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P J Twomey

Publications and source records attributed to P J Twomey.

16 recordsLinked to original sources
PubMed2006

Adjusting copper concentrations for caeruloplasmin levels in routine clinical practice.

BACKGROUND: An investigation on copper metabolism usually includes the measurement of serum levels of copper and caeruloplasmin. Using these levels, some laboratories derive levels of non-caeruloplasmin-bound copper (NCC); however, a considerable number of patients may show negative values, which is not physiologically possible. AIM: To derive an equation for adjusted copper in a manner similar to that widely accepted for adjusted calcium. METHODS: A linear regression equation for the relationship between caeruloplasmin and copper was used: [copper] (micromol/l) = 0.052x[caeruloplasmin] (mg/l). An equation for copper adjusted for caeruloplasmin was derived using this equation and the reference interval of 10-25 micromol/l for copper. RESULTS: The derived equation was [adjusted copper] (micromol/l) = [total copper] (micromol/l)+0.052x[caeruloplasmin] (mg/l)+17.5 (micromol/l). The adjusted copper concentrations on the 2.5th and 97.5th centiles were 12.7 and 21.5 micromol/l, respectively, with the population having a gaussian distribution. The relationship between NCC and the adjusted copper concentrations is linear and independent of caeruloplasmin concentration. CONCLUSION: Calculation of copper adjusted for caeruloplasmin uses the same variables as those for NCC. Accordingly, the problems that are caused by the lack of specificity of caeruloplasmin immunoassays are the same as those identified for NCC. This calculation, however, overcomes the negative values that are found in a considerable minority of patients with NCC, as well as age and sex differences in the caeruloplasmin reference interval. As the concept is already familiar to non-laboratory healthcare professionals in the form of calcium adjusted for albumin, this method is potentially less confusing than that for NCC.

Ceruloplasmin↗
PubMed2005

Differences between serum and plasma for intact parathyroid hormone measurement in patients with chronic renal failure in routine clinical practice.

BACKGROUND: Parathyroid hormone (PTH) is important in the evaluation of patients with calcium metabolism disorders and/or chronic renal disease. AIMS: To assess the differences between serum and plasma PTH measurements using the Advia Centaur. METHODS: Twenty six paired serum and edetate samples from patients with chronic renal failure were analysed using the Advia Centaur. RESULTS: The EDTA results ranged from 2.3 to 76.1 pmol/litre and the Deming regression equation was: serum = 0.8927 EDTA - 0.447. The percentage difference plot had a mean difference of 13.8% (95% confidence interval, 2.2% to 25.4%; significant). The available time to separation and freezing ranged from 10 to 231 (median, 85) minutes. The correlation coefficient for the percentage difference against the time to separation and the percentage difference against the mean PTH concentration were -0.13 and -0.07, respectively. CONCLUSIONS: These results go beyond the previous controlled research conditions by showing that such differences between serum and edentate plasma exist in routine clinical practice. They also show that intra-individual PTH differences as large as 25.0% can exist on the same day between serum and edetate plasma. This may partly explain some of the variability of PTH concentrations found in some patients with chronic renal failure.

Blood Specimen Collection↗
PubMed2005

An unusual case of hyponatraemia in diabetic ketoacidosis.

This report outlines a case of diabetic ketoacidosis associated hyponatraemia in an 18 year old woman with type 1 diabetes who presented to the accident and emergency department and was quickly admitted to the intensive treatment unit. Causes of hyponatraemia include sodium depletion, pseudohyponatraemia, and extracellular hypertonicity. Hypertonicity secondary to hyperglycaemia is thought to be the major cause of hyponatraemia in diabetic ketoacidosis. Indirect and direct sodium measurements were performed until the glucose concentration stabilised. The large difference between the presenting sodium concentrations is consistent with pseudohyponatraemia. However, the causes of pseudohyponatraemia (large increases in total protein, triglyceride, and cholesterol concentrations) were excluded. Analytical error should always be considered when the laboratory results do not agree with the clinical picture. Sometimes, however, even after excluding all known effects, the cause may remain unexplained, as in this case.

Adolescent↗
PubMed2005

Estimated GFR.

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Creatinine↗
PubMed2004

Upregulation of the CD40/CD40 ligand dyad and platelet-monocyte aggregation in cigarette smokers.

BACKGROUND: Smoking is a potent cardiovascular risk factor and is associated with proinflammatory and prothrombotic responses. The CD40/CD40 ligand (CD40L) dyad and platelet-monocyte aggregation mediate a range of proinflammatory and prothrombotic processes thought to be important in atherothrombosis. We investigated whether expression of the CD40/CD40L dyad and platelet-monocyte aggregation are altered in cigarette smokers. METHODS AND RESULTS: C-reactive protein (CRP), soluble (s) CD40L, and surface expression of CD40L on platelets and T cells and of CD40 on monocytes and platelet-monocyte aggregates were compared in 25 cigarette smokers and 25 age- and gender-matched nonsmokers. Cigarette smokers had increased serum CRP (2.47+/-2.60 versus 0.94+/-0.96 mg/L, P=0.008) and appeared to have elevated plasma sCD40L (0.8+/-1.09 versus 0.37+/-0.21 ng/mL, P=0.07) concentrations. Smokers also had increased surface expression of CD40 on monocytes (45.9+/-7.7% versus 39.9+/-6.5%, P=0.006), of CD40L on platelets (2.9+/-1.0% versus 2.3+/-0.6%, P=0.03), and of platelet-monocyte aggregates (26.6+/-10.9% versus 19.7+/-8.6%, P=0.02). Plasma cotinine concentrations correlated with monocyte CD40 expression, platelet CD40L expression, and platelet-monocyte aggregates. CONCLUSIONS: Cigarette smokers have upregulation of the CD40/CD40L dyad and platelet-monocyte aggregation that may account for the atherothrombotic consequences of this major cardiovascular risk factor.

Adult↗
PubMed2004

Increased CD40 ligand and platelet-monocyte aggregates in patients with type 1 diabetes mellitus.

BACKGROUND: Diabetes mellitus is a major risk factor for cardiovascular disease and is associated with a proinflammatory and prothrombotic state. We investigated whether CD40 ligand (L) expression and platelet-monocyte aggregation are increased in patients with type 1 diabetes. METHODS: Serum C-reactive protein (CRP) and soluble (s) CD40L concentrations, platelet surface CD40L expression and platelet-monocyte aggregates were measured in 22 patients with uncomplicated type 1 diabetes and 22 age- and sex-matched non-diabetic control subjects. RESULTS: In comparison to controls, patients with type 1 diabetes had higher serum CRP concentrations (3.29 +/- 0.9 mg/L versus 0.99 +/- 0.2mg/L, P = 0.01), serum sCD40L concentrations (10.0 +/- 1.4 ng/mL versus 4.6 +/- 0.6 ng/mL, P = 0.006), and platelet surface expression of CD40L (13.8 +/- 0.9% versus 8.5 +/- 1.1%, P < 0.001). Platelet-monocyte aggregates were also significantly elevated in type 1 diabetes (35.9 +/- 3.3% versus 26.4 +/- 2.9%, P = 0.005; n = 10). We also observed a significant correlation between plasma glucose and serum CRP (r = 0.53, P = 0.01) as well as platelet-monocyte aggregates (r = 0.69, P = 0.03). CONCLUSIONS: Type 1 diabetes is associated with increased CD40L expression and platelet-monocyte aggregation, which may contribute to the proinflammatory and prothrombotic state as well as the accelerated atherogenesis associated with this disorder.

Adult↗
PubMed2004

The number of unexpected HbA variants may be a greater problem in routine practice than is generally realized.

BACKGROUND: The majority of variant and abnormal haemoglobins are clinically silent but may not be biochemically silent when it comes to HbA1c estimation. CASE REPORT: We describe several cases in which there were problems in the determination of HbA1c for monitoring diabetes in patients that would not normally be classified as being at risk. Four of these cases were sufficiently unusual to warrant individual publication but all came from a very restricted geographical area with a population of only approximately 500,000. The significance of this is not that variant haemoglobins affect HbA1c analysis but that the occurrence of unexpected/unusual variant haemoglobins may be more frequent than most clinicians would expect, considering that only a small proportion of the basal population are diabetic and have their HbA1c monitored. Differences will exist between different areas due to differences in both the prevalence of variants and the analytical methods employed. CONCLUSIONS: Consequently, we propose greater interaction between diabetologists and the laboratory in an attempt to identify these clinically but not biochemically silent variants to achieve a true estimation of the glycaemic control in affected patients.

Adult↗
PubMed2004

Reflective testing.

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Clinical Chemistry Tests↗
PubMed2004

Plasma glucose measurement with the Yellow Springs Glucose 2300 STAT and the Olympus AU640.

BACKGROUND: Diabetes mellitus is an important diagnosis. New criteria have been defined for impaired glucose metabolism and, accordingly, there is a need for precise and accurate glucose analysis for the correct classification of patients. However, neither the World Health Organisation nor the National Service Framework for Diabetes in England and Wales deal with the associated analytical issues for plasma glucose. AIMS/METHODS: To compare two different methods for plasma glucose with respect to European and CLIA '88 quality requirements. RESULTS: Using several different graphical and statistical techniques, the YSI 2300 STAT was found to be 8.1-8.4% negatively biased for plasma glucose when compared with the Olympus AU640 method. CONCLUSIONS: Such a large bias would have a large impact on the detection of diabetes mellitus in clinical practice and therefore this method should not be used to make a definitive diagnosis. The bias probably results from the fact that the YSI 2300 STAT uses an aqueous based standard.

Bias↗
PubMed2004

The casino of life.

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Clinical Laboratory Information Systems↗
PubMed2003

Unreliability of triglyceride measurement to predict turbidity induced interference.

Lipaemic specimens are a common problem in clinical chemistry. Most laboratories will measure the concentration of triglycerides and then decide whether the analytical result is valid or not. There is a poor association between the concentration of triglycerides and an objective assessment of turbidity for visually turbid specimens. Extrapolation of triglyceride concentrations derived from the use of intravenous emulsions to visually turbid specimens found in clinical practice will overestimate the turbidity induced interference in assays (non-turbid interferences are probably the same). The evaluation of turbidity induced interference needs to be standardised using objective assessments of turbidity.

Artifacts↗