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Iron deposits and dietary patterns in familial combined hyperlipidemia and familial hypertriglyceridemia
Authors:Rocio Mateo-Gallego  Maria Solanas-Barca  Elena Burillo  Ana Cenarro  Iva Marques-Lopes  Fernando Civeira
Affiliation:1.Instituto Aragonés de Ciencias de la Salud (I+CS),Unidad de Lípidos and Laboratorio de Investigación Molecular, Hospital Universitario Miguel Servet,Zaragoza,Spain;2.Facultad de Ciencias de la Salud y del Deporte,Universidad de Zaragoza,Zaragoza,Spain
Abstract:Iron deposits are associated with lipid phenotype in familial hypertriglyceridemias, mainly familial combined hyperlipidemia (FCH) and familial hypertriglyceridemia (FHTG). In turn, diet plays an important role in hypertriglyceridemias although it is not known if dietary patterns are associated with iron concentration in these disorders. The objective was to determine the relationship between diet and iron deposits, measured through serum ferritin concentration, in patients with FCH and FHTG. The study was composed of 140 patients, 107 with FCH and 33 with FHTG. Subjects completed a validated 137-item food frequency questionnaire. Dividing subjects by ferritin tertiles adjusted by sex, there were no significant differences in dietary patterns except in dairy products consumption which was lower in the highest ferritin tertile. Subjects were also divided by triglycerides tertiles adjusted by sex. Those subjects in the highest tertile had lower HDL cholesterol and higher ferritin concentrations. Regarding to dietary parameters, there were significant differences in marine omega three fatty acids and vegetables presenting higher and lower consumption, respectively, those patients in the highest tertile of triglycerides. Moreover, there was not a significant correlation between dietary iron intake and any parameter, both biochemical and dietary, including ferritin concentrations. In conclusion, in patients with primary hypertriglyceridemia, triglycerides are associated with ferritin concentrations but dietary patterns are not related to iron deposits. Our results highly support the concept that the genetic mechanisms driven to hypertriglyceridemia also favor iron overload.
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