Spomenka Ljubić

Validation of Point-of-Care Glucose Testing for Diagnosis of Type 2 Diabetes

Point-of-care (POC) glucose technology is currently considered to be insufficiently accurate for the diagnosis of diabetes. The objective of this study was to investigate the diagnostic accuracy of an innovative, interference-resistant POC glucose meter (StatStrip glucose hospital meter, Nova Biomedical, USA) in subjects with a previous history of dysglycaemia, undergoing a 75 g diagnostic oral glucose tolerance test (oGTT). Venous and capillary blood sampling for the reference laboratory procedure (RLP) and POC-glucose measurement was carried out at fasting and 2 h oGTT, and categories of glucose tolerance were classified according to 2006 WHO diagnostic criteria for the respective sample type. We found an excellent between-method correlation at fasting (r = 0.9681, P < 0.0001) and 2 h oGTT (r = 0.9768, P < 0.0001) and an almost perfect diagnostic agreement (weighted Kappa = 0.858). Within a total of 237 study subjects, 137 were diagnosed with diabetes with RLP, and only 6 of them were reclassified as having glucose intolerance with POC. The diagnostic performance of POC-fasting glucose in discriminating between the normal and any category of disturbed glucose tolerance did not differ from the RLP (P = 0.081). Results of this study indicate that StatStrip POC glucose meter could serve as a reliable tool for the diabetes diagnosis, particularly in primary healthcare facilities with dispersed blood sampling services.

Lipoprotein(a) predicts progression of carotid artery intima-media thickening in patients with type 2 diabetes: A four-year follow-up

ZusammenfassungHINTERGRUND: Ziel dieser Studie war es, herauszufinden ob erhöhtes Serum Lipoprotein(a) (Lpa) bei Patienten mit Diabetes mellitus Typ 2 signifikant zu einem Anstieg der Intima-Media-Dicke und der Zahl der Plaques der Carotiden beiträgt und so das kardiovaskuläre Risiko dieser Patienten erhöht. METHODEN: Bei 146 Patienten mit Diabetes mellitus Typ 2 wurden die Lipoprotein(a)-Spiegel, die Intima-Media-Dicke und die Zahl der Plaques in den Carotiden erhoben. Die Intima-Media-Dicke und die Anzahl der Plaques wurde nach 4 Jahren Follow-up kontrolliert. Die Patienten wurden entsprechend ihrem Serum-Lipoprotein(a)-Spiegel in 2 Gruppen (> oder ≤30 mg/dl) eingeteilt. Die Intima-Media-Dicke wurde mit hochauflösendem B-Mode Ultraschall erhoben. ERGEBNISSE: Anfangs bestand kein signifikanter Unterschied in der Intima-Media Dicke der Carotiden der beiden Gruppen. Bei der Kontrolle waren die Intima-Media-Dicken der Gruppe mit höherem Lipoprotein(a)-Spiegel signifkant höher als jene der Gruppe mit niedrigem Lipoprotein(a) Spiegel (1,24 + 0,22 vs. 1,15 + 0,17 mm; p = 0.005), Die mittlere Zunahme der Intima-Media Dicke betrug in der Gruppe mit niedrigem Lipoprotein(a) Spiegel nach 4 Jahren 0,12 mm (0,030 mm/Jahr) und in der Gruppe mit höherem Lipoprotein(a) Spiegel 0,17 mm (0,043 mm/Jahr). Die Multivarianzanalyse ergab, dass die Intima-Media Dicke nur vom Lipoprotein(a)- und nicht vom Triglyzerid- beziehungsweise vom HDL-Cholesterin-Spiegel oder dem Taille-Hüfte Quotienten abhing. Die Anzahl der Plaques unterschied sich weder bei der Erstuntersuchung noch bei der Kontrolle zwischen den beiden Gruppen signifikant (p = 0,276 respektive p = 0,355). In der Gruppe mit höherem Lipoprotein(a)-Spiegel traten mehr kardiovaskuläre Ereignisse ein als in der anderen Gruppe – der Unterschied war allerdings statistisch nicht signifikant. SCHLUSSFOLGERUNGEN: Unsere Ergebnisse weisen daraufhin, dass Lipoprotein(a) ein unabhängiger, genetisch determinierter Risikofaktor ist, der eng mit der Zunahme der Intima-Media-Dicke bei Diabetes mellitus Typ 2 assoziiert ist.SummaryBACKGROUND: The aim of the study was to establish whether increased levels of serum lipoprotein(a) significantly contribute to an increase in intima-media thickness and the number of carotid artery plaques, and consequently to cardiovascular risk in patients with type 2 diabetes mellitus. METHODS: Lipoprotein(a) levels, intima-media thickness and the number of carotid artery plaques were determined at the beginning of the study in 146 patients with type 2 diabetes. Patients were divided into two groups according to serum lipoprotein(a) levels (> or ≤30 mg/dl). Intima-media thickness and the number of plaques were again determined after four years of follow-up. Intima-media thickness was assessed using high-resolution B-mode ultrasound. RESULTS: The two groups of patients revealed no significant differences in baseline intima-media thickness (P = 0.112) in relation to lipoprotein(a) level. After follow-up, intima-media thickness was significantly greater in patients with higher lipoprotein(a) levels (1.24 + 0.22 vs. 1.15 + 0.17 mm, respectively; P = 0.005). The mean increase in thickness over four years was 0.12 mm (0.030 mm/year) in the group with low lipoprotein(a) levels and 0.17 mm (0.043 mm/year) in the group with high lipoprotein(a). Multivariate analysis indicated that intima-media thickness depended on lipoprotein(a), and not on triglyceride, HDL-cholesterol levels or waist-to-hip ratio. No significant difference in baseline and follow-up number of plaques was observed between the study groups (P = 0.276 vs. P = 0.355, respectively). Although the group with lipoprotein(a) >30 mg/dl had more cardiovascular events, the difference was not statistically significant. CONCLUSIONS: These results indicate that lipoprotein(a) is an independent, genetically determined risk factor closely associated with progression of intima-media thickness in type 2 diabetes.