Clinical Chemistry Department Research Articles

Indications that paraoxonase-1 contributes to plasma high density lipoprotein levels in familial hypercholesterolemia

HDL-associated paraoxonase type 1 (PON1) can protect LDL and HDL against oxidative modification in vitro and therefore may protect against cardiovascular disease. We investigated the effects of PON1 levels, activity, and genetic variation on high density lipoprotein-cholesterol (HDL-C) levels, circulating oxidized LDL (OxLDL), subclinical inflammation [high-sensitive C-reactive protein (Hs-CRP)], and carotid atherosclerosis. PON1 genotypes (L55M, Q192R, -107C/T, -162A/G, -824G/A, and -907G/C) were determined in 302 patients with familial hypercholesterolemia. PON1 activity was monitored by the hydrolysis rate of paraoxon, diazoxon, and phenyl acetate. PON1 levels, OxLDL, and Hs-CRP were determined using an immunoassay. The genetic variants of PON1 that were associated with high levels and activity of the enzyme were associated with higher HDL-C levels (P values for trend: 0.008, 0.020, 0.042, and 0.037 for L55M, Q192R, -107C/T, and -907G/C, respectively). In addition to the PON1 genotype, there was also a positive correlation between PON1 levels and activity and HDL-C (PON1 levels: r = 0.37, P < 0.001; paraoxonase activity: r = 0.23, P = 0.01; diazoxonase activity: r = 0.29, P < 0.001; arylesterase activity: r = 0.19, P = 0.03). Our observations support the hypothesis that both PON1 levels and activity preserve HDL-C in plasma.

Generation of aldehyde-derived protein adducts and alcohol-dependent liver toxicity is inhibited by kupffer cell destruction by gadolinium chloride: Onni Niemel, EP Central Hospital, Seinäjoki, and Department of Clinical Chemistry, University of Oulu, Finland, Seinäjoki Finland; Seppo Parkkila, Department of Clinical Chemistry, Anatomy, and Cell Biology, University of Oulu, Oulu Finland; Blair Bradford, Yuji Iimuro, Ronald G Thurman, Laboratory of Hepatobiology

Generation of aldehyde-derived protein adducts and alcohol-dependent liver toxicity is inhibited by kupffer cell destruction by gadolinium chloride: Onni Niemel, EP Central Hospital, Seinäjoki, and Department of Clinical Chemistry, University of Oulu, Finland, Seinäjoki Finland; Seppo Parkkila, Department of Clinical Chemistry, Anatomy, and Cell Biology, University of Oulu, Oulu Finland; Blair Bradford, Yuji Iimuro, Ronald G Thurman, Laboratory of Hepatobiology

Proteomic analysis using SELDI-TOF in cervical and amniotic fluid to detect biomarkers released in response to intra-amniotic inflammation

DETECT BIOMARKERS RELEASED IN RESPONSE TO INTRA-AMNIOTIC INFLAMMATION BO JACOBSSON, ULLA RUESCHI, ASA ROSEN, LARS RYMO, HENRIK HAGBERG, Perinatal Center, Dept Obstetrics and Gynecology, Goteborg, Sweden, Department of Clinical Chemistry and Transfusion Medicine, Department of Clinical Chemistry and Transfusion Medicine, Goteborg, Sweden OBJECTIVE: There is an urgent need to understand the pathophysiological mechanisms behind preterm birth in order to develop therapeutic and preventive strategies. Lately, evidence has grown strong for an association between intrauterine inflammation (IAI) and preterm birth in women with preterm labor (PTL) or preterm premature rupture of membranes (pPROM). In that perspective identification of novel biomarkers is of great importance. Our objective was to use a proteomic strategy, SELDI-TOF-MS, to determine whether protein profiling could reveal novel biomarkers present in cervical and amniotic fluid of PTL/pPROM patients with IAI (defined as elevated amniotic IL-6) compared to non-IAI cases. STUDY DESIGN: The study-material included amniotic fluid samples from 27 individuals with either PTL (n = 13) or pPROM (n = 14) before 34 weeks of gestation. Cervical fluid were present from those in PTL. Fourteen of the 27 women had IAI defined as elevated concentrations of IL-6 in amniotic fluid. Cervical and amniotic fluid proteins were analyzed by SELDI-TOF-MS using a strong anion array surface (Q 10) using sinapinic acid as the energy-absorbing molecule. RESULTS: Protein profiles revealed large individual variation in the amniotic fluid protein composition. However, we detected five peaks that were strongly over-expressed (P ! .0002) in amniotic fluid in IAI samples compared non-IAI samples. Four of the peaks were detected in the mass range 3400-4100 Da, the fifth peak was detected at 24 600 Da. The difference was not present regarding these five peaks in cervical fluid. CONCLUSION: Preliminary data suggest that novel biomarkers could be detected with proteomic analysis using SELDI-TOF and these proteins might S108 SMFM Abstracts

PROSTATE CANCER CHARACTERISTICS AND PROSTATE SPECIFIC ANTIGEN CHANGES IN SCREENING DETECTED PATIENTS INITIALLY TREATED WITH A WATCHFUL WAITING POLICY

We evaluated prostate cancer (PCa) characteristics at diagnosis and changes in prostatic specific antigen (PSA) with time in males with screening detected PCa that was initially managed with a watchful waiting policy. Patients with histologically proven PCa and PSA less than 10 ng/ml were selected from the European Randomized Study of Screening for Prostate Cancer, section Rotterdam. The choice of initiating a watchful waiting policy was patient desire or physician advice. PSA slope and PSA doubling time (PSADT) were calculated in patients with 3 or more PSA tests results available. A total of 191 patients were included. Mean age at diagnosis was 69 years and mean PSA was 3.9 ng/ml. Of the patients 92.6% had a Gleason score of 3 + 3 or lower, 133 had a followup of greater than 12 months (mean 40) and 35 (29.2%) had a negative PSA slope. Mean PSADT was 9.7 years (range 0.3 to 155) in 85 males with a positive PSA slope. During followup 30 patients changed therapy. Watchful waiting remains a controversial prostate cancer treatment strategy. In select screening detected patients with PCa there appears to be a subgroup with stable or even decreasing PSA values with time. These males could profit from a watchful waiting policy with possible deferred treatment. Together with conventional tumor parameters at diagnosis PSADT and PSA slope during followup could be used to monitor tumor activity and possibly aid in determining the time of deferred treatment. Further followup is mandatory to validate these results.

How to improve the specificity and sensitivity of biopsy technique in screening.

BJU InternationalVolume 92, Issue s2 p. 79-83 How to improve the specificity and sensitivity of biopsy technique in screening S. Ciatto, S. Ciatto Centro per lo Studio e la Prevenzione Oncologica, Florence, Italy,Search for more papers by this authorA. Vis, A. Vis Department of Pathology, Josephine Nefkens Institute, Erasmus University, Rotterdam, the Netherlands, andSearch for more papers by this authorP. Finne, P. Finne Department of Clinical Chemistry, Biomedicum, Helsinki, FinlandSearch for more papers by this author S. Ciatto, S. Ciatto Centro per lo Studio e la Prevenzione Oncologica, Florence, Italy,Search for more papers by this authorA. Vis, A. Vis Department of Pathology, Josephine Nefkens Institute, Erasmus University, Rotterdam, the Netherlands, andSearch for more papers by this authorP. Finne, P. Finne Department of Clinical Chemistry, Biomedicum, Helsinki, FinlandSearch for more papers by this author First published: 13 January 2004 https://doi.org/10.1111/j.1465-5101.2003.04403.xCitations: 3 Stefano Ciatto, Cspo, Viale A. Volta 171, Florence, Italy. e-mail: s.ciatto@cspo.it Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume92, Issues2December 2003Pages 79-83 RelatedInformation

Dietary reference values for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium and zinc

Journal of Human Nutrition and DieteticsVolume 16, Issue 3 p. 199-200 Dietary reference values for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium and zinc Alan Shenkin, Alan Shenkin Department of Clinical Chemistry, University of Liverpool, UK. E-mail: shenkin@liverpool.ac.ukSearch for more papers by this author Alan Shenkin, Alan Shenkin Department of Clinical Chemistry, University of Liverpool, UK. E-mail: shenkin@liverpool.ac.ukSearch for more papers by this author First published: 12 May 2003 https://doi.org/10.1046/j.1365-277X.2003.00439.xCitations: 5Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume16, Issue3June 2003Pages 199-200 RelatedInformation

Insufficient use of lipid-lowering drugs and measurement of serum cholesterol among patients with a history of myocardial infarction.

The effect of lipid-lowering drugs (LLDs) on coronary heart disease is well documented, particularly in patients with established ischaemic heart disease. However, intensity of the use of these drugs is low. The aim of this linkage study was to analyse the use of serum cholesterol measurements and LLDs among patients with a history of myocardial infarction (MI) in a Danish population. Information on serum cholesterol values was retrieved from the hospital's Department of Clinical Chemistry for all patients from the Odense municipality and four surrounding municipalities (213,868 inhabitants) hospitalised at Odense University Hospital for MI between 1994-1997. Information on LLD use was obtained from a prescription database. Only patients alive at discharge were included in the investigation. The total observation period was from 1993-1998. In all, 1,018 patients were eligible for observation and 39% of the patients who met the criteria for LLD reimbursement (MI and serum cholesterol >5.4 mmol/L) started treatment. Relatively more males than females and relatively more patients under the age of 70 years were treated. Patients above the age of 70 years were prescribed these drugs at a slower rate. More attention to the insufficient use of lipid-lowering drug treatment in patients with established coronary heart disease is needed.

Validation of albumin determined in urine with the HemoCue point‐of‐care analyser

Albumin concentrations persistently between 20 and 200 mg/L in first morning spot urine or urine collected overnight, referred to as microalbuminuria, indicate incipient nephropathy in diabetes mellitus. This study validates a new point‐of‐care device, the HemoCue Urine Albumin analyser, for handling, accuracy precision and predictive values (PV±) at 20 mg/L. Over a period of 2 months, 200 microalbuminuria samples were selected at the Department of Clinical Chemistry according to the results from the Integra 700 instrument (Roche, R) and analysed on the same day using the HemoCue analyser (HemoCue, H) and the Immage instrument (Beckman, B), in all cases closely following the manufacturers' instructions. Only 137 results were within the measuring range of H, 10–150 mg/L. Comparisons yielded regression lines H=1.06R–7.2 (r2=0.94), H=1.08B–3.1 (r2=0.94) and R=1.00B+4.3 (r2=0.99). Inter‐assay (n=24) CV% at 12 mg/L was H=18.2, R=4.2 and B=2.9 and at 65 mg/L: H=6.1, R=1.8 and B=2.6. Intra‐assay duplicate CV% for H at 21–40 mg/L was 13.2, at 41–80 mg/L 10.8 and at 81–150 mg/L 9.2. Intra‐assay repeatability (n=8) CV% at 28 mg/L was 7.2–13.8, at 57 mg/L 6.4–8.4 and at 105 mg/L 4.3–7.1. External quality assurance urine albumin (B) was +5.7% cf. nephelometry and (R) +1.0% cf. turbidimetry (n=6) method–group means. PV± values were (H versus R) 0.98/0.37 and (H versus B) 0.95/0.65. HemoCue is easy to handle. Results below 20 mg/L need to be confirmed at the central laboratory to exclude microalbuminuria. Values above 20 mg/L can be used to follow microalbuminuria, as precision allows discerning steps of 10 mg/L.

Cost-benefit analysis of total, free/total, and complexed prostate-specific antigen for prostate cancer screening

Refinements in prostate-specific antigen (PSA) through the use of its derivatives have augmented early detection rates of prostate cancer. However, these improvements are coupled with relatively large increases in unit cost per detected cancer. We used decision-analytic modeling to determine the most appropriate PSA derivative for population-based screening. We constructed a decision-analytic model to determine the PSA derivative with the highest cost-benefit ratio for prostate cancer screening. We defined 5 screening strategies: total PSA (tPSA) 4.0 ng/mL; free PSA/tPSA (f/tPSA) in conjunction with tPSA; and complexed PSA (cPSA) 3.8, 3.4, and 3.0 ng/mL. Prostate cancer prevalence, false-positive rates, and false-negative rates for each test strategy were calculated from a database of 2138 men. The direct costs were obtained from literature review and our department of clinical chemistry. The derivative cPSA with a positive threshold of 3.8 ng/mL was the dominant strategy. The average cost of screening was $138.93. The strategy of tPSA became dominant when the cost of cPSA was >$35.00 or the cost of a prostate biopsy was <$67.30. To match the false-negative rate of tPSA 4.0 ng/mL, a cPSA threshold of 3.0 ng/mL is necessary (sensitivity 92.5%). At this level, the marginal cost increase over tPSA is $9.40. The dominant strategy for population-based prostate cancer screening is use of cPSA with a positive threshold of 3.8 ng/mL. The use of cPSA with a threshold of 3.0 ng/mL identifies a similar number of cancers with fewer biopsies than tPSA at 4.0 ng/mL.

Report on the potential allergenicity of genetically modified organisms and their products.

Clinical & Experimental AllergyVolume 32, Issue 8 p. 1131-1143 Report on the potential allergenicity of genetically modified organisms and their products BSACI working party: , BSACI working party: Department of Paediatric Allergy & Immunology, St Mary's Hospital, London, UK,Search for more papers by this authorG. Lack, G. Lack Department of Paediatric Allergy & Immunology, St Mary's Hospital, London, UK,Search for more papers by this authorM. Chapman, M. Chapman Health Sciences Centre, Charlottesville, Virginia, USA,Search for more papers by this authorN. Kalsheker, N. Kalsheker Department of Clinical Chemistry, University Hospital, Nottingham, UK,Search for more papers by this authorV. King, V. King Ministry for the Environment, Wellington, New Zealand,Search for more papers by this authorC. Robinson, C. Robinson Department of Pharmacology & Clinical Pharmacology, St George's Hospital Medical School, London, UK, andSearch for more papers by this authorK. Venables, K. Venables Institute of Health Sciences, University of Oxford, Oxford, UKSearch for more papers by this author BSACI working party: , BSACI working party: Department of Paediatric Allergy & Immunology, St Mary's Hospital, London, UK,Search for more papers by this authorG. Lack, G. Lack Department of Paediatric Allergy & Immunology, St Mary's Hospital, London, UK,Search for more papers by this authorM. Chapman, M. Chapman Health Sciences Centre, Charlottesville, Virginia, USA,Search for more papers by this authorN. Kalsheker, N. Kalsheker Department of Clinical Chemistry, University Hospital, Nottingham, UK,Search for more papers by this authorV. King, V. King Ministry for the Environment, Wellington, New Zealand,Search for more papers by this authorC. Robinson, C. Robinson Department of Pharmacology & Clinical Pharmacology, St George's Hospital Medical School, London, UK, andSearch for more papers by this authorK. Venables, K. Venables Institute of Health Sciences, University of Oxford, Oxford, UKSearch for more papers by this author First published: 19 August 2002 https://doi.org/10.1046/j.1365-2222.2002.01464.xCitations: 32 Gideon Lack, Department of Paediatric Allergy & Immunology, St Mary's Hospital, Praed Street, London W2 1NY, UK. E-mail: gideon.lack@st-marys.nhs.uk Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume32, Issue8August 2002Pages 1131-1143 RelatedInformation

In Memoriam

The present generation active in epileptology may be only vaguely or not at all acquainted with the acronym, WODADIBOF, which stood for Workshops On the Determination of Antiepileptic Drugs In Body Fluids. Yet those who write science history will probably agree that the workshops formed the basis for therapeutic drug monitoring in the field of epilepsy. One of its founding fathers, Jaap (Jacobus Wilhelmus Antonius) Meijer, died on April 28, 2001, at age 74 years. He finished pre-university education at the end of World War II in Breda, The Netherlands. He hesitated between careers as a pianist and as a chemist and solved the problem by playing in ensembles to finance his academic studies. In 1953 he accepted a job at the Leiden University Laboratory of Endocrinology (Prof. Dr. A. Querido and Dr. A.A.H. Kassenaar) and collaborated with J.B. Stanbury, leading to the discovery of dehalogenase deficiencies. In this laboratory, he met two co-workers who were pivotal in his later work in the field of epilepsy. However, first he joined the atherosclerosis group of Prof. Dr. C.J.F. Böttcher at the Department of Physical Chemistry, where he acquired his expertise in gas chromatography. In 1968 he was appointed head of the Clinical Chemistry and Research Department of the Instituut voor Epilepsiebestrijding Meer en Bosch-De Cruquiushoeve in Heemstede. This institute, now renamed SEIN, is the oldest (founded 1882) and largest special center for epilepsy in the Netherlands. His focus was on all aspects of antiepileptic drugs in body fluids. In the international scene, his first epilepsy article appeared in Epilepsia in 1971; it was entitled “Simultaneous Quantitative Determination of Antiepileptic Drugs, including Carbamazepine, in Body Fluids.” Twenty years later, he summarized his work in a thesis defended at Nijmegen University: “Knowledge, Attitude, and Practice in Antiepileptic Drug Monitoring,” which also was published as a supplement to Acta Neurologica Scandinavica (1991;(suppl 134):1–128). He was awarded the distinction Ambassador for Epilepsy by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE) in 1986. His innovative thinking, his musical and graphic talents, but above all, his amiable character ensure that he will be long and fondly remembered by his many friends and his family.

Familial phosphofructokinase deficiency is associated with a disturbed calcium homeostasis in erythrocytes.

To critically evaluate whether an altered calcium homeostasis in erythrocytes could be contributing to the symptomatology of the Tarui's disease, which is an inherited phosphofructokinase (PFK) deficiency of the muscle isoenzyme. PFK is a tetrameric enzyme with three different isoenzymes, muscle (M), liver (L), and platelet (P). Erythrocytes contain a 50 : 50 hybrid of M and L type. The deficiency of the muscle isoenzyme displays a symptomatology which is mainly characterized by myopathy, and a compensated haemolytic anaemia. Erythrocyte deformability was assessed before and after autoincubation. Energy related metabolites and energy charge was determined in erythrocytes under various experimental conditions. The clinical part of the study was performed at the Departments of Cardiology and Clinical Chemistry, Umeå University Hospital, and the experimental investigation was carried out at the Department of Clinical Chemistry of the University Hospital of Uppsala, Sweden. Four family members with Tarui's disease participated in the study: the proband (patient 1), a 39-year-old male and two siblings, patient 2 (male, aged 46 years) and patient 3 (female, 30 years). Patient 4 (male, 16 years) was the son of the patient 2. Five healthy persons served as controls (controls 1-5). None. Cell-physiological variables were determined after autoincubation of erythrocytes (i.e. incubation in their own plasma at 37 degrees C) and after incubation in a composite buffered medium. Erythrocyte deformability as assessed by the erythrocyte fluidity was substantially decreased in patients compared to the moderate decrease in the control after 24 h of autoincubation, in presence of endogenous Ca2+ (heparin plasma). Moreover, autoincubation of erythrocytes shows that the patient's erythrocytes, although being moderately deficient in PFK activity, exhibit a normal (or slightly increased) lactate production compared to controls. Despite this, we show an increased ATP turnover with an Ca2+-induced AMP deaminase (and 5'-nucleotidase) activation leading to an increase in hypoxanthine content in patients' erythrocytes of about 100% after 24 h of autoincubation in heparin plasma, when compared to controls. A loss of volume in patient's erythrocytes after 24 h of autoincubation (in presence of Ca2+), as revealed by a diminished MCV, was consistent with an increased metabolic pool of intracellular calcium ions with a selective loss of K+ due to the activation of the K+ channel by intracellular Ca2+ (Gardos-effect). We conclude that the different calcium ion-induced effects on energy metabolism, structure and function of patients' erythrocytes are due to an augmented membrane leakage of Ca2+ and therefore an accumulated intracellular Ca2+ pool. This will result in an increased energy demand by the Ca2+-stimulated ATPase (calcium pump) to compensate for the dissipated Ca2+ gradient across the plasma membrane. The concomitant haemolysis may be explained by a diminished erythrocyte deformability due to Ca2+ overload.

Increased erythrocyte content of Ca2+ in patients with Tarui's disease.

To establish by flow cytometry and fluorophores an increased calcium ion load in erythrocytes of four patients with Tarui's disease. Calcium ion levels were determined in erythrocytes of patients and controls under normal and energy-deprived conditions. Adenylates were measured to assess energy status of incubated erythrocytes. The experiments were carried out at the Department of Clinical Chemistry of the University Hospital of Uppsala, Sweden. Four family members with Tarui's disease participated in the study. The proband (patient 1) was a 39-year-old male; patients (male, aged 46 years) 2 and 3 (female, 30 years) were his two siblings. Patient 4 (male, 16 years) was the son of patient 2. None. Calcium ion homeostasis was measured under basic conditions and under energy-deprived conditions and related to cellular adenylate content. All patients showed enhanced erythrocyte calcium ion loading compared to controls under energy-deprived conditions. Under normal conditions, however, three out of the four patients showed an increased erythrocyte calcium ion level compared to controls. We conclude that erythrocytes from patients with Tarui's disease have an increased Ca2+ permeability, initiating compensatory mechanisms involving increased Ca2+ pump activity and increased glycolytic flux, which are not always sufficient to keep erythrocyte calcium ion concentration within physiological range.

USE OF THE COMPLEX BETWEEN PROSTATE SPECIFIC ANTIGEN AND α1-PROTEASE INHIBITOR FOR SCREENING PROSTATE CANCER

We assess whether the complex between prostate specific antigen (PSA) and alpha1-protease inhibitor in serum can be used to reduce further the number of false-positive PSA screen results independent of total and free PSA. Sera from 304 consecutive screen positive subjects, including 78 with and 226 without prostate cancer, and serum PSA of 4 to 10 microg./l. or higher in the Finnish, randomized, population based prostate cancer screening trial were analyzed for PSA-alpha-protease inhibitor, and total and free PSA. Main outcome measures were specificity, sensitivity and area under receiver operating characteristics curve for proportions of free PSA and PSA-alpha 1-protease inhibitor, and for a combination of these among screen positive cases. The proportion of serum PSA-alpha 1-protease inhibitor of total PSA was lower in cancer cases than in controls (0.9% versus 1.6%, p <0.001). Logistic regression analysis of total PSA, free PSA and PSA-alpha 1-protease inhibitor showed that PSA-alpha 1-protease inhibitor in serum was an independent variable for discrimination between subjects with and without prostate cancer (p = 0.006) in the PSA range of 4 to 10 microg./l. The proportion of PSA-alpha 1-protease inhibitor alone improved specificity less than the proportion of free PSA but when these were combined by logistic regression they performed better than the proportion of free PSA alone at sensitivities of 85% to 95% (p <0.001). Serum PSA-alpha 1-protease inhibitor improves the specificity of total and free PSA in a screening population with total PSA 4 to 10 microg./l.

The application of HPLC/ESI tandem mass spectrometry on urine-soaked filter-paper strips for the screening of disorders of purine and pyrimidine metabolism.

Journal of Inherited Metabolic DiseaseVolume 23, Issue 4 p. 434-437 Article The application of HPLC/ESI tandem mass spectrometry on urine-soaked filter-paper strips for the screening of disorders of purine and pyrimidine metabolism T. Ito, T. Ito Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. B. P. van Kuilenburg, A. B. P. van Kuilenburg Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. H. Bootsma, A. H. Bootsma Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. J. Haasnoot, A. J. Haasnoot Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. van Cruchten, A. van Cruchten Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorY. Wada, Y. Wada Department of Pediatrics, Nagoya City University Medical School, Nagoya, JapanSearch for more papers by this authorA. H. van Gennip, A. H. van Gennip Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this author T. Ito, T. Ito Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. B. P. van Kuilenburg, A. B. P. van Kuilenburg Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. H. Bootsma, A. H. Bootsma Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. J. Haasnoot, A. J. Haasnoot Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorA. van Cruchten, A. van Cruchten Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this authorY. Wada, Y. Wada Department of Pediatrics, Nagoya City University Medical School, Nagoya, JapanSearch for more papers by this authorA. H. van Gennip, A. H. van Gennip Emma Children's Hospital and Department of Clinical Chemistry, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsSearch for more papers by this author First published: 01 June 2000 https://doi.org/10.1023/A:1005628624520Citations: 11AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume23, Issue4June 2000Pages 434-437 RelatedInformation

Molecular basis of classical mevalonic aciduria and the hyperimmunoglobulinaemia D and periodic fever syndrome: high frequency of 3 mutations in the mevalonate kinase gene.

Journal of Inherited Metabolic DiseaseVolume 23, Issue 4 p. 367-370 Article Molecular basis of classical mevalonic aciduria and the hyperimmunoglobulinaemia D and periodic fever syndrome: High frequency of 3 mutations in the mevalonate kinase gene S. M. Houten, S. M. Houten Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this authorJ. Frenkel, J. Frenkel Department of General Pediatrics, University Children's Hospital ‘Het Wilhelmina Kinderziekenhuis’, Amsterdam, The NetherlandsSearch for more papers by this authorW. Kuis, W. Kuis Department of Immunology, University Children's Hospital ‘Het Wilhelmina Kinderziekenhuis’, Amsterdam, The NetherlandsSearch for more papers by this authorR. J. A. Wanders, R. J. A. Wanders Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this authorB. T. Poll-The, B. T. Poll-The Department of Metabolic Disorders, University Children's Hospital ‘Het Wilhelmina Kinderziekenhuis’, Amsterdam, The NetherlandsSearch for more papers by this authorH. R. Waterham, H. R. Waterham Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this author S. M. Houten, S. M. Houten Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this authorJ. Frenkel, J. Frenkel Department of General Pediatrics, University Children's Hospital ‘Het Wilhelmina Kinderziekenhuis’, Amsterdam, The NetherlandsSearch for more papers by this authorW. Kuis, W. Kuis Department of Immunology, University Children's Hospital ‘Het Wilhelmina Kinderziekenhuis’, Amsterdam, The NetherlandsSearch for more papers by this authorR. J. A. Wanders, R. J. A. Wanders Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this authorB. T. Poll-The, B. T. Poll-The Department of Metabolic Disorders, University Children's Hospital ‘Het Wilhelmina Kinderziekenhuis’, Amsterdam, The NetherlandsSearch for more papers by this authorH. R. Waterham, H. R. Waterham Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this author First published: 01 June 2000 https://doi.org/10.1023/A:1005687415434Citations: 14AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume23, Issue4June 2000Pages 367-370 RelatedInformation

First trimester nuchal anomalies as a prenatal sign of Zellweger syndrome

Prenatal DiagnosisVolume 20, Issue 6 p. 520-521 Letter to the Editor First trimester nuchal anomalies as a prenatal sign of Zellweger syndrome G.C.M.L. Christiaens, G.C.M.L. Christiaens Division Obstetrics, Neonatology and Gynaecology, University Medical Center Utrecht, The NetherlandsSearch for more papers by this authorJ.M. de Pater, J.M. de Pater Department Medical Genetics, University Medical Center Utrecht, The NetherlandsSearch for more papers by this authorPh. Stoutenbeek, Ph. Stoutenbeek Division Obstetrics, Neonatology and Gynaecology, University Medical Center Utrecht, The NetherlandsSearch for more papers by this authorA. Drogtrop, A. Drogtrop Twee steden Hospital, Tilburg, The NetherlandsSearch for more papers by this authorR.J.A. Wanders, R.J.A. Wanders Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this authorF.A. Beemer, F.A. Beemer Department Medical Genetics, University Medical Center Utrecht, The NetherlandsSearch for more papers by this author G.C.M.L. Christiaens, G.C.M.L. Christiaens Division Obstetrics, Neonatology and Gynaecology, University Medical Center Utrecht, The NetherlandsSearch for more papers by this authorJ.M. de Pater, J.M. de Pater Department Medical Genetics, University Medical Center Utrecht, The NetherlandsSearch for more papers by this authorPh. Stoutenbeek, Ph. Stoutenbeek Division Obstetrics, Neonatology and Gynaecology, University Medical Center Utrecht, The NetherlandsSearch for more papers by this authorA. Drogtrop, A. Drogtrop Twee steden Hospital, Tilburg, The NetherlandsSearch for more papers by this authorR.J.A. Wanders, R.J.A. Wanders Departments of Clinical Chemistry and Pediatrics, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, The NetherlandsSearch for more papers by this authorF.A. Beemer, F.A. Beemer Department Medical Genetics, University Medical Center Utrecht, The NetherlandsSearch for more papers by this author First published: 09 June 2000 https://doi.org/10.1002/1097-0223(200006)20:6<520::AID-PD842>3.0.CO;2-UCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume20, Issue6June 2000Pages 520-521 RelatedInformation

Oxalate in human seminal plasma: possible significance and problems of oxalate determination

Objective: To determine the level of oxalate in seminal plasma and to correlate it with andrologic variables. Design: Laboratory examination. Setting: University-based department of andrology and department of clinical chemistry. Patient(s): One hundred male outpatients with infertility. Intervention(s): Isolated seminal plasma was stored for 120 days at −20°C. Main Outcome Measure(s): Levels of oxalic acid in seminal plasma. Result(s): Oxalate levels in seminal plasma depend on the degradation of ascorbic acid to oxalic acid during storage. There was a linear nonenzymatic increase of oxalate with storage time. After 120 days of storage, the values were 133 ± 50 μmol/L (n = 100). Oxalic acid correlated significantly with the number of sperm head anomalies, the pH value, and the age of the donors and correlated negatively with the volume of ejaculate. Conclusion(s): Oxalic acid in seminal plasma may influence male fertility.

The clinical value of procalcitonin in the prediction of infected necrois in acute pancreatitis

Infection of pancreatic necrosis (IN) has a major impact on management and outcome in acute pancreatitis (AP). Currently, guided fine-needle aspiration (FNA) is the only means for an accurate diagnosis of IN. Procalcitonin (PCT), a 116 amino acid pro-peptide of calcitonin has been found in high concentrations in patients with sepsis. In the present study we analyzed the clinical value of serum PCT for predicting IN in AP and compared the results to guided FNA. Clinical study. A collaborative study between the Departments of General Surgery and Clinical Chemistry/ Pathobiochemistry of the University of Ulm, Germany. 61 patients with AP entered this study and were stratified into three groups according to morphological and bacteriological data: I. 22 patients with edematous pancreatitis (AIP), II. 18 patients with sterile necrosis (SN), III. 21 patients with IN. During an observation period of 14 days PCT was measured by immunoluminometry, CRP was determined by lasernephelometry on a routine base. In patients with IN overall PCT concentrations were significantly higher than in those with SN, whereas CRP levels did not differ in both groups. In contrast, only low concentrations of both parameters were found in patients with AIP. By ROC analysis the best PCT cut-off level for predicting IN or persisting pancreatic sepsis was obtained at > or =1.8 ng/ml. If this cut-off was reached on at least two consecutive days, IN could be predicted with a sensitivity of 95%, a specificity, of 88%, and an accuracy of 90%. Guided FNA achieved a sensitivity, specificity, and accuracy of 91%. 79%, and 84% in differentiating IN from SN, respectively. After surgical treatment of IN median PCT values continued to be significantly higher in patients with persisting pancreatic sepsis (n=12) compared to those with an uneventful postoperative course (n=7). Our results demonstrate that monitoring of serum PCT could serve as a noninvasive and accurate method to predict IN in AP as well as to select patients with persisting septic complications after surgical debridement.

Adsorption of small hydroxy acids on glass: a pitfall in quantitative urinary organic acid analysis by GC-MS.

Journal of Inherited Metabolic DiseaseVolume 22, Issue 3 p. 293-296 Article Adsorption of small hydroxy acids on glass: A pitfall in quantitative urinary organic acid analysis by GC-MS A. A. J. van Landeghem, A. A. J. van Landeghem Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorY. T. J. Somers-Pijnenburg, Y. T. J. Somers-Pijnenburg Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorW. J. H. M. Somers, W. J. H. M. Somers Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorC. Stokwielder, C. Stokwielder Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorW. de Bruyn, W. de Bruyn Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorG. B. van den Berg, G. B. van den Berg Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this author A. A. J. van Landeghem, A. A. J. van Landeghem Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorY. T. J. Somers-Pijnenburg, Y. T. J. Somers-Pijnenburg Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorW. J. H. M. Somers, W. J. H. M. Somers Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorC. Stokwielder, C. Stokwielder Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorW. de Bruyn, W. de Bruyn Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this authorG. B. van den Berg, G. B. van den Berg Department of Clinical Chemistry and Haematology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, 5022 GC The NetherlandsSearch for more papers by this author First published: 01 May 1999 https://doi.org/10.1023/A:1005527315019Citations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume22, Issue3May 1999Pages 293-296 RelatedInformation