One in Five Laboratories Using Various Hemoglobin A(1c) Methods Do Not Meet the Criteria for Optimal Diabetes Care Management

Background: We assessed the reference change value (RCV) of currently available hemoglobin A(1c) (HbA(1c)) laboratory assays, which is defined as the critical difference between two consecutive HbA(1c) measurements representing a significant change in health status. Methods: We examined the individual laboratory coefficients of variation (CVs) in the Dutch/Belgian quality scheme based on 24 lyophilized samples and calculated the RCV per laboratory (n-220) and per assay method. In addition, two pooled whole blood samples were sent to the participating laboratories. The individual laboratory results were compared to the assigned value +/- an allowable total error (TEa) of 6%. Results: At HbA(1c) values of 41.0 mmol/mol (5.9%-Diabetes Control and Complications Trial [DCCT]) and 61.8 mmol/mol (7.8%-DCCT), 99% and 98%, respectively, of the laboratories reported a value within a TEa limit of 6%. The analytical CV of the HbA(1c) method used in 78% of the laboratories is Conclusions: The analytical performance of the majority of laboratory HbA(1c) methods is within the clinical requirements. However, based on the calculated RCV, 21.8% of the laboratories using different HbA(1c) methods are not able to distinguish an HbA(1c) result of 59 mmol/mol (7.5%-DCCT) from a previous HbA(1c) result of 53 mmol/mol (7.0%-DCCT). It can be presumed that differences in HbA(1c) results of 5 mmol/mol (0.5%-DCCT) do influence treatment decisions

Ethnic differences in cardiometabolic risk profile in an overweight/obese paediatric cohort in the Netherlands: a cross-sectional study

<p>Abstract</p> <p>Background</p> <p>Differences in prevalence of cardiometabolic risk factors between different ethnic groups are largely unknown. We determined the variation in cardiometabolic risk profile according to ethnicity in a cohort overweight/obese Dutch children.</p> <p>Methods</p> <p>An oral glucose tolerance test was performed in 516 overweight/obese Dutch children of multi-ethnic origin, attending an obesity out-patient clinic of an urban general hospital (mean age 10.6 ± 3.2; 55.2% boys). Anthropometric parameters and blood samples were collected, and the prevalence of (components of) the metabolic syndrome (MetS) and insulin resistance were determined in each ethnic group.</p> <p>Results</p> <p>Major ethnic groups were Dutch native (18.4%), Turkish (28.1%), and Moroccan (25.8%). The remaining group (27.7%) consisted of children with other ethnicities. Turkish children had the highest mean standardized BMI compared to Dutch native children (<it>P </it>< 0.05). As compared to Moroccan children, they had a higher prevalence of MetS (22.8% vs. 12.8%), low HDL-cholesterol (37.9% vs. 25.8%), hypertension (29.7% vs. 18.0%) and insulin resistance (54.9% vs. 37.4%, all <it>P </it>< 0.05). Although Turkish children also had higher prevalences of forementioned risk factors than Dutch native children, these differences were not statistically significant. Insulin resistance was associated with MetS in the Turkish and Moroccan subgroup (OR 6.6; 95%CI, 2.4–18.3 and OR 7.0; 95%CI, 2.1–23.1, respectively).</p> <p>Conclusion</p> <p>In a Dutch cohort of overweight/obese children, Turkish children showed significantly higher prevalences of cardiometabolic risk factors relative to their peers of Moroccan descent. The prospective value of these findings needs to be established as this may warrant the need for differential ethnic-specific preventive measures.</p

Haemoglobin A1c: Historical overview and current concepts

Since the discovery of the relation between increased concentrations of fast haemoglobin fractions in patients with diabetes mellitus compared to concentrations in subjects without diabetes mellitus by Samuel Rahbar and co-workers in 1969, glycated haemoglobin A1c (HbA1c) has become a "gold standard" for glucose management in patients with diabetes mellitus. Recently, HbA1c has been advocated as a diagnostic marker for diabetes mellitus, which further underlines the importance of HbA1c. There are currently more than 30 methods available on the market with an analytical performance ranging from poor to state of the art. This review describes the biochemistry of HbA1c and the concepts of analytical and biological variation with respect to the measurement of HbA1c. Subsequently, aspects regarding the discovery of HbA1c are described. In addition, an overview is given on the assays methods that are currently available for the measurement of HbA1c. Finally, recommendations for the minimally required analytical performance characteristics of the current HbA1c assays are presented. (C) 2012 Elsevier Ireland Ltd. All rights reserved

Haemoglobin A1c:Historical overview and current concepts

<p>Since the discovery of the relation between increased concentrations of fast haemoglobin fractions in patients with diabetes mellitus compared to concentrations in subjects without diabetes mellitus by Samuel Rahbar and co-workers in 1969, glycated haemoglobin A1c (HbA1c) has become a "gold standard" for glucose management in patients with diabetes mellitus. Recently, HbA1c has been advocated as a diagnostic marker for diabetes mellitus, which further underlines the importance of HbA1c. There are currently more than 30 methods available on the market with an analytical performance ranging from poor to state of the art. This review describes the biochemistry of HbA1c and the concepts of analytical and biological variation with respect to the measurement of HbA1c. Subsequently, aspects regarding the discovery of HbA1c are described. In addition, an overview is given on the assays methods that are currently available for the measurement of HbA1c. Finally, recommendations for the minimally required analytical performance characteristics of the current HbA1c assays are presented. (C) 2012 Elsevier Ireland Ltd. All rights reserved.</p>

A Patient with a Prolonged Activated Partial Thromboplastin Time and a Deep Intracerebral Haemorrhage

We report on a 57-year-old woman with a pontine haemorrhage and an extremely prolonged activated partial thromboplastin time (aPTT) of more than 240 s, suggestive of a coagulation disorder. Given the location of the haemorrhage, which is associated with a high mortality rate, recombinant factor VIIa was administered, although not all necessary laboratory analyses could be performed at that time. In our case, a deficiency of factor XII was found, which is not associated with an increased bleeding risk. In an acute setting, evaluation of a prolonged aPTT may cause diagnostic and therapeutic challenges, in particular in situations where additional laboratory investigations may not be readily available

Pancreatic fat content and β-cell function in men with and without type 2 diabetes

OBJECTIVE - Insulin resistance, associated with increased lipolysis, results in a high exposure of nonadipose tissue to lipids. Experimental data indicate that fatty infiltration of pancreatic islets may also contribute to β-cell dysfunction, but whether this occurs in humans in vivo is unknown. RESEARCH DESIGN AND METHODS - Using proton magnetic resonance spectroscopy and oral glucose tolerance tests, we studied the association of pancreatic lipid accumulation in vivo and various aspects of β-cell function in 12 insulin-naive type 2 diabetic and 24 age- and BMI-matched nondiabetic men. RESULTS - Patients versus control subjects had higher A1C, fasting plasma glucose, and insulin and triglyceride levels and lower HDL cholesterol, but similar waist circumference. Median (interquartile range) pancreatic fat content in patients and control subjects was 20.4% (13.4-43.6) and 9.7% (7.0-20.2), respectively (P = 0.032). Pancreatic fat correlated negatively with β-cell function parameters, including the insulinogenic index adjusted for insulin resistance, early glucose-stimulated insulin secretion, β-cell glucose sensitivity, and rate sensitivity (all P < 0.05), but not potentiation. However, these associations were significantly affected by the diabetic state, such that a significant association of pancreatic fat with β-cell dysfunction was only present in the nondiabetic group (all P < 0.01), suggesting that once diabetes occurs, factors additional to pancreatic fat account for further β-cell function decline. In control subjects, the association of pancreatic fat and β-cell function remained significant after correction for BMI, fasting plasma glucose, and triglycerides (P = 0.006). CONCLUSIONS - These findings indicate that pancreatic lipid content may contribute to β-cell dysfunction and possibly to the subsequent development of type 2 diabetes in susceptible humans