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J Chalas

Publications and source records attributed to J Chalas.

At least 37 records · Page 2Linked to original sources
PubMed1994

Hyperchloremic acidosis during grand mal seizure lactic acidosis.

OBJECTIVE: To evaluate the prevalence and the mechanism of hyperchloremic acidosis component (HClA) during lactic acidosis secondary to grand mal seizures. DESIGN: Retrospective study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: 35 patients admitted for grand mal seizures with lactic acidosis (pH < 7.35, TCO2 < 20 mmol/l and PaCO2 < 8 kPa). MEASUREMENTS: HClA was defined by the ratio: excess anion gap/HCO3 deficit (delta AG/delta TCO2) < 0.8. A difference in the distribution space of protons and their accompanying anion, i.e., a displacement of chloride from cells by the entering lactate, was evaluated by the ratio natremia/chloremia (Na+/Cl-). RESULTS: Immediately after seizures, a profound lactic acidosis was observed (pH = 7.22 +/- 0.17 (mean +/- SD), AG: 23.8 +/- 7.1 mmol/l, TCO2 = 14.5 +/- 5.3 mmol/l, lactate: 14.6 +/- 6.9 mmol/. HClA was present on admission in 11 patients (31.5%). Its prevalence increased to 73% after recovery. delta AG/delta TCO2 ratios were unrelated to creatinine, level and PaCO2, but dependent on the ratio Na+/Cl- (r = 0.803; p < 0.001, delta AG/delta TCO2 = 6.4 x (Na+/Cl-)-7.9). These data demonstrate that HClA is not a respiratory or renal phenomenon and suggest differences in the distribution spaces of hydrogen ions and their accompanying anions. CONCLUSION: HClA component may be associated with lactic acidosis in grand mal seizures and appears to be secondary to a lactate antiport. This phenomenon could be an immediate physiological response to a sudden metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1994

Serum concentrations of albumin, C-reactive protein, alpha 2-macroglobulin, prealbumin, fibronectin, fibrinogen, transferrin, and retinol binding protein in 55 patients with hepatic glycogen storage diseases.

Hepatic glycogen storage diseases are hereditary metabolic disorders involving the metabolism of glycogen. This study was designed to investigate the serum protein status in such diseases. Fifty-five patients with glycogen storage disease types I, III, VI, and IX, whose ages ranged from 1 month to 27 years, were included in this work. C-reactive protein, fibrinogen, alpha 2-macroglobulin, albumin, transferrin, fibronectin, retinol binding protein, and prealbumin serum concentrations were measured in each patient. In patients affected with type I glycogen storage disease, serum concentrations of alpha 2-macroglobulin, fibrinogen, C-reactive protein, and transferrin were significantly increased. In patients with types III, VI, and IX glycogen storage diseases, the concentration of alpha 2-macroglobulin was the only one that was significantly increased. Thus, even though this study raises more questions than it answers, it seems likely that the hepatic synthesis of some proteins may be increased in patients affected by hepatic glycogen storage diseases. This may indicate some degree of mild hepatic dysfunction in such metabolic disorders. However, further investigations are required to elucidate the discrepancies observed among the different types of diseases.

Adolescent↗
PubMed1994

[Enzymatic determination of sodium, potassium and chloride in plasma].

The Boehringer enzymatic reagents for Na, K and Cl determination on a Hitachi 717 automatic analyser at 37 degrees C were evaluated. Except for Na, the within-run and between-run precision assays gave CV within the SFBC ranges but were higher than those of the comparison analysers: Ektachem 500 Kokak, Dimension Ars Du Pont-De-Nemours and flame photometry. The linear ranges were larger than the usual clinical results. Accuracy, estimated from human controls, was 99 to 103% for Na and K, and 105% for Cl. Comparison of plasma from 102 to 152 patients showed a good concordance for sodium with the Dimension ARS (y = 1x + 0). On the contrary, with Ektachem Kodak, differences appeared, particularly for high values (y = 0.91x + 13.6). For potassium, the concordance was good with flame photometry (y = 1x + 0.1) and Ektachem Kodak (y = 0.94x - 0.16). For chloride, comparison was satisfactory except for high values which were underestimated by the enzymatic method: Dimension ARS (y = 1.03x - 4.8), Ektachem Kodak (y = 0.91x + 9.8). The enzymatic methods were very easy to perform and can be adapted on any autoanalyser at 37 degrees C. We conclude that they are suitable for routine clinical determination. Urinary assays are currently being developed.

Autoanalysis↗
PubMed1994

[Evaluation of the technique of CKMB assay using Ektachem (500 and 700)].

The aim of this study was to compare the dry-chemistry CKMB Ektachem method to a liquid immunoinhibition method (Merck/Cobas Bio) and to the electrophoretic method (Helena France), both on patients (n = 95) and control (4 specimens from different commercial origin) sera. The Ektachem method was found linear in the range tested (7 to 97 U/l). Within run imprecision tested with low, medium and high control sera were satisfying (CV 3-4%) as well as between run imprecision (CV < 10%), for CKMB activities of at least 30 U/l. As compared to the liquid immunoinhibition method (Merck), the results of patient sera were very close but slightly lower (y = 0.97x-1; r = 0.74; y = Ektachem, x = Merck). As compared to the electrophoretic method, the Kodak Ektachem method showed a specificity of 74% and a sensitivity of 85% (n = 95). A close agreement (r = 0.73) between these two methods was obtained for samples with a total CK activity at least 3 times over the upper limit of normal range. We therefore conclude that the Kodak Ektachem CKMB method allows a rapid and easy determination of CKMB activity for samples undergoing total CK activity 3 times over the upper limit of normal range. Like all liquid immunoinhibition methods, the Kodak Ektachem method shows some lack of specificity and does not show a better concordance with the electrophoretic method than does the Merck/Cobas Bio method.

Creatine Kinase↗
PubMed1990

[Anti-radical enzymes, oxygenated free radicals and lipoperoxydation in rheumatoid polyarthritis. Effects of treatment with D-penicillamine].

Three aspects of the action of oxygenated free radicals were studied in 10 controls and 20 patients with rheumatoid arthritis, 11 not treated and 9 treated with D-penicillamine. Free radical production was evaluated in whole blood, malondialdehyde was measured in plasma, the concentration of antiradicular enzymes (copper and manganese superoxide dismutase, catalase and glutathion peroxydase) in hemolysate, platelets and plasma and copper superoxide dismutase activity in a chloroform erythrocyte extract. Only patients treated with D-penicillamine showed a significant decrease in the concentration of platelet anti-radicular enzymes and plasma manganese superoxide dismutase. The involvement of oxygenated free radicals in the pathophysiology of rheumatoid arthritis and in the mechanism of action of D-penicillamine in this pathology is discussed.

Arthritis, Rheumatoid↗
PubMed1989

[Clinical electrophysiologic properties of magnesium and correlations with its anti-arrhythmia efficacy in acquired torsade de pointes].

Recently, intravenous administration of low doses of magnesium has proved remarkably effective in the treatment of acquired torsade de pointe, but its electrophysiologic effects remain poorly understood. Three clinical cases are reported in three distinct situations (quinidine treatment, hypokalemia, bradycardia with complete atrioventricular block). These cases confirm the efficacy of magnesium, which acts without notable modification of ventricular cycles or the duration of repolarization. In ten patients undergoing intracavitary exploration, the electrophysiologic parameters were analyzed before and after injection of magnesium sulfate (35 mg/kg). Only three parameters were significantly altered; the corrected sinusal recovery time (increase from 245 +/- 92 ms to 296 +/- 96 ms), the effective nodal refractory period (increase from 333 +/- 98 ms to 346 +/- 93 ms), and the Wenckebache period (decrease from 157 +/- 28/min to 144 +/- 21/min). No changes were noted in other parameters, notably ventricular (QT interval, QRS duration, HV interval, and effective ventricular refractory period). The arrhythmic action on the ventricle is therefore remarkable and is not accompanied by patent electrophysiologic effects. The efficacy of magnesium in torsade de pointe may suggest action on calcium currents.

Aged↗
PubMed1989

[Determination of blood level of muscle enzymes in glycogenoses with liver involvement: a diagnostic criterion].

Serum muscle enzyme activity assays were routinely performed in 36 patients with glycogen storage diseases (15 types 1a and 1b, 12 type III, and 9 types VI and IX). Creatine phosphokinase serum activity was increased only in type III. Glutamate-pyruvate transaminase, aldolase and lactate dehydrogenase serum activities were increased in all the forms of glycogen storage disease studied. Muscle involvement may at least partly explain the increased serum enzyme activities in type III.

Alanine Transaminase↗
PubMed1987

[Fructosamine, a new marker of blood glucose control in the diabetic].

Serum fructosamine assay is a new, simple and fast method used to evaluate serum glycosylprotein concentrations. We performed this assay in 96 healthy controls, 95 patients with diabetes (insulin-dependent in 71, non insulin-dependent in 24) and 23 non diabetic pregnant women. Serum fructosamine concentrations were increased and correlated with percents of glycosyl haemoglobin in all diabetics, irrespective of the type of diabetes. However, the low correlation coefficient and the fact that some individual values plotted were distant from the regression slope suggested that fructosamine does not have the same biological significance as glycosyl haemoglobin: the formation and degradation kinetics of these two substances are known to be very different. Fructosamine values were tightly close together in controls and in pregnant women, the latter showing lower values.

Adolescent↗
PubMed1987

[Toxicity of oxygen and (Cu) superoxide dismutase and (Mn) superoxide dismutase in newborn infants with respiratory distress. Preliminary results].

Twelve premature newborns mechanically ventilated with high FiO2 for hyaline membrane disease were tested for SOD contents during their first two weeks of life. CuSOD and MnSOD were measured in plasma, platelets and red cells using a radioimmunology method. No correlation was found between FiO2 levels neither with CuSOD and MnSOD contents. Furthermore no correlation was found between the SOD contents, at birth, and the constitution of bronchopulmonary dysplasia (BPD). Our results don't prove any relationship between lack of SOD and BPD. BPD pathogeny is certainly plurifactorial. Other protecting systems against O2 toxicity are also known to play an important role.

Bronchopulmonary Dysplasia↗
PubMed1987

[Concentrations of superoxide dismutase (copper and manganese), catalase and glutathione peroxidase in red cells, platelets and plasma in patients with rheumatoid polyarthritis].

Antioxidant enzymes assays (CuZnSOD, MnSOD, catalase glutathione peroxidase) have been performed by radioimmunoassay in erythrocytes, platelets and plasma of rheumatoid polyarthritis patients. No difference has been shown as compared with control subjects whatever the therapy or the length of time for which the patients have been affected. If a deficiency in antioxidant enzymes is related to the destruction of joint tissues by free radicals, it cannot be detected in blood tissue elements.

Adult↗
PubMed1987

[Determination of fructosamine on the Cobas-Bio centrifuge system. Importance of white reagent].

An automated assay for fructosamine on Cobas-Bio centrifugal analyzer with subtracting the contribution of the albumin matrix present in standards is described. This rapid and simple test has suitable analytical performances. Fructosamine concentrations were measured in 100 healthy subjects and in 95 diabetic patients. For the diabetic patients, results were compared with those obtained from a commercialized test kit.

Adult↗
PubMed1981

[Modifications of disulfiram and its metabolites in blood in alcoholic hepatopathy (author's transl)].

In cirrhotic, steatosic and healthy subjects, the authors studied the metabolism of disulfiram (TETD) administrated orally (500 mg) 3 consecutive days. Carbon disulfide (CS2) and the whole TETD, diethyl dithiocarbamate (DDC) disulfides, were determined by a gas chromatographic method. The evolution of metabolites is similar in steatosic and healthy subjects. In cirrhotics the CS2, DDC and disulfides level increase within the 3 days. This phenomenon may be related with hepatic toxicity of TETD and with the persistence of disulfiram-alcohol reaction. The authors suggest to use low doses of disulfiram in cirrhotic.

Adult↗