the question of what really happens when ADAMTS13 is (temporarily) unavailable. In this review, we explore the possible role of complementary mechanisms that are capable of modifying the thrombogenic potential of VWF.

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