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R Couderc

Publications and source records attributed to R Couderc.

65 records · Page 4Linked to original sources

[Comparison of plasma total homocysteine determinations in 9 French hospital laboratories by using 6 different methods].

A lot of methods are now available for total plasma homocysteine (tHcy) determination. Commercial kits using immunoassay, easier to use, begin to supplant in-house laboratory methods. Our aim is to evaluate the interchangeability of tHcy measurements in 9 French hospital laboratories. Six different method types were used: 2 gas chromatography-mass spectrometry (GC-MS), 2 HPLC with fluorescence detection subdivided in one in-house method and one commercial kit (Bio-Rad ), 3 fluorescence polarization immunoassays (FPIA), 1 enzyme immunoassay, 1 amino acid analyser, 1 capillary electrophoresis coupled with laser-induced fluorescence detection (EC-LIF). Each laboratory analysed 41 patient's plasma samples in which 8 samples contained added homocystine. Results were analysed for imprecision, recovery, and methodological differences. The mean among-laboratory imprecision (CV) ranged from 12.5 to 18% in function of plasma sample type and was identical to the mean among-method variation. In terms of recovery, we obtained underestimated results with immunoassays. The bias relative to the GC-MS method was less than 12.5% except for two laboratories, one using FPIA assay and the other EC-LIF. In conclusion, the interchangeability of tHcy results between laboratories is not satisfactory and does not allow us to evaluate cardiovascular risk linked to moderate increases of tHcy.

Blood Chemical Analysis↗

[Acute meningitidis, acute phase proteins and procalcitonin].

The prognosis of bacterial meningitis is critically dependent on a rapid causal diagnosis and implementation of an accurate treatment. However, clinical and biological parameters available within the few hours that follow the patient's admission are not reliable enough, except when bacteria are to be found in cerebrospinal fluid under the microscope. Therefore, the initial treatment of acute meningitis is still most of time presumptive so that the definitive diagnosis, however difficult, is often established when the therapeutic management has already been initiated. The use of biological markers, especially lymphokines and acute-phase proteins, has been proposed to facilitate the accuracy of the initial diagnosis. Today, C-reactive protein (CRP) is the most widely used inflammatory marker in emergency departments with aim to discriminate bacterial from viral infections. In 1998, Gerdes et al. published a meta-analysis from 35 studies questioning the usefulness of CRP in discriminating bacterial meningitis from viral meningitis. They outlined that the majority of authors proposed to use this inflammation marker as an additional tool for discriminating bacterial meningitis from viral meningitis, without having evaluated its independent contribution relative to other parameters such as white blood cell count, cerebrospinal fluid (CSF) white cell count, protein or glucose. Procalcitonin (PCT) is an acute-phase protein with faster kinetics than CRP, its concentration in serum rising within the few hours that follow the inception of a bacterial infection. Two French studies published in 1997 and 1998 have shown that, using a cut-off range of 0.5 through 2 ng/mL, the sensitivity and specificity of PCT were 100% in discriminating bacterial meningitis from viral meningitis. Some of the seven studies published since seemed to demonstrate the usefulness of PCT in diagnosing meningitis. Finally, PCT was used effectively to shorten unnecessary antibiotic treatment for children seen in an hospital in Paris (France) during summer 2000.

Acute Disease↗

[Multicenter evaluation of four homogenous LDL-cholesterol assays].

International guidelines emphasize the importance of LDL cholesterol (LDL-C) assay in the care and follow-up of patients with cardiovascular risk. Most studies and common practice use Friedewald's formula for LDL-C calculation. The accuracy of the result depends closely on the precision of the input parameters (total cholesterol, triglycerides (TG) and HDL cholesterol), and discrepancies between calculated LDL-C and measurement by reference methods appear when TG exceed 4.5 mmol/L, or in the presence of abnormal lipoproteins. These restrictions and uncertainties in calculations have prompted the recent development of direct and homogeneous methods that fit all analyzers. A multicenter evaluation of four direct assays of LDL-C (Daiichi, Denka Seiken, Kyowa, Wako) was carried out on 45 serum samples (TG below 3.1 mmol/L) in eight laboratories using different analyzers. For three methods (Daiichi, Kyowa, Wako), the interlaboratory reproducibility was markedly improved relative to that of calculation. A strong correlation was found for all new methods when compared with a beta-quantification assay. Average bias in Denka Seiken assays was greater than Kyowa's and Daiichi's (although less dispersed for the latter) and for Wako all bias were positive. The relationship between bias variations and the lipid parameters of the samples was studied. Three methods, Daiichi, Kyowa and Wako, revealed a significant positive correlation between bias and serum VLDL-C/TG ratio, clearly indicating that cholesterol enrichment of VLDL was a source of variability in these assays. Specificity of the four methods was tested in situation of dyslipidemia by spiking isolated lipoproteins (chylomicrons, VLDL and HDL). This experiment revealed differences in behavior, most evidently upon addition of VLDL. No method was truly specific, but up to 8 mmol/L of TG the variations were acceptable. In the presence of type III hyperlipoproteinemia, however, only the Denka Seiken method was reliable. Linearity up to 20 mmol/L (Daiichi, Denka Seiken) or 14 mmol/L (Kyowa, Wako) of LDL-C allows these tests to be used in main routine cases. New direct assays are an obvious technological advance in terms of analytical performance and conveniency. Their use for the diagnosis and follow-up of hyperlipidemic patients offers an alternative that overcomes the limitations of the Friedewald calculation.

Blood Chemical Analysis↗

[Arginine and statins: relationship between the nitric oxide pathway and the atherosclerosis development].

Arginine, a semi-essential amino acid, plays a major nutritional and metabolic role. In particular, arginine is the precursor of nitric oxide which is involved in the endothelial function. Several factors, such as hypercholesterolemia, diabetes, ageing and hypertension are established risk factors for atherosclerosis, in particular by decreasing the availability of nitric oxide. Thus, endothelial nitric oxide synthase has a pivotal role against atherosclerosis. A suitable amount of cofactor and a sufficient intake of arginine have been shown to modulate nitric oxide-induced vasodilatation: despite the fact that the intracellular concentration of arginine is well above the Km of endothelial nitric oxide synthase, an arginine supplemented-diet is effective in increasing the production of nitric oxide. Several mechanisms have been proposed to explain this "arginine paradox": co-localization of the arginine transporter with endothelial nitric oxide synthase, intracellular arginine regeneration from citrulline, balance between endothelial arginase and nitric oxide synthase. Statins which are HMG-CoA reductase inhibitors inhibit the synthesis of mevalonate, and thus that of cholesterol. In addition, statins increase the stabilization of endothelial nitric oxide synthase mRNA. The co-operation between cholesterol synthesis and the upregulation of caveolin-1 on the one hand, and the activation of endothelial nitric oxide synthase on the other hand, is very tight. A depletion of cholesterol in the caveolae induces a decrease in caveolin-1 at the cell surface allowing NOS activation. Thus statins improve nitric oxide production and vasodilatation. In a recent work in the hypercholesterolemic Watanabe rabbit, we have demonstrated that the combination of arginine with a statin, namely atorvastatin, significantly hinders the spreading of atherosclerotic plaques as compared with monotherapies. Such association of a nutriment and a drug open a new area of therapeutic strategy.

Aging↗

[Reference values of apolipoproteins A1 and B. Contribution of international standardization. Travail collaboratif entre la SFBC, l'Arcol et le SFRL].

The utilization of two WHO reference materials, liquid and lyophilized, permitted international standardization of apolipoprotein measurements. We report here the results of a collaborative study between Arcol, SFBC and SFRL in order to establish reference ranges for apo A1 and B on nine standardized systems. A population of 1027 men and women supposed healthy, 4 to 60 year old, have been selected in two Centers for Preventive Medicine. The serum samples were aliquoted frozen at -20 degrees C the day of sampling and analysed by the manufacturers with IFCC standardized calibrants. A specific quality control was performed using a frozen pool of sera. For apo A1, the centile 2.5 of the reference population varies from 1.04 to 1.16 g/l. The range values for the centile 97.5 varies from 1.87 to 2.24 g/l. For apoB, the centile 2.5 varies from 0.43 to 0.57 g/l, and the centile 97.5 from 1.30 to 1.39 g/l. Only one system has a problem of dispersion with an upper limit equal to 1.20 g/l. These results improve that international standardization allowed actually a good comparability of the results, especially for apoB.

Adolescent↗

[Apolipoprotein B and LDL cholesterol: which parameter(s) should be included in the assessment of cardiovascular risk?].

High level of plasma apo B lipoproteins is a risk factor for coronary artery disease. However, which lipid parameters should be routinely assayed is a question still in debate. For this purpose, the authors have studied issues since 1992 comparing predictive and discriminative values of LDL-cholesterol and apo B in order to assess coronary artery disease. Indeed the respective advantages of these markers were still being discussed after an exhaustive review had been completed in 1992. Despite the number of the debates, none of the few studies about this topic rise any decisive arguments. In conclusion it is proposed that a true comparison of the predictive values of LDL-cholesterol and apo B should be carried out before making definitive recommendations concerning their clinical utility.

Apolipoproteins B↗

[Apolipoprotein E and its alleles in healthy subjects and in atherosclerosis].

Apolipoprotein E (apo E) plays a central role in lipoprotein metabolism as a ligand for LDL-, VLDL- and remnant receptors. It is mainly synthesized by hepatocytes and also by monocytes-macrophages. There are three common codominant isoforms E2, E3 and E4. Apo E2 binds defectively to LDL- and to remnant-receptors. Apo E alleles frequency varies from population to population around the world. In Europe, E4 allele frequency increases from south to north along the cardiovascular disease frequency gradient. On the other hand, the association between E2 allele and these diseases remains to be proved except for type III hyperlipoproteinemia. Apo E4 role in atherosclerosis could be explained, at least in part, by its high solubility in apo B lipoproteins. The average cholesterolemia of E4/E3 subjects is higher than E3/E3 subjects and E3/E3 subjects' cholesterolemia is higher than in E3/E2 subjects, probably because of a faster uptake of chylomicrons and VLDL remnants in E4/E3 subjects. The E4 allele also seems to play a role not only in diet response in combination with other genetic factors such as the Eco RI polymorphism of apo B but also in hypolipemic treatment. Apo E plays also a role in triglyceridemia control in association with other genetic and environmental factors such as lipoprotein lipase, apo B, LDL receptor and diet. Models of apo E knockout mice suggest a protective effect of monocyte-macrophageapo E in the vessel wall and HDL-apo E probably induces a high cholesterol efflux from macrophages. This effect counteracts the proatherogenic effect of VLDL- and IDL-apo E. The balance between these effects could be influenced by apo E phenotype.

Alleles↗