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Bone loss in chronic liver diseases: Could healthy liver be a requirement for good bone health?

期刊

WORLD JOURNAL OF GASTROENTEROLOGY
卷 29, 期 5, 页码 825-833

出版社

BAISHIDENG PUBLISHING GROUP INC
DOI: 10.3748/wjg.v29.i5.825

关键词

Chronic liver disease; Fracture risk; Hepatic osteodystrophy; Osteoporosis; Bone strength

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Given that the liver is involved in many metabolic mechanisms, chronic liver disease (CLD) can lead to complications such as secondary osteoporosis and increased bone fragility, which are often overlooked. Studies have shown that up to one-third of CLD patients meet diagnostic criteria for osteopenia or osteoporosis. Recent publications indicate that the risk of bone fragility in CLD patients depends on the etiology, duration, and stage of liver disease. This poses a significant socioeconomic burden and calls for more effective prevention, diagnosis, and treatment measures.
Given that the liver is involved in many metabolic mechanisms, it is not surprising that chronic liver disease (CLD) could have numerous complications. Secondary osteoporosis and increased bone fragility are frequently overlooked complications in CLD patients. Previous studies implied that up to one-third of these individuals meet diagnostic criteria for osteopenia or osteoporosis. Recent publications indicated that CLD-induced bone fragility depends on the etiology, duration, and stage of liver disease. Therefore, the increased fracture risk in CLD patients puts a severe socioeconomic burden on the health system and urgently requires more effective prevention, diagnosis, and treatment measures. The pathogenesis of CLD-induced bone loss is multifactorial and still insufficiently understood, especially considering the relative impact of increased bone resorption and reduced bone formation in these individuals. It is essential to note that inconsistent findings regarding bone mineral density measurement were previously reported in these individuals. Bone mineral density is widely used as the golden standard in the clinical assessment of bone fragility although it is not adequate to predict individual fracture risk. Therefore, microscale bone alterations (bone microstructure, mechanical properties, and cellular indices) were analyzed in CLD individuals. These studies further support the thesis that bone strength could be compromised in CLD individuals, implying that an individualized approach to fracture risk assessment and subsequent therapy is necessary for CLD patients. However, more well-designed studies are required to solve the bone fragility puzzle in CLD patients.

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