肝硬変症におけるビタミンD代謝障害

概要

論文の詳細を見る
Liver cirrhosis (LC) is often associated with osteomalacia and osteoporosis. Since it has been shown that serum levels of 25 hydroxy vitamin D (25-OH-D) are reduced in LC, defective hepatic hydroxylation of vitamin D has been postulated to be responsible for the low serum 25-OH-D levels and skeletal demineralization. This study was designed, therefore, to determine serum 25-OH-D and 1α, 25-(OH)2 -D levels in patients with LC. Further, the response of serum 1α, 25-(OH)2-D to a single oral dose of 1α-OH-D3(2μEg) was investigated. In 5 patients with severe decompensated LC and 3 patients with compensated LC, serum 25-OH-D and 1α, 25-(OH)2-D levels were respectively measured by the modified method of Belsey and by that of Eisman. Serum 25-OH-D in patients with compensated and decompensated LC was significantly higher than that in normals. Serum levels of 1α, 25-(OH)2-D in patients with decompensated LC were significantly lower than those in patients with compensated LC and normals. After a single oral administration of 1α-OH-D3 at a dose of 2μg, the 1α, 25-(OH)2 -D rose in each patient within 6h, reaching the maximum levels at 12h. The percent increase over the basal value in decompensated LC was similar to that in compensated LC. Since 25-OH-D is known to be hydroxylated to 1α, 25-(OH)2 -D in renal tubules, the relationship between renal function and serum 1α, 25-(OH)2 -D levels has been investigated, and a significant positive correlation was found between creatinine clearance and serum 1α, 25-(OH)2-D levels. Contrary to the previous observations, the present study has demonstrated high serum 25-OH-D levels in patients with LC. Although the reason for this discrepancy is unknown, the modified method of Belsey for determining serum 25-OH-D levels might be responsible for the high serum 25-OH-D levels. In this study, all 8 patients treated with 1α-OH-D3 responded with elevation of the serum 1α, 25-(OH)2-D. This observation has demonstrated that hepatic 25-hydroxylation is not impaired even in patients with severe LC. To function physiologically, vitamin D must be hydroxylated in the liver to 25-OH-D and subsequently by the kidney to 1α, 25-(OH)2-D. A significant positive correlation was observed between creatinine clearance and serum 1α, 25-(OH)2 -D levels in LC. These results imply a defect in the la-hydroxylation step of vitamin D metabolism in LC, probably due to hepatorenal syndrome. Thus it may be conceivable that osteoporosis and osteomalacia associated with LC is due to a defect in the 1α-hydroxylation by the kidney rather than a hepatic hydroxylation defect.
一般社団法人日本内分泌学会の論文

肝硬変症におけるビタミンD代謝障害

スポンサーリンク

概要

著者

関連論文

スポンサーリンク