Suzuki K, Arakawa Y, Chino S, Yagi K
Third Department of Internal Medicine, Nihon University School of Medicine.
Nihon Rinsho. 1998 Jun;56(6):1604-8.
Bone thinning causing both fractures and severe pain not associated with fractures has been recognized in patients with chronic liver diseases. The patients most commonly affected are those with primary or secondary biliary cirrhosis, but those with alcoholic liver disease and cirrhosis after active chronic hepatitis may also be involved. Chronic liver disease has also been recognized as an important cause of osteoporosis in both sexes, with the mechanism thought to be a combination of calcium and/or vitamin D. The 9.1% patients with chronic active hepatitis accompanied with osteodystrophy. But 50% cirrhotic patients accompanied with osteodystrophy. Bone densitometry was determined by Digital Image Processing Method (Osteodystrophy < mean-2SD: age- and sex-matched normal value). Serum levels of osteocalcin (BGP) and parathyroid hormone (PTH) in patients of hepatic cirrhosis without osteodystrophy were lower than those with osteodystrophy. These results were suggested that hepatic osteodystrophy was rapidly turnover osteodystrophy. To function physiologically, vitamin D must be hydroxylation in liver to 25-(OH)-D and subsequently by the kidney to 1 alfa, 25-(OH)2-D. Osteodystrophy associated with hepatic cirrhosis is due to a defect in the 1 alfa-hydroxylation by the kidney rather than a hepatic hydroxylation defect. 1 alfa OH-D3 is very useful for treatment for hepatic osteodystrophy.
慢性肝病患者中已认识到存在导致骨折以及与骨折无关的严重疼痛的骨质变薄情况。最常受影响的患者是原发性或继发性胆汁性肝硬化患者,但酒精性肝病患者以及活动性慢性肝炎后肝硬化患者也可能受累。慢性肝病也已被确认为男女骨质疏松的重要原因,其机制被认为是钙和/或维生素D的综合作用。9.1%的慢性活动性肝炎患者伴有骨营养不良。但50%的肝硬化患者伴有骨营养不良。采用数字图像处理方法测定骨密度(骨营养不良<均值-2标准差:年龄和性别匹配的正常值)。无骨营养不良的肝硬化患者血清骨钙素(BGP)和甲状旁腺激素(PTH)水平低于有骨营养不良的患者。这些结果提示肝性骨营养不良是快速转换型骨营养不良。为发挥生理功能,维生素D必须在肝脏中羟化为25-(OH)-D,随后在肾脏中进一步羟化为1α,25-(OH)2-D。与肝硬化相关的骨营养不良是由于肾脏1α-羟化缺陷而非肝脏羟化缺陷所致。1α-OH-D3对治疗肝性骨营养不良非常有用。