This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues.Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. IntroductionThere is compelling evidence suggesting that magnesium depletion may play a role in the pathophysiology of insulinresistance and/or altered glucose homeostasis in type 2 diabetes mellitus [1][2][3]. Magnesium is the second most abundant intracellular cation after potassium, and it is involved in a number of fundamental biochemical processes, comprising all ATP transferAbbreviations: ATP, adenosine triphosphate; BMI, body mass index; DBP, diastolic blood pressure; ESRD, end stage renal disease; FBG, fasting blood glucose; HbA1c, hemoglobin A1c; ISE, ion-selective electrode; NADPH, nicotinamide adenine dinucleotide phosphate-oxidase; NMR, nuclear magnetic resonance; Mg-tot, total serum magnesium; Mg-ion, extracellular free levels of magnesium; SBP, systolic blood pressure. ☆ None of the authors has any conflict of interest or financial support to disclose. ☆☆ There was no external funding for the study.

AIM:To investigate the relationship between ferritin and steatosis in patients with chronically abnormal liver function tests (LFTs) and high ferritin level. METHODS:One hundred and twenty-four consecutive patients with hyperferritinemia (male > 300 ng/mL, female > 200 ng/mL) were evaluated; clinical, biochemical and serological data, iron status parameters, HFE gene mutations and homeostasis model assessment score were obtained. Steatosis was graded by ultrasound as absent or present. Histology was available in 53 patients only.RESULTS: Mean level of ferritin was 881 ± 77 ng/mL in men and 549 ± 82 ng/mL in women. The diagnosis was chronic hepatitis C in 53 (42.7%), non-alcoholic fatty liver disease/non-alcoholic steatohepatitis in 57 (45.9%), and cryptogenic liver damage in 14 (11.3%). None was diagnosed as hereditary hemochromatosis (HH). Hepatic siderosis on liver biopsy was present in 17 of 54 (32%) patients; grade 1 in eight and grade 2 in nine. Overall, 92 patients (74.2%) had steatosis. By logistic regression, ferritin and g-glutamyltransferase were independent predictors of steatosis. Ferritin levels were significantly related to low platelet count, steatosis and hepatitis C virus infection. CONCLUSION:In a non-obese cohort of non-alcoholic patients with chronically abnormal LFTs without HH, high serum ferritin level is a risk factor for steatosis.

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