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OBJECTIVE--1,5-anhydroglucitol (1,5-AG) is a short-term marker of metabolic control in diabetes. Its renal loss is stimulated in hyperglycemic conditions by glycosuria, which results in a lowered plasma concentration. As a [...]

The K121Q polymorphism in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) is associated with type 2 diabetes and obesity. The possibility of other ENPP1 polymorphisms influencing these phenotypes has received little attention. Our aim was to examine the associations of tagging single nucleotide polymorphisms (SNPs) and haplotypes of the linkage disequilibrium (LD) block containing K121Q polymorphism with type 2 diabetes in a Polish population, controlling for any effect of obesity. We genotyped 426 type 2 diabetic case and 370 control subjects for seven SNPs in ENPP1. In the total group, neither type 2 diabetes nor obesity was significantly associated with any SNP. However, in obese subjects, two SNPs were significantly associated with type 2 diabetes: the Q allele of K121Q (odds ratio 1.6 [95% CI 1.003-2.6]) and T allele of rs997509 (4.7 [1.6-13.9]). In the LD block, four SNPs plus the K121Q polymorphism distinguished six haplotypes, three of which carried the Q allele. Interestingly, the T allele of rs997509 sufficed to distinguish a 121Q-carrying haplotype that was significantly more associated with type 2 diabetes than the other two (4.2 [1.3-13.5]). These other two 121Q-carrying haplotypes were not associated with type 2 diabetes. In conclusion, we found a new SNP, rs997509, in intron 1 that is strongly associated with risk of type 2 diabetes in obese individuals. The molecular mechanisms underlying this association are unknown., The ectonucleotide pyrophosphatase/phosphodiesterase 1 gene (ENPP1 or PC-1) is located on the long arm of chromosome 6 (6q23.2) and encodes for a protein that inhibits insulin signaling (1). A polymorphism [...]

Decreased availability of nitric oxide (NO), which contributes to the development of diabetes vascular complications (1), is partially related to asymmetric dimethylarginine (ADMA). ADMA is an endogenous NO synthase inhibitor [...]

Heterozygous activating mutations in the KCNJ11 gene are a common cause of permanent neonatal diabetes (PNDM) (1,2). In contrast to the autoimmune type 1 diabetes, patients with KCNJ11 mutations do [...]

Activating mutations in the KCJN11 gene encoding in the ATP-sensitive [K.sup.+] channel ([K.sub.ATP]channel) subunit Kir6.2 were reported (1) as the most common cause of permanent neonatal diabetes (PND). Recently, it [...]

Maturity-onset diabetes of the young (MODY) is an autosomaldominant form of disease characterized by β-cell defects and early age of diagnosis. So far, six MODY genes have been identified (1,2). [...]

About 50% patients with newly diagnosed type 2 diabetes already have diabetes related complications. Early diagnosis and treatment of diabetes may reduce the complications. In order to early detection of [...]

Hyperglycemia in type 2 diabetes may cause microvascular disease as well as may cause or contribute to macrovacular disease. In 1997 the American Diabetes Association (ADA)has presented revised diagnostic criteria [...]

We present results for quality control (QC) on glucometers used in a diabetes outpatient clinic. The QC included inspection of glucometer blood glucose measurement by patients and a comparison of glucose results from the patients' meters with the point-of-care analyzer used in a clinic and with a central laboratory method. In the study, results from 86 patient glucometers were compared with the reference HemoCue glucose analyzer, and results from 72 glucometers were compared with the reference laboratory method. Glucometers studied were Accutrend (11), Glucotrend (32), Precision QiD (22), One Touch (11), and Glucocard II (11). Reference glucose assays were performed using the glucose oxidase method on a Hitachi 912 analyzer. Glucose concentrations measured using patient glucometers ranged from 36 to 425 mg/dL. The analytical bias of glucometers varied from −1.45% to 9.54%. Correlation coefficient between results obtained by the patient glucometers and HemoCue analyzer or laboratory method ranged from 0.964 to 0.983 and from 0.955 to 0.986, respectively. Passing-Bablok agreement test and Deming regression analysis indicated good concordance of results between all the patient glucometers and the HemoCue analyzer, whereas good agreement with the laboratory method was found only for the Accutrend, Glucotrend, and One Touch glucometers. Differences between results did not exceed 20 mg/dL, and the mean difference between results for the patient glucometers and HemoCue analyzer ranged from 0.06 to 5.55 mg/dL and between the glucometers and the laboratory method from 1.82 to 12.9 mg/dL. In conclusion, good analytical performance of the glucometers studied and a bias of <10% from the reference values were found. Results of this study show the possibility for routine QC of glucometers in an outpatient clinic.

AbstractIn this study analytical and functional performance of the Precision GTM“point-of-care” glucometer (MediSense Inc.) was evaluated. Studies were carried-out using capillary blood collected for routine monitoring of glycemia in diabetic patients. Each glucose test measurement with the glucometer was paralleled by the laboratory measurement of glucose on the same blood sample, using the GOD/PAP method. Mean accuracy error in the glucose concentration range of 1.1–33.3 mmol/l calculated for the glucometer vs.the laboratory method amounted to only 0.2%. However, for glucose concentrations below 4.4 mmol/l the mean accuracy error was 3.9%, and for the concentrations above 10.0 mmol/l it was 4.6%. Within-run CV for three concentration levels was 2.76%, 2.89%, and 4.22%, respectively. Linearity of the meter response in samples with glucose concentration ranging from 1.7 mmol/l to 16.7 mmol/l, expressed as the correlation coefficient r, yielded r=0.996 and linear regression equation [y1= 0.996 y2–0.005], where y1is the measured glucose concentration and y2 is the target glucose concentration calculated in diluted samples. Correlation studies on a set of 114 blood samples collected from patients and assayed by glucometer and by the laboratory method yielded a relationship expressed by the equation: y = 0.84x + 1.13 where yis glucometer read-out and xis glucose concentration obtained by the laboratory method. Passing-Bablok test showed a significant agreement between the glucometer measurements and the reference laboratory results in the studied glucose concentration range. The error grid analysis of series of the paired patient's samples showed that 95% of results were in the clinically acceptable zone A and 1% of results in zone