Duarte M P, Farias M L, Coelho H S, Mendonça L M, Stabnov L M, do Carmo d Oliveira M, Lamy R A, Oliveira D S
Division of Endocrinology, Hospital Universitário Clementino Fraga Filho, Federal University of Rio de Janeiro, Brazil.
J Gastroenterol Hepatol. 2001 Sep;16(9):1022-7. doi: 10.1046/j.1440-1746.2001.02561.x.
The main process involved in hepatic osteodystrophy seems to be osteoporosis, but decreased 25-hydroxylation of vitamin D might lead to osteomalacia and secondary hyperparathyroidism.
We studied bone mineral density (BMD) by using DEXA-Expert Lunar, biochemical markers of bone turnover and calcium-parathyroid hormone (PTH)-vitamin D axis in 100 patients with chronic viral hepatitis secondary to hepatitis C virus: 49 non-cirrhotic (NCir) and 51 with cirrhosis (Cir) confirmed by liver biopsy and/or clinical and biochemical features. When compared to the age-matched population, 25% of the patients had low BMD at the lumbar spine (LS), 26.2% at Ward's triangle, 15.5% at the femoral neck (FN), and 20.2% at the trochanter. No difference was found either between Cir and NCir groups or between sexes. Urinary N-telopeptide was increased in 31.86% of the patients, and negatively correlated with BMD at the LS and trochanter (P < 0.02). Serum bone-specific alkaline phosphatase was elevated in 21% of the patients and negatively correlated with BMD at the trochanter and Ward's triangle (P < 0.02). Fasting 25-hydroxyvitamin D was low in only three Cir patients, with no difference between the Cir and NCir groups, but it was higher in men (51.8 +/- 16.0 ng/mL) compared to women (40.4 +/- 14.4 ng/mL; P = 0.001). Fasting serum calcium was lower in Cir than NCir patients, P = 0.019. Fasting intact PTH was elevated in 42% of the patients, but the mean serum levels were similar in Cir and NCir groups.
We found no evidence of vitamin D deficiency, but cannot exclude the participation of PTH in the high bone turnover and bone loss in the population with chronic viral hepatitis.
肝性骨营养不良所涉及的主要过程似乎是骨质疏松症，但维生素D的25-羟化作用降低可能导致骨软化症和继发性甲状旁腺功能亢进。
我们使用DEXA-Expert Lunar研究了100例丙型肝炎病毒所致慢性病毒性肝炎患者的骨密度（BMD）、骨转换生化标志物以及钙-甲状旁腺激素（PTH）-维生素D轴：49例非肝硬化（NCir）患者和51例经肝活检和/或临床及生化特征确诊为肝硬化（Cir）的患者。与年龄匹配的人群相比，25%的患者腰椎（LS）骨密度低，26.2%的患者沃德三角区骨密度低，15.5%的患者股骨颈（FN）骨密度低，20.2%的患者大转子骨密度低。Cir组和NCir组之间以及男女之间均未发现差异。31.86%的患者尿N-端肽升高，且与LS和大转子处的BMD呈负相关（P<0.02）。21%的患者血清骨特异性碱性磷酸酶升高，且与大转子和沃德三角区的BMD呈负相关（P<0.02）。仅3例Cir患者空腹25-羟维生素D水平低，Cir组和NCir组之间无差异，但男性（51.8±16.0 ng/mL）高于女性（40.4±14.4 ng/mL；P = 0.001）。Cir患者空腹血清钙低于NCir患者，P = 0.019。42%的患者空腹完整PTH升高，但Cir组和NCir组的平均血清水平相似。
我们未发现维生素D缺乏的证据，但不能排除PTH参与慢性病毒性肝炎患者高骨转换和骨质流失过程。
