Clinical Chemistry (CLIN CHEM)

Publications in this journal

• Article: Time-Dependent Degradation Pattern of Cardiac Troponin T Following Myocardial Infarction

  Cardinaels EP, Mingels AM, van Rooij T, Collinson PO, Prinzen FW, van Dieijen-Visser MP
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  ABSTRACT: BACKGROUND: Cardiac troponin T (cTnT) is widely used for the diagnosis of acute myocardial infarction (AMI). However, it is still unclear whether degraded cTnT forms circulate in the patient's blood. We therefore aimed to elucidate which cTnT forms are detected by the clinical assay.METHODS: Separation of cTnT forms by gel filtration chromatography (GFC) was performed in sera from 13 AMI patients to examine cTnT degradation. The GFC eluates were subjected to Western blot analysis with the original antibodies from the Roche immunoassay used to mimic the clinical cTnT assay. To investigate the degradation pattern with time, standardized serum samples of 18 AMI patients collected 0-72 h postadmission were analyzed by Western blot analysis.RESULTS: GFC analysis of AMI patients' sera revealed 2 cTnT peaks with retention volumes of 5 and 11 mL. Western blot analysis identified these peaks as cTnT fragments of 29 and 14-18 kDa, respectively. Furthermore, the performance of direct Western blots on standardized serum samples demonstrated a time-dependent degradation pattern of cTnT, with fragments ranging between 14 and 40 kDa. Intact cTnT (40 kDa) was present in only 3 patients within the first 8 h after hospital admission.CONCLUSIONS: These results demonstrate that the Roche cTnT immunoassay detects intact as well as degraded cTnT forms in AMI patients' sera during the period of diagnostic testing. Moreover, following AMI, cTnT is degraded in a time-dependent pattern.
  Clinical Chemistry 03/2013;
• Article: MicroRNAs in Idiopathic Childhood Nephrotic Syndrome

  Johan Lorenzen, Thomas Thum
  Clinical Chemistry 02/2013;
• Article: Drug-induced changes in risk/biomarkers and their relationship with renal and cardiovascular long-term outcome in patients with diabetes

  Yan Miao Paul A. Smink Dick de Zeeuw Hiddo J. Lambers Heerspink
  Clinical Chemistry 02/2011;
• Article: Quantitative Protein Bioanalysis by Online High Flow Peptide Immunoaffinity Enrichment and Nanoflow LC-MS/MS: Assay Development for Measuring Total Salivary Pepsin/Pepsinogen.

  Neubert H, Gale J, Muirhead D
  Clinical Chemistry 01/2010; 56:1413-1423.
• Article: Use of biomarkers to predict cardiac risk from medications: getting to the heart of the matter.

  James L Januzzi
  Clinical Chemistry 08/2008; 54(7):1107-9.
• Article: The Hitchhiker's Guide to Self-Management & Leadership: Strategies for Success. Seven Steps to Overachieving in Business and Life, 2nd ed. Christopher S. Frings, PhD, CSP. Washington, DC: AACC Press, 2007, 106 pp., $25. ISBN 078-1-59425-069-9.

  Anthony Kurec
  Clinical Chemistry 08/2008; 54(7):1260.
• Article: Electrospray ionization mass spectrometric analysis of the globin chains in hemoglobin heterozygotes can detect the variants HbC, D, and E.

  Robert H Bateman, Brian N Green, Michael Morris
  Clinical Chemistry 08/2008; 54(7):1256-7.
• Article: A girl with goiter and inappropriate thyroid-stimulating hormone secretion.

  Mark D Kellogg, Terence C Law, Stephen Huang, Nader Rifai
  Clinical Chemistry 08/2008; 54(7):1241-4.
• Source

  Available from: clinchem.org

  Article: Dehydrogenase interference with enzymatic ethanol assays: forgotten but not gone.

  Angineh Gharapetian, Daniel T Holmes, Nadine Urquhart, Frances Rosenberg
  Clinical Chemistry 08/2008; 54(7):1251-2.
• Article: Highly sensitive cardiac troponin T values remain constant after brief exercise- or pharmacologic-induced reversible myocardial ischemia.

  Kerstin Kurz, Evangelos Giannitsis, Joerg Zehelein, Hugo A Katus
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  ABSTRACT: Using a new precommercial high-sensitivity cardiac troponin T (hsTnT) assay, we evaluated whether hsTnT increases after reversible myocardial ischemia. In 195 patients undergoing nuclear stress testing (ST) using single-photon emission computed tomography (SPECT) for suspected ischemic heart disease, we measured hsTnT before and 18 min, 4 h, and 24 h after the stress test. Thirty patients were excluded before ST because of cardiac troponin T (cTnT) >30 ng/L (0.03 mug/L) as measured by the fourth-generation commercial test. Another 65 patients were excluded because of a combination of fixed and reversible perfusion defects (PDs) after SPECT. We studied 18 patients with reversible PDs, 41 patients with fixed PDs, and 41 patients without any PDs. Of these 100 patients, 61 received dynamic ST and 39 pharmacological ST. Median baseline hsTnT concentrations (25th, 75th percentile) were comparable in patients with reversible, fixed, and no PDs [5.57 (2.47, 12.60), 8.01 (4.55, 12.44), and 6.90 (4.63, 10.59) ng/L, respectively]. After ST, median hsTnT concentrations did not change in the reversible, fixed, or no PD groups from baseline to 18 min [-0.41 (-0.81, 0.01), 0.01 (-0.75, 0.79), and 0.36 (-0.42, 1.01) ng/L] or from baseline to 4 h [-0.56 (-1.82, 0.74), 0.24 (-0.60, 1.45), and 0.23 (-0.99, 1.15) ng/L]. Median baseline hsTnT concentrations tended to be higher in patients undergoing pharmacological vs dynamic ST; however, there were no significant increases in hsTnT concentrations after either type of ST. Elevation of cTnT is rather a consequence of irreversible myocyte death than reversible myocardial ischemia after exercise or pharmacologic myocardial ischemia.
  Clinical Chemistry 08/2008; 54(7):1234-8.
• Source

  Available from: clinchem.org

  Article: Macromolecular cystatin C can be a caveat for estimating glomerular filtration rate in biliary obstruction.

  Liesbeth Vynckier, Veronique Stove, Joris R Delanghe
  Clinical Chemistry 08/2008; 54(7):1257-9.
• Article: Commentary: discordant measurements of serum triiodothyronine (T4), thyroxine (T3) and thyroid-stimulating hormone (TSH).

  Kenneth D Burman
  Clinical Chemistry 08/2008; 54(7):1246.
• Article: Utility of oligonucleotide array-based comparative genomic hybridization for detection of target gene deletions.

  Lee-Jun C Wong, David Dimmock, Michael T Geraghty, Richard Quan, Uta Lichter-Konecki, Jing Wang, Ellen K Brundage, Fernando Scaglia, A Craig Chinault
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  ABSTRACT: direct DNA sequencing is the primary clinical technique for identifying mutations in human disease, but sequencing often does not detect intragenic or whole-gene deletions. Oligonucleotide array-based comparative genomic hybridization (CGH) is currently in clinical use to detect major changes in chromosomal copy number. a custom oligonucleotide-based microarray was constructed to provide high-density coverage of an initial set of 130 nuclear genes involved in the pathogenesis of metabolic and mitochondrial disorders. Standard array CGH procedures were used to test patient DNA samples for regions of copy number change. Sequencing of regions of predicted breakpoints in genomic DNA and PCR analysis were used to confirm oligonucleotide array CGH data. oligonucleotide array CGH identified intragenic exonic deletions in 2 cases: a heterozygous single-exon deletion of 4.5 kb in the SLC25A13 gene [solute carrier family 25, member 13 (citrin)] in an individual with citrin deficiency and a homozygous 10.5-kb deletion of exons 13-17 in the ABCB11 gene [PFIC2, ATP-binding cassette, sub-family B (MDR/TAP), member 11] in a patient with progressive familial intrahepatic cholestasis. In 2 females with OTC deficiency, we also found 2 large heterozygous deletions of approximately 7.4 Mb and 9 Mb on the short arm of the X chromosome extending from sequences telomeric to the DMD gene [dystrophin (muscular dystrophy, Duchenne and Becker types)] to sequences within or centromeric to the OTC gene (ornithine carbamoyltransferase). these examples illustrate the successful use of custom oligonucleotide arrays to detect either whole-gene deletions or intragenic exonic deletions. This technology may be particularly useful as a complementary diagnostic test in the context of a recessive disease when only one mutant allele is found by sequencing.
  Clinical Chemistry 08/2008; 54(7):1141-8.
• Article: Plasma dehydroepiandrosterone and risk of myocardial infarction in women.

  John H Page, Jing Ma, Kathryn M Rexrode, Nader Rifai, Joann E Manson, Susan E Hankinson
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  ABSTRACT: In this study we prospectively evaluated the relationships between plasma concentrations of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) and subsequent myocardial infarction in women. Using case-control sampling, we selected participants from the Nurses' Health Study cohort. Blood samples were collected from 1989 to 1990 when the women were 43 to 69 years old. During follow-up through June 1998, 239 women were diagnosed with myocardial infarction (fatal and nonfatal). We matched cases 1:2 by age, cigarette smoking status, fasting status, and month of blood collection and used conditional logistic regression to adjust for potential confounders, including anthropometric factors and dietary intake. Baseline median (10th, 90th percentiles) concentrations of DHEA were 17.1 (4.3, 46.7) nmol/L among women who subsequently developed myocardial infarction and 16.6 (6.1, 37.9) among controls. The risk of myocardial infarction increased with plasma concentrations of DHEA and its sulfate. Women in the highest DHEA quartile had a rate ratio (RR) of 1.27 (95% CI 0.92-1.74, P for trend = 0.008) for myocardial infarction compared with those in the lowest quartile, after adjusting for covariates. The results did not vary significantly by menopausal status, postmenopausal estrogen therapy, fasting status, or age at time of blood collection. Similar relationships between concentrations of DHEA-S and risk were observed, with an RR of 1.58 (95% CI 1.13-2.21; P for trend = 0.06) for myocardial infarction in the highest vs lowest quartile. We observed a modest positive relationship between plasma concentrations of DHEA and its sulfate and the risk of subsequent myocardial infarction among predominantly postmenopausal women.
  Clinical Chemistry 08/2008; 54(7):1190-6.
• Article: New horizons for diagnostic applications of circulating nucleosomes in blood?

  Stefan Holdenrieder, Frank T Kolligs, Petra Stieber
  Clinical Chemistry 08/2008; 54(7):1104-6.
• Article: Low testosterone and risk of premature death in older men: analytical and preanalytical issues in measuring circulating testosterone.

  Elizabeth A Platz
  Clinical Chemistry 08/2008; 54(7):1110-2.