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Non‐Transferrin‐Bound Iron in Alcohol Abusers
Author(s) -
Feo Tullia Maria,
Fargion Silvia,
Duca Lorena,
Cesana Bruno Mario,
Boncinelli Lodovico,
Lozza Paola,
Cappellini Maria Domenica,
Fiorelli Gemino
Publication year - 2001
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2001.tb02152.x
Subject(s) - transferrin , transferrin saturation , cirrhosis , alcohol , medicine , chemistry , endocrinology , gastroenterology , biochemistry , physiology , anemia , iron deficiency
Background: Non‐transferrin‐bound iron, a low‐molecular‐weight iron complex capable of initiating free radical formation and lipid peroxidation, has been detected in the serum of animals experimentally fed with alcohol, but no data have been reported in alcohol abusers. The purpose of this study was to evaluate whether non‐transferrin‐bound iron is present in chronic alcohol abusers with liver involvement and whether alcohol plays any part in its appearance. Methods: We measured non‐transferrin‐bound iron in a cohort of chronic alcohol abusers with and without liver cirrhosis at presentation, when 43 were active abusers and 33 were abstainers, and in a smaller group during a follow‐up period. Results: At presentation, non‐transferrin‐bound iron was detectable in 83.7% of active abusers but only in 21.2% of abstainers, and within the group of abusers, patients with cirrhosis had significantly higher non‐transferrin‐bound iron than patients without. Non‐transferrin‐bound iron was present not only in patients with transferrin saturation >45% but also in those with transferrin saturation ≤45%. Multiple regression analyses revealed that only alcohol intake and total bilirubin were associated independently with non‐transferrin‐bound iron values. Longitudinal study confirmed the data of the cross‐sectional study. Conclusions: Non‐transferrin‐bound iron could have a role in initiating or promoting alcohol‐induced liver damage.