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The metabolic syndrome, clinically defined by the Adult Treatment Panel III (ATPIII) (1), affects ∼25% of western adults (2). The metabolic syndrome is closely linked to insulin resistance and implies an increased cardiovascular risk (3,4). Accumulating evidence suggests a link between body iron excess and insulin metabolism (5). Studies have shown an association between serum ferritin and one or more metabolic syndrome feature (6–11). Moreover, a syndrome characterized by hepatic iron overload (HIO) associated with insulin resistance features (insulin resistance–associated HIO IR-HIO), unrelated to genetic hemochromatosis, has been described (12,13). IR-HIO currently represents the most frequent indication to venesection in referral care units for iron overload (14). 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. Within the registry of the Verona Heart Project (15), we identified metabolic syndrome subjects according to ATPIII because of three of more of the following: 1 ) fasting glucose ≥110 mg/dl or antidiabetes medication, 2 ) hypertension (blood pressure ≥135/85 mmHg or medication), 3 ) triglycerides ≥150 mg/dl, 4 ) HDL cholesterol <40 mg/dl in men and <50 mg/dl in women, and 5 ) obesity (BMI ≥27 kg/m2 instead of waist circumference, due to unavailability of waist circumference measurement in all subjects). An age-matched control group was extracted from the registry, requiring the absence of either metabolic syndrome or any evidence of cardiovascular disease. We excluded patients who were homozygous for the main HFE mutation associated with genetic hemochromatosis (C282Y) or who …
Bozzini et al. (Mon,) studied this question.