Bone Abstracts

Chronic liver diseases (CLD) leads to an imbalance of bone remodeling, bone mass decrease with the development of hepatic osteodystrophy, which is most often seen in osteoporosis. In the development of structural and functional deficiency of bone plays an important role of calcium–phosphorus homeostasis and coherence calcium-regulating hormones (CRH), which include parathyroid hormone (PTH) and active metabolites of vitamin D.

The aim of this study was to determine violations of mineral metabolism, the concentration of calcium-regulating hormones, as well as to establish the influence of disturbances in these systems of osteoporosis associated with liver cirrhosis LC.

We observed 172 patients with LC, the average age – 49.3±7.7 years. The men were 108 (62.8%), women – 64 (37.2%). Bone mineral density (BMD) was determined by DXA ‘Challenger’ (DMS, France). We also determined the serum concentration of calcium and phosphorus, urinary excretion, the level of PTH, and 25-hydroxyvitamin D (25(OH)D).

We was found significant violations of the calcium–phosphorus metabolism, changes in the CRH, and reduced bone mineral density in patients with LC, but the severity of the imbalance depended on the severity of the disease and correlated with the main laboratory criteria of liver dysfunction. We observed decrease serum concentration of total and ionized calcium, as well as the expressive tendency to hypercalciuria.

The concentration of 25(OH)D was 9.88±4.36 ng/ml (in control 26.76±9.27 ng/ml; P<0.01). The level of deficit depended on the degree of liver dysfunction. In the case of compensated of LC the level of 25(OH)D was 12.93±5.42 ng/ml and decompensated – 4.53±1.22 ng/ml (a decrease of 2.8 times). It emphasizes that with abnormal liver function significantly affected the formation of this 25(OH)D, i.e. mechanism of the first hydroxylation of vitamin D, which occurs in the liver. PTH level was elevated in a majority of patients. Serum concentrations of PTH were on average 82.2±5.3 pg/ml in patients with LC. It significantly changed at different degrees of disease activity and severity of hepatocellular insufficiency. In the compensation stage of LC the PTH level was 39.8±3.1 pg/ml (P> 0.05), with subcompensation 89.8±4.2 (P<0.05), decompensation 103.2±11.7 (P<0.001). PTH correlated with bone mineral density of the radius and lumbar spine.

Thus, in patients with cirrhosis of the observed violation of mineral metabolism with the emergence of resistant hypocalcemia, lack of active metabolites of vitamin D, the development of secondary hyperparathyroidism, especially in severe liver dysfunction. It is in these patients is determined by the high incidence of osteoporosis.