2009 Publications

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    EDTA sample contamination is common and often undetected, putting patients at unnecessary risk of harm.
    (Wiley Open Access, 2009-08-01) Sharratt, Caroline L; Gilbert, Christopher J; Cornes, Michael P; Ford, Clare; Gama, Rousseau
    Background: Potassium ethylenediaminetetraacetic acid (EDTA) is a sample tube anticoagulant used for many laboratory analyses. Gross potassium EDTA contamination of blood samples is easily recognised by marked hyperkalaemia and hypocalcaemia. However, subtle contamination is a relatively common, often unrecognised erroneous cause of spurious hyperkalaemia. Potassium EDTA contamination may also cause hypomagnesaemia and hypozincaemia. There are, however, no data on the prevalence of EDTA contamination as a cause of hypocalcaemia, hypomagnesaemia and hypozincaemia. Methods: Following a recent service evaluation, we measure EDTA in serum samples from patients with unexplained hyperkalaemia (serum potassium > 6.0 mmol/l). In addition, over a 1‐month period EDTA concentrations were measured in hypocalcaemic (serum adjusted calcium < 2.0 mmol/l), hypomagnesaemic (serum magnesium < 0.7 mmol/l) and hypozincaemic (serum zinc < 11 μmol/l) serum samples. Results: Ethylenediaminetetraacetic acid contamination was detected in 31 samples, nine of which were detected by our routine screening programme. The remaining 22 samples represented 14.3% (19/133) of hypocalcaemic samples, 4.8% (5/104) of hypomagnesaemic samples and 1.4% (2/139) of hypozincaemic samples. A total of 25/31 (80.6%) of patients were re‐bled, of which 23/25 (92%) results normalised. Conclusions: Factitious hyperkalaemia, hypocalcaemia and hypomagnesaemia caused by potassium EDTA contamination in our studies are relatively common, and if unrecognised may adversely affect patient care and waste scarce healthcare resources. Correct order of draw of blood samples, improved education and routine laboratory screening of EDTA are necessary to prevent and identify EDTA contamination.
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    Algorithm combining HbA and fasting plasma glucose for screening subjects for OGTT.
    (Wiley Online, 2009-07-30) Likhari, Taruna; Gama, Rousseau
    No abstract available
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    Glycaemia‐independent ethnic differences in HbA1c in subjects with impaired glucose tolerance.
    (Wiley Online, 2009-10-01) Likhari, Taruna; Gama, Rousseau
    Aim: To study the ethnic differences in HbA(1c) between Whites and South Asians with impaired glucose tolerance. Methods: We audited 75g oral glucose tolerance tests (OGTT) performed in Clinical Chemistry, New Cross Hospital, Wolverhampton over 1 year. HbA(1c) and glycaemia were compared between Whites and South Asians with impaired glucose intolerance (IGT). Results: There were 46 South Asians (22 female) and 88 Whites (41 female). South Asian subjects were younger (59.2 +/- 14.31 vs. 67.6 +/- 12.63 yrs; P < 0.001) and weighed less (78.1 +/- 17.2 vs. 87.47 +/- 19.1 kgs; P < 0.001) than White subjects. HbA(1c) levels were higher (6.5 +/- 0.7 vs. 6.1 +/- 0.6%; P < 0.001) in South Asians compared to Whites. Fasting glucose (5.71 +/- 0.5 vs. 5.93 +/- 0.7; P = 0.039) was lower in South Asians but 2hour glucose (10.5 +/- 1.0 vs. 10.40 +/- 0.9; P = 0.404) was similar in both ethnic groups. Conclusion: South Asians have higher HbA(1c) levels than Whites despite lower fasting glucose value on OGTT, indicating ethnic differences in HbA(1c) are due to glycaemia-independent factors.
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    Revised national guidelines for the analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage: interpret with caution.
    (BMJ Publishing Group, 2009-11-01) Griffiths, Melaine J; Ford, Clare; Gama, Rousseau
    No abstract available.
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    Avoiding spurious hyperkalaemia.
    (BMJ Publishing Group, 2009-11-17) Gama, Rousseau; Cornes, Michael P; Ford, Clare
    No abstract available.