[Prevention of neonatal hyperbilirubinemia by enzyme inducers. Effectiveness of a phenobarbital-nikethamide association].
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Biomedical subjects
Publications and source records attributed to S Marcovina.
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BACKGROUND: The Veterans Affairs Cooperative Study in Type II Diabetes Mellitus prospectively studied insulin-treated patients with type 2 (non-insulin-dependent) diabetes mellitus, achieving 2.1% glycosylated hemoglobin separation between intensive- and standard-treatment arms (P<.001) for 2 years. OBJECTIVE: To assess the effect of intensive therapy on serum fibrinogen and lipid levels, compared with standard treatment. METHODS: One hundred fifty-three male subjects with type 2 diabetes mellitus and who required insulin treatment were recruited from 5 Veterans Affairs medical centers. The subjects were divided into intensive- and standard-treatment arms for a randomized prospective study. Dyslipidemia was managed identically in both arms (diet, drugs). Fibrinogen levels and lipid fractions were measured in the full cohort. Lipid fractions are separately reported in patients not treated with hypolipidemic agents. RESULTS: There were no baseline differences between arms. Fibrinogen levels rose in the intensive-treatment arm at 1 year (from 3.34+/-0.12 to 3.75+/-0.15 g/L; P<.001) but returned to baseline at 2 years (3.47+/-0.12 g/L). There was no change in the standard-treatment arm. Triglyceride levels decreased in the intensive-treatment arm from 2.25+/-0.27 to 1.54+/-0.14 mmol/L (199+/-24 to 136+/-12 mg/ dL) at 1 year (P = .004) and to 1.74+/-0.18 mmol/L (154+/-16 mg/dL) at 2 years (P = .03); there was no change in the standard-treatment arm. Cholesterol levels decreased in the intensive-treatment arm at 1 year from 5.4+/-0.21 to 4.99+/-0.13 mmol/L (207+/-8 to 193+/-5 mg/dL) (P = .02); there was no change in the standard-treatment arm. Levels of low- and high-density lipoprotein cholesterol decreased in the standard-treatment arm only by 2 years, from 3.44+/-0.13 to 3.16+/-0.10 mmol/L (133+/-5 to 122+/-4 mg/ dL) (P =.02) and from 1.10+/-0.03 to 1.00+/-0.03 mmol/L (42+/-1 to 38+/-1 mg/dL) (P<.001) for low-density and high-density lipoprotein cholesterol, respectively. Levels of apolipoprotein B decreased in both treatment arms (P<.001), and apolipoprotein A1 levels decreased in the standard-treatment arm (P<.01). Lipoprotein (a) levels did not change in either treatment arm. Lipid results were essentially identical whether examined in the full cohort or excluding those patients receiving hypolipidemic agents. CONCLUSIONS: Intensive insulin therapy led to a potentially beneficial reduction in serum triglyceride levels and preservation of high-density lipoprotein cholesterol and apolipoprotein A1 levels. However, it caused transient elevation in plasma fibrinogen levels, a possible thrombogenic effect.
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A user programmable microcomputer-based integrated system for automatic analysis in the clinical chemistry laboratory is presented. Friendly user-instrument interaction helps the operator when defining tests and analytical conditions or entering sample data and test requests. Quality control data are retained for the automatic production of various statistical lists and graphs. Routine operator intervention is limited to reagent preparation, sample loading onto the autosampler plate, definition of the tests to be performed on each of the samples and data validation before the generation of reports. Finally, connection with an existing laboratory management system is provided by means of a standard serial interface.
The aim of this study was to evaluate the ability of plasma levels of apo A-I and apo B to discriminate between male patients with and without angiographically determined coronary artery disease (CAD) in comparison to the levels of cholesterol, HDL-cholesterol and triglycerides. The plasma apo A-I and B levels were measured by a radial immunodiffusion assay that made use of well characterized monoclonal antibodies. Univariate statistical analysis showed that the mean values for HDL-cholesterol and apo A-I were significantly lower in patients with single-, double- and triple-vessel disease than in the control subjects. The mean values for plasma cholesterol and apo B were significantly higher in the group with double- and triple-, but not single-vessel disease, than in the group without CAD. No statistically significant difference among groups was found for plasma triglyceride values. Since the considered variables failed to assess the severity of the disease, as determined by the number of vessels involved, the 3 groups of patients with CAD were combined into one group. A multiple logistic analysis, performed in order to assess the independent role of the variables and to estimate the corresponding odds ratio, indicated an independent association of HDL-cholesterol, apo A-I and apo B with CAD. When the multiple logistic analysis was repeated with a stepwise procedure, only apo A-I and B entered into the model. The results of our study indicate that plasma levels of apo A-I and B are more useful than plasma lipid in detecting the presence or absence of coronary artery disease in a group of male patients undergoing coronary angiography.
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The DNCB skin test was carried out on 47 patients with solid tumours. Fifteen deaths were noted among subject displaying a negative response and in 1/24 positives. A statistically significant relation was found between negativity and several blood chemistry parameters: increased IgG, positive PCR, inversion of the A/G ratio and the fall in peripheral lymphocytes. The method employed for the test is described.