Validation of the Finnish diabetes risk score (FINDRISC) questionnaire for screening for undiagnosed type 2 diabetes, dysglycaemia and the metabolic syndrome in Greece.

AIM: The present study aimed to validate the Finnish Type 2 Diabetes Risk Score (FINDRISC) questionnaire for its ability to predict the presence of any glucose homoeostasis abnormalities and the metabolic syndrome (MetS) in the Greek population. METHODS: Validation was performed on a sample of individuals who had agreed to participate in a screening program for type 2 diabetes (T2D) prevention (the Greek part of the DE-PLAN study), using both FINDRISC and oral glucose tolerance tests (OGTT). Impaired fasting glucose (IFG) was defined as a fasting plasma glucose level of 6.1-6.9 mmol/L, and impaired glucose tolerance (IGT) as a 2-h plasma glucose of 7.8-11.0 mmol/L. The predictive value of the FINDRISC was cross-sectionally evaluated using the area under the receiver operating characteristic (AUROC) curve method. RESULTS: A total of 869 individuals (379 men, aged 56.2 ± 10.8 years) were screened from the general population living in the city and suburbs of Athens. OGTT revealed the presence of unknown diabetes in 94 cases (10.8%), IFG in 85 (9.8%) and IGT in 109 (12.6%). The sensitivity of a FINDRISC score greater or equal to 15 (45% of the population) to predict unknown diabetes was 81.9% and its specificity was 59.7%. The AUROC curve for detecting unknown diabetes was 0.724 (95% CI: 0.677-0.770). For any dysglycaemia, the AUROC curve was 0.716 (0.680-0.752) while, for detection of the MetS, it was 0.733 (0.699-0.767). CONCLUSION: The FINDRISC questionnaire performed well as a screening tool for the cross-sectional detection of unknown diabetes, IFG, IGT and the MetS in the Greek population.

Antiphospholipid antibodies: laboratory and pathogenetic aspects.

Antiphospholipid antibodies (aPL) constitute a heterogeneous group of autoantibodies that share the ability to bind phospholipids (PL) alone, protein-PL complexes, or PL-binding proteins. They have been detected in isolation, in association with autoimmune diseases such as systemic lupus erythematosus (SLE), and during the course of different infections. aPL have been associated with an array of clinical manifestations in virtually every organ, although deep vein and arterial thrombosis as well as pregnancy morbidity are predominant. The co-occurrence of these clinical findings with aPL constitutes the so-called antiphospholipid syndrome (APS). aPL can be detected by immunological methods [e.g., anticardiolipin antibodies (aCL)] or by functional methods that exploit the effect of aPL on blood coagulation [lupus anticoagulant (LA)]. Since aPL are heterogeneous, numerous immunological and coagulation assays have been developed. These assays have not been fully standardized, and, therefore, problems such as high interlaboratory variation are relatively frequent. Recently, recommendations have been published regarding LA and aCL testing. Not all aPL are pathogenic. However, when they are not associated with infections, they have a role in the pathogenesis of APS. Clinical and experimental data have shown that aPL exert their pathogenic activity by interfering with the function of coagulation factors, such as thrombin and factors X, XI and XII, and with the function of anticoagulant proteins of the protein C system. In addition, aPL interaction with platelets and endothelial cells induces a pro-adhesive activated phenotype.