Prevalence of body iron excess in the metabolic syndrome.

The metabolic syndrome, clinically de\ufb01ned by the Adult Treatment Panel III (ATPIII), affects 25% of western adults. The metabolic syndrome is closely linked to insulin resistance and implies an increased cardiovascular risk. Accumulating evidence suggests a link between body iron excess and insulin metabolism. Studies have shown an association between serum ferritin and one or more metabolic syndrome feature. Moreover, a syndrome characterized by hepatic iron overload (HIO) associated with insulin resistance features (insulin resistance\u2013associated HIO [IR-HIO]), unrelated to genetic hemochromatosis, has been described. IR-HIO currently represents the most frequent indication to venesection in referral care units for iron overload. Data on the other side of the phenomenon, namely the prevalence of a potentially relevant iron overload in subjects selected for having metabolic syndrome, are scanty

Interaction between smoking and PON2 Ser311 Cys polymorphism as a determinant of the risk of myocardial infarction

Background Increased oxidative stress is thought to play a role in the pathogenesis of the atherothrombotic process. Paraoxonases (PONs) are closely related antioxidant enzymes encoded by clustered genes on chromosome 7q. We evaluated three PON polymorphisms (PON1 Leu(55)Met and Gln(192)Arg; PON2 Ser(311)Cys) as possible risk factors for coronary atherosclerotic disease (CAD) and/or its main thrombotic complication, myocardial infarction (MI).Materials and methods We studied 890 subjects with angiographic documentation of coronary vessels (272 = CAD-free; 618 = CAD). In the CAD group, 341 subjects had a previous MI.Results Frequencies of various genotypes were not significantly different between CAD-free subjects and the entire CAD population. In the latter group, there were more carriers of the PON2 (311)Cys variation among those who had suffered a MI than among those who had not (P < 0.01 by chi(2)). The adjusted OR for MI among PON2 (311)Cys carriers was 1.5 (95%CI, 1.03-2.19). A gene-environmental interaction was found between PON2 Ser(311)Cys and smoking. Smoking by itself was associated with an increased MI risk. Among smokers, however, the MI risk was related to PON2 genotype: Cys/Cys homozygotes (OR = 5.3; 95%CI, 1.7-16.4) and Ser/Cys heterozygotes (OR = 2.1; 95%CI, 1.3-3.6) were at greater risk than Ser/Ser subjects (OR = 1.2; 95%CI, 0.8-1.8). The PON2 polymorphism did not influence the MI risk among nonsmokers.Conclusions In CAD subjects, a proportion of the risk of MI may be influenced by the interaction between smoking and a polymorphism in the antioxidant enzyme PON2