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Hemochromatosis and Osteoporosis
What is Hemochromatosis (iron overload or "bronze" diabetes)?
Hemochromatosis is a disease that causes the body to store excessive amounts of iron in the body. It is an inherited disorder that can lead to the onset of type 1 diabetes after years of iron overload which can damage the pancreas. The number of persons with hemochromatosis for those with diabetes is not higher than is seen in the general population but about 40% of those diagnosed with hemochromatosis will also be diagnosed with type 1 diabetes at the same time.
Diabetes did not cause hemochromatosis, but hemochromatosis causes diabetes. For this reason, this form of diabetes is considered a “secondary” diabetes because it is caused by damage to the pancreas from excessive levels of iron. Healthy people usually absorb about 10 percent of the iron contained in the food they eat to meet the body needs. People with hemochromatosis absorb more than the body needs. The body has no natural way to rid itself of the excess iron, so it is stored in body tissues, especially the liver, heart, and pancreas. Hemochromatosis is often called “bronze” diabetes because of an accompanying skin discoloration.
Prognosis
The sooner a diagnosis of hemochromatosis is made, the more favorable the long-term outcome for the patient. If treatment beings prior to complications (organ damage) many problems associated with hemochromatosis can often be avoided. Even if some organ damage has occurred, it may be able to be reverse or minimized the impact by early detection and treatment.
If the disease is not detected early and treated, iron may accumulate in body tissues and may eventually lead to serious problems such as:
Arthritis
Liver disease, including an enlarged liver, cirrhosis, cancer, and liver failure
Damage to the pancreas, possibly causing diabetes
Heart abnormalities, such as irregular heart rhythms or congestive heart failure
Impotence
Early menopause
Changes in secondary sex characteristics; loss of sexual desire
Abnormal pigmentation of the skin, making it look gray or bronze
Thyroid deficiency
Damage to the adrenal gland
Iron inhibits hydroxyapatite crystal growth in vitro.
Guggenbuhl P, Filmon R, Mabilleau G, Baslé MF, Chappard D. Metabolism. 2008 Jul;57(7):903-10. INSERM, U 922-LHEA, Faculté de Médecine, Angers Cédex Fr.49045,
Hemochromatosis is a known cause of osteoporosis in which the pathophysiology of bone loss is largely unknown and the role of iron remains questionable. We have investigated the effects of iron on the growth of hydroxyapatite crystals in vitro on carboxymethylated poly(2-hydroxyethyl methacrylate) pellets. This noncellular and enzyme-independent model mimics the calcification of woven bone (composed of calcospherites made of hydroxyapatite crystals).
Polymer pellets were incubated with body fluid containing iron at increasing concentrations (20, 40, 60 micromol/L). Hydroxyapatite growth was studied by chemical analysis, scanning electron microscopy, and Raman microscopy. When incubated in body fluid containing iron, significant differences were observed with control pellets. Iron was detected at a concentration of 5.41- to 7.16-fold that of controls. In pellets incubated with iron, there was a approximately 3- to 4-fold decrease of Ca and P and a approximately 1.3- to 1.4-fold increase in the Ca/P ratio. There was no significant difference among the iron groups of pellets, but a trend to a decrease of Ca with the increase of iron concentration was noted.
Calcospherite diameters were significantly lower on pellets incubated with iron. Raman microspectroscopy showed a decrease in crystallinity (measured by the full width of the half height of the 960 Deltacm(-1) band) with a significant increase in carbonate substitution (measured by the intensity ratio of 1071 to 960 Deltacm(-1) band). Energy dispersive x-ray analysis identified iron in the calcospherites. In vitro, iron is capable to inhibit bone crystal growth with significant changes in crystallinity and carbonate substitution.
Studies:
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