title: Bloodletting therapy in hemochromatosis: Does it affect trace element homeostasis?
abstract: Hemochromatosis is the most common hereditary disorder in the Nordic population, if left untreated it can result in severe parenchymal iron accumulation. Bloodletting is mainstay treatment. Iron and trace elements partially share cellular uptake and transport mechanisms, and the aim of the present study was to see if bloodletting for hemochromatosis affects trace elements homeostasis. We recruited patients referred for diagnosis and treatment of hemochromatosis, four women and 22 men 23-68 years of age. Thirteen were C282Y homozygote, one was C282Y heterozygote, three were H63D homozygote, seven were compound heterozygote and two had none of the mutations above. Iron and liver function tests were performed; serum levels of trace elements were measured using inductively coupled plasma mass spectrometry. Results before the start of treatment and after normalization of iron parameters were compared. On completion of the bloodlettings the following average serum concentrations increased: Co from 5.6 to 11.5 nmol/L, serum Cu 16.2-17.6 μmol/L, Ni increased from 50.0 to 52.6 nmol/L and Sb from 13.2 to 16.3 nmol/L. Average serum Mn concentration declined from 30.2 to 28.3 nmol/L. All changes were statistically significant (by paired t-test). B, Ba, Cs, Mo, Se, Sr and Zn were not significantly changed. We conclude that bloodlettings in hemochromatosis lead to changes in trace element metabolism, including increased absorption of potentially toxic elements.
authors.affiliation: Department of Clinical Science, University of Bergen, Bergen, Norway; Laboratory of Clinical Biochemistry, Haukeland University Hospital, Bergen, Norway. Electronic address: bjbolann@gmail.com.
authors.forename: Bjørn J
authors.initials: BJ
authors.lastname: Bolann
authors.affiliation: Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway.
authors.forename: Sonia
authors.initials: S
authors.lastname: Distante
authors.affiliation: Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway.
authors.forename: Lars
authors.initials: L
authors.lastname: Mørkrid
authors.affiliation: Department of Clinical Science, University of Bergen, Bergen, Norway; Laboratory of Clinical Biochemistry, Haukeland University Hospital, Bergen, Norway.
authors.forename: Rune J
authors.initials: RJ
authors.lastname: Ulvik
mesh_terms: D000328:Adult; D000368:Aged; D003035:Cobalt / Q000097:blood; D005260:Female; D006432:Hemochromatosis / Q000097:blood / Q000235:genetics / Q000628:therapy*; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I / Q000235:genetics*; D006720:Homozygote; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D008875:Middle Aged; D009154:Mutation; D018962:Phlebotomy; D014131:Trace Elements / Q000097:blood* / Q000652:urine; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: C103673:HFE protein, human; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I; D008565:Membrane Proteins; D014131:Trace Elements; D003035:Cobalt
keywords: Bloodletting; Hemochromatosis; Iron overload; Trace elements