Iron effects versus metabolic alterations in hereditary hemochromatosis driven bone loss
Hereditary hemochromatosis (HH) is a genetic disorder in which mutations affect systemic iron homeostasis. Most subtypes of HH result in low hepcidin levels and iron overload. Accumulation of iron in various tissues can lead to widespread organ damage and to various complications, including liver ci...
Saved in:
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article (Journal) |
| Language: | English |
| Published: |
9 August 2022
|
| In: |
Trends in endocrinology and metabolism
Year: 2022, Volume: 33, Issue: 9, Pages: 652-663 |
| ISSN: | 1879-3061 |
| DOI: | 10.1016/j.tem.2022.06.004 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.tem.2022.06.004 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S1043276022001163 |
| Author Notes: | Ulrike Baschant, Sandro Altamura, Peter Steele-Perkins, Martina U. Muckenthaler, Maja Vujić Spasić, Lorenz C. Hofbauer, Andrea U. Steinbicker, and Martina Rauner |
| Summary: | Hereditary hemochromatosis (HH) is a genetic disorder in which mutations affect systemic iron homeostasis. Most subtypes of HH result in low hepcidin levels and iron overload. Accumulation of iron in various tissues can lead to widespread organ damage and to various complications, including liver cirrhosis, arthritis, and diabetes. Osteoporosis is another frequent complication of HH, and the underlying mechanisms are poorly understood. Currently, it is unknown whether iron overload in HH directly damages bone or whether complications associated with HH, such as liver cirrhosis or hypogonadism, affect bone secondarily. This review summarizes current knowledge of bone metabolism in HH and highlights possible implications of metabolic dysfunction in HH-driven bone loss. We further discuss therapeutic considerations managing osteoporosis in HH. |
|---|---|
| Item Description: | Gesehen am 17.02.2023 |
| Physical Description: | Online Resource |
| ISSN: | 1879-3061 |
| DOI: | 10.1016/j.tem.2022.06.004 |