Regular donor plasmapheresis of up to 45 l of plasma per year appears to be as safe as more moderate plasmapheresis programmes, with respect to the parameters analysed in this study. Individuals donating under these conditions did not develop impaired humoral and cellular immunity, iron store depletion, or increased cardiovascular risk with regard to established biochemical risk markers. Prospective studies are required to determine more exactly than in retrospective analyses the reasons why donors withdraw from plasmapheresis programmes.
Background-Type 2 diabetes mellitus (T2DM) increases the risk of coronary artery disease (CAD). A G(Ϫ30)Apolymorphism in the -cell-specific promoter of glucokinase (GK-30PM) has been implicated in reduced pancreatic -cell function. Its impact on CAD has not been examined. Methods and Results-The glucokinase G(Ϫ30)A variant was determined in 2567 patients with angiographic CAD and in 731 individuals in whom CAD had been ruled out by angiography. In carriers of the A allele, the adjusted OR of CAD was 1.39 (95% CI, 1.15 to 1.70). Corresponding ORs were 1.27 (95% CI, 1.02 to 1.59) and 1.92 (95% CI, 1.26 to 2.93) in individuals without and with T2DM, respectively. The prevalence of the A allele increased in parallel with the Friesinger coronary score. Patients with T2DM were more frequent among carriers of Ն1 A allele (OR, 1.17; 95% CI, 1.00 to 1.28). This association was stronger if CAD patients only were considered. The A allele was associated with higher glucose (fasting, Pϭ0.002; 2 hours after oral glucose, Pϭ0.017) and glycohemoglobin (HbA1c; Pϭ0.002). Furthermore, presence of 1 A allele was negatively related to -cell function, estimated by  percent (Pϭ0.012) and by the ratios of proinsulin to insulin (Pϭ0.025) and proinsulin to C peptide (Pϭ0.019). Conclusions-The A allele of the pancreatic promoter of glucokinase increases the risk of CAD in individuals with and without T2DM. Furthermore, at least in CAD, it is associated with an augmented prevalence of T2DM. (Circulation.
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