[The disorder of vitamin D metabolism in patients with liver cirrhosis].
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 1 alpha, 25-(OH)2-D levels in patients with LC. Further, the response of serum 1 alpha, 25-(OH)2-D to a single oral dose of 1 alpha-OH-D3 (2 micrograms) was investigated. In 5 patients with severe decompensated LC and 3 patients with compensated LC, serum 25-OH-D and 1 alpha, 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 1 alpha, 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 1 alpha-OH-D3 at a dose of 2 micrograms, the 1 alpha, 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.(ABSTRACT TRUNCATED AT 250 WORDS)
D004100:Dihydroxycholecalciferols / Q000097:blood; D005260:Female; D006801:Humans; D006887:Hydroxycholecalciferols / Q000097:blood; D006900:Hydroxylation; D007668:Kidney / Q000378:metabolism; D008103:Liver Cirrhosis / Q000097:blood / Q000150:complications / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010018:Osteomalacia / Q000209:etiology; D010024:Osteoporosis / Q000209:etiology; D014807:Vitamin D / Q000378:metabolism*
D004100:Dihydroxycholecalciferols; D006887:Hydroxycholecalciferols; D014807:Vitamin D