Liver osteodystrophy

Hepatic osteodystrophy, which is a disorder of bone metabolism, is a common side effect among patients with chronic liver diseases. It can be observed among approximately 20-100% of patients with chronic liver disease, both parenchymatous and cholestatic. The pathogenesis of hepatic osteodystrophy is complex and still unknown. Hypothetical causes of liver osteodystrophy can be impairment of vitamin D liver hydroxylation, vitamin D receptor, increased level of PTH in blood, decreased level of IGF-1, hyperbilirubinaemia, hypogonadism, decreased level of osteoprotegerin, effect of pharmacotherapy, impairment of digestion of vitamin D, calcium, phosphorus, present in chronic liver diseases. Clinically the most significant after-effects are bone tenderness and fractures. Calcitriol, 1,25(OH)2D3, is the active form of vitamin D. It is produced due to a two-step hydroxylation process, the first in the liver and the second in the kidneys. Calcitriol acts on the cells of the intestine to promote the absorption of calcium from food and on bone to mobilize calcium from the bone to the blood. Disturbances of vitamin D metabolism can be an important cause of liver osteodystrophy. However, the correlation between vitamin D and liver osteodystrophy is not very clear; thus we discuss in our article other hypothetical causes of liver osteodystrophy.