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there is significant bone loss
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Osteoporos Int. 2005 Dec;16(12):1809-14. Epub 2005 Jun 1. Related
Articles, Links

Bone mineral density in men with genetic hemochromatosis and HFE gene
mutation.

Guggenbuhl P, Deugnier Y, Boisdet JF, Rolland Y, Perdriger A, Pawlotsky
Y, Chales G.

Rheumatology Department, University Hospital, Rennes, France.
pascal.guggenbuhl@chu-rennes.fr

Genetic hemochromatosis (GH) is an iron overload disorder mainly due to
the C282Y mutation of the HFE gene. The possibility of bone involvement
was only recently recognized. The aims of this study were to assess
bone mineral density (BMD) and bone remodeling in men with GH, and to
examine the influence of iron overload. Thirty-eight men (mean age
47.2+/-9.4 years) with well-defined HFE-related GH were studied. They
had an important iron overload with liver iron concentration to age
ratio >2.5, no previous venesection therapy and were C282Y homozygotes
(n=37) or compound C282Y/H63D heterozygote (n=1). BMD measured by DXA
was 0.925+/-0.15 g/cm2 at the lumbar spine (LS) and 0.778+/-0.13 g/cm2
at the femoral neck (FN). Osteopenia (T-score<-1 SD) was observed in
78.9% of patients and osteoporosis (T-score<-2.5 SD) in 34.2%. Vitamin
D levels were normal, and no 1-84 parathyroid hormone dysfunction was
found. Hypogonadism was found in only 13.2% of patients. Patients with
hypogonadism had lower LS BMD than eugonadal patients (0.788+/-0.16 and
0.954+/-0.14 g/cm2). Bone remodeling and parathyroid hormone levels
were lower in patients with cirrhosis, but BMD values were similar to
those in patients without cirrhosis. FN BMD appeared to fall with
rising hepatic iron concentrations (r=-0.399). We conclude that there
is significant bone loss in HFE-related hemochromatosis that cannot
solely be explained by hypogonadism or cirrhosis. Further
investigations are needed to determine the role of iron overload
itself.

PMID: 15928800 [PubMed - indexed for MEDLINE]

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