ABSTRACT
Five different commercial immunoassays for the measurement of creatine kinase isoenzyme 2 mass concentration were compared using human plasma samples covering a wide range of creatine kinase 2 concentrations. The immunoassays studied differ in the detection systems, in the specificity of the antibodies and in the calibrators used. Intermethod comparison by regression analysis showed differences in the results of creatine kinase 2 mass concentration. The following ratios were deduced from the obtained equations: Elecsys=1.10xImmulite=1.20xIMx=1.26xACS:180= 1.33 x Stratus. The commutability of different materials prepared by diluting purified human creatine kinase 2 in biological and synthetic matrices was studied using the different immunoassays in comparison with human plasma specimens. Almost all the materials tested were not commutable.
Subject(s)
Creatine Kinase/blood , Immunoassay/methods , Calibration , Creatine Kinase/chemistry , HumansABSTRACT
BACKGROUND: Serotonergic system alterations were studied in 51 depressed patients classified according to DSM-III-R criteria for major depression with melancholia compared to 31 healthy controls. METHOD: [3H]Imipramine and [3H]paroxetine binding sites and the 5HT2 receptor were simultaneously determined in blood platelet membranes. RESULTS: A significantly lower maximum binding in [3H]imipramine binding was observed in depressed patients compared to controls (1134+/-74 vs. 1712+/-106 fmol/mg protein, P<0.0001) without changes in the equilibrium dissociation constant (1.10+0.05 vs. 1.25-/+0.09 nM). [3H]Paroxetine binding did not differ between the two groups (Bmax, 1441+/-55 vs. 1280+/-81 fmol/mg protein; Kd, 0.060+/-0.002 vs. 0.062+/-0.002 nM). The K(d) value of 5HT2 binding was lower in depressed patients than controls (0.95+/-0.04 vs. 1.15+/-0.09 nM, P<0.039) without changes in maximum binding (140+/-11 vs. 127+/-14 fmol/mg protein). CONCLUSIONS: Taken together, these results suggest that [3H]imipramine and 5HT2 receptors may be good biological markers for serotonergic dysfunction in depressive disorders.