Semiquantitative measurement of drugs in urine samples and measurement of pharmaceutical active substances in serum samples using the Beckman Coulter Synchron LX20 PRO clinical system.

Our manuscript describes the investigation of options for the detection and semiquantitative assay of drug (metabolites) and the assay of relevant pharmaceutical active substances using the LX20 PRO (Beckman Coulter) in comparison with the Dimension RxL (Dade Behring) and the TDx or AxSYM (Abbott) system. Drug tests carried out with the LX system satisfy sensitivity and selectivity requirements. The assay of the pharmaceutical active substances revealed a few noticeable clusters of values with valproate and, in particular, digitoxin, that can be attributable to the reagents used rather than to the system itself, which is highly stable and reproducible in terms of operation. These values are thus devoid of any considerable clinical significance.

Quantitative bedside testing of troponin T: is it equal to laboratory testing? The Cardiac Reader Troponin T (CARE T) study.

The progressive evolution of cardiac marker testing in patients with acute coronary syndromes has extended their role into risk stratification and guidance of therapeutic regimen. To provide utilization of cardiac markers around the clock and facilitate the diagnostic work-up of patients with acute chest pain in the emergency room, a point-of-care system for quantitative troponin T and myoglobin testing in whole blood samples was developed. Aim of this multicenter study was to evaluate bedside quantitative determination of myoglobin and troponin T in chest pain patients in a clinical routine setting. Five hospitals in Germany were contributing to blood sampling and 741 patients were included four hours (median) after onset of cardiac pain. Comparison between the rapid test and the established laboratory-based method showed a sufficient agreement of results with a correlation of r = 0.89 (Y = 0.856x + 0.029) for troponin T and r = 0.912 (Y= +1.145x + 3.457) for myoglobin. Diagnostic sensitivity and prognostic power of the troponin T results obtained in the emergency unit were thoroughly equivalent to the laboratory-based method. The results show that the cardiac reader system represents a promising alternative to central laboratory testing with an accuracy sufficiently for rapid decision making in the emergency room. Myoglobin results in this study did not add supplementary information to the cardiac reader troponin result. However, point-of-care testing of troponin T is advantageous whenever marker results could positively effect initial triage decisions and interventional management choices.

Increased plasma concentrations of soluble CD40 ligand in acute coronary syndrome depend on in vitro platelet activation.

BACKGROUND: Soluble CD40 ligand (sCD40L) was suggested as a novel biomarker of cardiovascular risk. We examined the effect of preanalytical variation on the measurement of sCD40L concentration. METHODS: From healthy control individuals (n = 20) and patients with acute coronary syndrome (ACS) (n = 20) or sepsis (n = 20), we obtained blood drawn into 5 tubes containing citrate or a mixture of citrate, theophylline, adenosine, and dipyridamole (CTAD). The tubes were incubated for 30 min at room temperature or 0 degrees C before a single or double centrifugation (15 min, 2500 g) at room temperature or 4 degrees C, respectively. sCD40L, beta-thromboglobulin (betaTG), and platelet factor 4 (PF4) concentrations were measured using immunoassays. RESULTS: Concentrations of sCD40L were very low in all CTAD and citrated samples maintained at 0 degrees C (median < or = 0.076 microg/L). Although increased betaTG and PF4 confirmed disease-related in vivo platelet activation, sCD40L was not higher in patients than in controls. In contrast, if the samples were processed at room temperature, sCD40L was significantly higher in ACS patients than in controls (P <0.02 in CTAD and citrated plasma at room temperature). Moreover, the betaTG:PF4 ratio decreased in patient but not control CTAD samples, suggesting a greater susceptibility of patient platelets to in vitro activation. CONCLUSIONS: Increased sCD40L concentrations resulted from in vitro platelet activation during sample preparation. Disease-related in vivo activation did not contribute to sCD40L concentrations in plasma. Therefore, published studies of sCD40L demand cautious interpretation, because their preanalytical conditions were not standardized.

Severe septic inflammation as a strong stimulus of myocardial NT-pro brain natriuretic peptide release.

BACKGROUND: Septic shock (SS) has recently been identified as stimulus of N-terminal pro-brain natriuretic peptide (NT-proBNP) release. We tested whether SS mediates NT-proBNP release through cardiomyocyte necrosis. Moreover, the discriminative value of NT-proBNP for the distinction between SS and non-septic shock (NSS) was assessed. METHODS: The study included 50 ICU patients with SS (n=25) and NSS (n=25), 40 patients with acute coronary syndrome and elevated troponin-I (ACStrop+) and 16 patients with unstable angina and normal troponin-I (UAtrop-). Eleven subjects without inflammation or cardiac disease served as controls. NT-proBNP levels of coronary patients were measured on admission, those of ICU patients 48 h after onset of shock symptoms. RESULTS: ACStrop+ (1525 [25th-75th percentile: 790-3820] pg/L) and NSS (687 [254-1552]) patients showed increased NT-proBNP levels above those of UAtrop- patients (107 [43-450], p<0.001) and controls (52 [42-99], p<0.001), but SS patients exhibited still higher levels (11,335 [4716-25,769], p<0.001 vs all others). Among ICU patients with shock symptoms, NT-proBNP discriminated SS and NSS with high sensitivity and specificity (area under ROC curve: 0.946 [95% confidence interval, 0.872-1.019]). NT-proBNP correlated with troponin-I, as marker of cardiomyocyte damage, among ACStrop+ (p<0.001) and SS patients (p=0.013). But, whereas SS patients showed the greatest NT-proBNP values, ACStrop+ patients had higher troponin-I levels (p<0.001), suggesting different mechanisms by which myocardial ischemia and SS mediate NT-proBNP release. CONCLUSIONS: SS is a more potent stimulus of NT-proBNP release than myocardial ischemia. NT-proBNP reliably distinguishes SS from other forms of shock. SS-related NT-proBNP release appears to involve cardiomyocyte damage but not genuine cardiomyocyte necrosis.