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Background: There is limited data and literature on the issue of cardiac troponin test requesting by general practitioners (GPs). It was therefore our aim to audit the cardiac troponin test requests made by GPs in our community with a view to develop an informed strategy for assay provision and reporting of results. Methods: A retrospective audit was undertaken of data in our laboratory database for all cardiac troponin T (cTnT) tests requested by GPs between January and June 2005. A prospective audit was then carried out between July and December 2005 using the telephone interview method. The number and distribution of tests, the reasons for the request and the intended action by the GPs were quantified. Results: Forty-five of 46 of the results of both the retrospective and prospective audits were negative based on the 99th percentile level with less than 10% imprecision (cTnT <0.03 μg/L). During the one-year study period, we had requests from 24 general practices with a mean and mode of two and one requests per general practice respectively. The most common reason for the request was found to be chest pain that had occurred more than 24 h ago. Conclusion: Bearing in mind the limitations of an audit study, our findings obviate the use of cTnT in general practice. We suggest that the laboratory should liase with the GP and advise referral for specialist care if clinical suspicion of acute coronary syndrome is high. [ABSTRACT FROM AUTHOR]

Laboratory monitoring is an important part of the assessment and management of all patients requiring enteral or parenteral nutritional support. The National Institute for Health and Clinical Excellence (NICE) has recently published a report on the provision of nutrition support in hospitals and in the community. Of special relevance are the recommendations that all laboratories which support a clinical nutrition service should be part of a multidisciplinary Nutrition Support Team, and that they should ensure that there is an agreed local protocol for laboratory testing and monitoring of patients receiving nutritional support. [ABSTRACT FROM AUTHOR]

Background: The cardiac troponins have been shown to be sensitive and specific biochemical markers of myocardial infarction and highly prognostic for future adverse events in patients with acute coronary syndromes. There have been reports suggesting that haemolysis causes a negative interference in the cardiac troponin T (cTnT) assay but the mechanism(s) involved remain unknown. Here we show the effects of haemolysis and haemoglobin per se on the cTnT assay. Methods: The effect of haemolysis was studied by the addition of prepared haemolysate to serum samples with known and clinically relevant cTnT levels. The effect of haemoglobin was studied by the addition of haemoglobin of increasing concentrations and noting its effect on the level of cTnT measured. The effect of putative proteases was determined indirectly by incubating samples with spiked cTnT with various protease inhibitors and observing the changes in the measured cTnT levels. Results: The results show that both haemolysis, which is the release of haemoglobin and corpuscular contents, and haemoglobin itself negatively interfere in the cTnT assay in a concentration-dependent manner, although the former had a greater magnitude of effect. On haemolysis, indirect evidence suggests that proteases are released which degrade the cTnT in serum, thus causing the decreased levels detected. Pepstatin A, a reversible inhibitor of aspartic proteinases, effectively inhibited the loss of cTnT in serum at 37°C and pH 7.4 over a 48-h period. We found that at a haemoglobin level of 0.75 g/L, cTnT declined by more than 10% of the initial concentration, suggesting that falsely decreased levels due to haemolysis may significantly affect the clinical utility of the assay. Conclusions: Haemolysis, haemoglobin per se and possibly proteolysis play a role in the negative interference in cTnT assays. Measures to reduce this interference must be implemented. [ABSTRACT FROM AUTHOR]

Background: Oxidative stress is a consequence of critical illness, and may have an impact on survival. We studied markers of oxidative damage and antioxidant (AO) protection and compared them with clinical scores and outcome. Methods: Blood sampling and clinical scoring was carried out on 60 consecutively admitted intensive therapy unit (ITU) patients within 24 h of admission and then every three days of ITU stay. The patients included 30 surgical and 30 medical patients, of whom 46 survived their stay in ITU. Clinical scoring was by Acute Physiology and Chronic Health Evaluation (APACHE) II score, multiple organ dysfunction (MOD) score and sepsis rating. Oxidative damage was assessed by measurement of plasma malondialdehyde (MDA) and F2 isoprostanes (F2 IsoPs). AO protection was assessed by measurement of plasma total AO status, AO gap, ascorbic acid and the enzymes glutathione peroxidase and superoxide dismutase. Results: Both clinical markers, APACHE II and MOD, and oxidative damage markers MDA and F2 IsoPs were significantly higher in non-survivors (NS) than in survivors (S) at the time of admission. Median (interquartile ranges) were (APACHE II), 14[12–17] (S), 20.5[16.7–22.2] (NS),P<0.0001; (MOD), 3.0[2.0–5.0] (S), 8.0[4.7–9.2] (NS), P<0.0005; (MDA, μmol/L), 0.22[0.19–0.27] (S), 0.25[0.20–0.34] (NS), P=0.04 and (F2 IsoPs, pg/mL), 9.7[6.0–9.9] (S), 11.0[9.0–12.0] (NS), P=0.01. Oxidative damage markers reduced (improved) in the survivors but increased in the non-survivors. There was little difference between the groups in AO protection markers. There was a significant positive correlation between MOD and markers of oxidative damage at the time of admission (r=0.40, P=0.003, F2 IsoPs; r=0.28, P=0.035, MDA) and between the oxidative damage markers themselves (r=0.32, P=0.017). Conclusion: Increased oxidative stress is associated with poor outcome in critically ill patients, and may be a prognostic indicator. Oxidative damage markers are more useful than AO protection markers in predicting outcome. [ABSTRACT FROM AUTHOR]