Metabolic bone disease associated with total parenteral nutrition.

G L Klein, J W Coburn
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引用次数: 41

Abstract

Patients receiving long-term treatment with total parenteral nutrition often develop bony abnormalities characterized by patchy osteomalacia and low bone turnover. The patients present evidence of physiologic hypoparathyroidism, although low levels of iPTH cannot entirely explain the osteomalacia. Abnormally low serum levels of 1,25(OH)2-vitamin D have been demonstrated, but the significance of these reduced levels in the pathogenesis of the bone lesions is not defined. Aluminum has been detected in large quantities in the plasma, urine, and bone of some patients treated with TPN, and there is mounting evidence that aluminum may be associated with skeletal pathology, particularly osteomalacia. There is, however, no clear documentation that aluminum accumulation produces the skeletal lesions observed, although it could be a contributing factor. There has been the unusual empiric observation that the removal of vitamin D2 from the infusate is associated with a decrease in the quantity of unmineralized osteoid in TPN patients. A possible role of vitamin D2 in producing osteomalacia is not easy to understand since normal serum levels of 25(OH)-D2, the circulating form of vitamin D2, have been reported. The long-term consequences of intravenous nutritional support for many aspects of metabolism remain unknown. Administration into the systemic circulation of predetermined quantities of calcium and phosphorus via a route that bypasses their passage across the intestinal mucosa, the portal system and the liver may have adverse consequences. It is possible that bypassing homeostatic mechanisms may affect bone formation and metabolism or lead to alterations in vitamin D sterols. Alternatively, a deficiency of an essential trace metal or the accumulation of a toxic trace substance could be responsible for the bony abnormalities. Much remains to be clarified concerning calcium homeostasis and bone disease during total parenteral nutrition. Among various possible factors, it seems likely that the significance of the low levels of 1,25(OH)2-vitamin D and of the accumulation of aluminum in this condition will soon be clarified.

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与全肠外营养相关的代谢性骨病。
长期接受全肠外营养治疗的患者经常出现以斑片状骨软化和低骨转换为特征的骨异常。患者表现为生理性甲状旁腺功能低下,尽管低iPTH水平不能完全解释骨软化。已证实血清中1,25(OH)2-维生素D水平异常低,但这些水平降低在骨病变发病机制中的意义尚不明确。在一些接受TPN治疗的患者的血浆、尿液和骨骼中检测到大量的铝,并且有越来越多的证据表明铝可能与骨骼病理,特别是骨软化症有关。然而,虽然铝的积累可能是一个促成因素,但没有明确的文献表明铝的积累会产生所观察到的骨骼病变。有一个不寻常的经验性观察,即从输液剂中去除维生素D2与TPN患者中未矿化类骨质的数量减少有关。维生素D2在产生骨软化症中的可能作用并不容易理解,因为已有报道称维生素D2的循环形式25(OH)-D2的正常血清水平。静脉营养支持对新陈代谢许多方面的长期影响尚不清楚。预定数量的钙和磷通过绕过肠粘膜、门静脉系统和肝脏的途径进入体循环,可能会产生不良后果。绕过体内平衡机制可能会影响骨形成和代谢或导致维生素D固醇的改变。另外,一种必需微量金属的缺乏或一种有毒微量物质的积累可能是导致骨骼异常的原因。在全肠外营养过程中,钙稳态和骨病的关系还有待进一步研究。在各种可能的因素中,在这种情况下,低水平的1,25(OH)2-维生素D和铝的积累的重要性似乎很快就会得到澄清。
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Advances in Nutritional Research
Advances in Nutritional Research Nutritional Physiological Phenomena-
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