Giouleme Olga I, Vyzantiadis Timoleon A, Nikolaidis Nikolaos L, Vasiliadis Themistoklis G, Papageorgiou Athanasios A, Eugenidis Nikolaos P, Harsoulis Fedon I
Second Propedeutic Department of Medicine, Aristotle University Hippocration Hospital, Thessaloniki, Greece.
Hepatogastroenterology. 2006 Nov-Dec;53(72):938-43.
BACKGROUND/AIMS: Osteoporosis has been recognized in patients with liver cirrhosis, although the prevalence and the exact mechanisms vary considerably in the literature. We have studied the prevalence of bone disease in cirrhotic patients, the pathogenesis and the relation to the etiology and the severity of liver failure.
The study included 83 hospitalized patients with various types of cirrhosis, where 25 healthy individuals served as controls. Patients were classified according to Child-Pugh's stages as follows: Child A: 49, Child B: 20, Child C: 14. Serum levels of iPTH, 250HD, LH, FSH, SHBG, testosterone, estradiol, IGF-I, osteocalcin and urine levels of cross-linked N-telopeptides of collagen type 1 (NTX) were measured in all patients. Bone mineral density (BMD) was measured by DEXA at the spine of both patients and controls.
The prevalence of osteoporosis was higher in patients (26/83) 31.3% than in controls (4/25) 16%. Osteopenia was positively related with the elevated levels of crosslinked N-telopeptides (p=0.048). There were no differences in BMD between the types of cirrhosis. BMD was found to be significantly lower in Child B and C male patients than in Child A (p=0.043). Patients' groups B, and C had lower testosterone levels with a trend to contribute to the low BMD (p=0.15). 250HD and IGF-1 were significantly lower in decompensated cirrhosis (p<0.002), but did not correlate with BMD.
Cirrhosis is a major cause of osteoporosis and the degree of osteopenia is related to the severity and not the etiology of the liver disease. The biochemical markers of bone remodeling suggest a high-turnover osteoporosis in cirrhosis.
背景/目的:肝硬化患者中已发现骨质疏松症,尽管其患病率和确切机制在文献中差异很大。我们研究了肝硬化患者骨病的患病率、发病机制及其与病因和肝衰竭严重程度的关系。
该研究纳入了83例住院的各种类型肝硬化患者,其中25名健康个体作为对照。患者根据Child-Pugh分期进行如下分类:Child A:49例,Child B:20例,Child C:14例。测定了所有患者的血清甲状旁腺激素(iPTH)、25羟维生素D(250HD)、促黄体生成素(LH)、促卵泡生成素(FSH)、性激素结合球蛋白(SHBG)、睾酮、雌二醇、胰岛素样生长因子-1(IGF-I)、骨钙素水平以及尿I型胶原交联N端肽(NTX)水平。采用双能X线吸收法(DEXA)测量患者和对照者脊柱的骨密度(BMD)。
患者骨质疏松症的患病率(26/83,31.3%)高于对照组(4/25,16%)。骨量减少与交联N端肽水平升高呈正相关(p = 0.048)。不同类型肝硬化之间的骨密度无差异。发现Child B和C组男性患者的骨密度显著低于Child A组(p = 0.043)。B组和C组患者的睾酮水平较低,有导致低骨密度的趋势(p = 0.15)。失代偿期肝硬化患者的250HD和IGF-1显著降低(p < 0.002),但与骨密度无关。
肝硬化是骨质疏松症的主要原因,骨量减少的程度与肝脏疾病的严重程度而非病因有关。骨重塑的生化标志物提示肝硬化患者存在高转换型骨质疏松症。