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[肾性骨营养不良:铝与继发性甲状旁腺功能亢进]

[Renal osteodystrophy: aluminium and secondary hyperparathyroidism].

作者信息

de Vernejoul M C

机构信息

INSERM U 18, Centre Viggo-Petersen, Paris.

出版信息

Rev Prat. 1990 Mar 1;40(7):613-8.

PMID:2326587
Abstract

Aluminium-related osteodystrophy results in osteomalacia or in the so-called aplastic bone. In this particular bone disease bone cells activities are distinctly reduced but there is no disorder of bone mineralization. Aluminium exerts a direct toxic effect on bone tissue, notably on osteoblasts which are always strongly depressed in case of major aluminium overload. Aluminium-related osteopathy is regularly accompanied by low levels of parathormone due to accumulation of aluminium in the parathyroid glands. Parathormone modulates the bone aluminium overload: hyperparathyroidism "protects" bones against the deleterious effect of aluminium, whereas aluminium deposit in bone increase after parathyroidectomy. The respective roles played by low parathormone levels and by aluminium deposits in aplastic bone lesions is difficult to determine since hypoparathyroidism itself can probably cause the aplastic osteopathy. The role of parathormone stands out more clearly now that in patients under dialysis the bone aluminium overload has markedly decreased. Many patients with aplastic bone (initially described in aluminium poisoning) show no aluminium deposits in bones but have, for some unknown reason, a normal or even low parathormone level. The clinical course of this type of osteopathy remains to be determined, but there seems to be no reason to worry since numerous patient are asymptomatic. Preventing secondary hyperparathyroidism while refraining from prescribing aluminium hydroxide is the principal therapeutic objective in osteodystrophy of haemodialysis patients.

摘要

铝相关性骨营养不良可导致骨软化症或所谓的再生障碍性骨病。在这种特殊的骨病中,骨细胞活性明显降低,但骨矿化并无紊乱。铝对骨组织有直接毒性作用,尤其是对成骨细胞,在铝严重超载的情况下,成骨细胞总是受到强烈抑制。铝相关性骨病常伴有甲状旁腺激素水平降低,这是由于铝在甲状旁腺中蓄积所致。甲状旁腺激素可调节骨铝超载:甲状旁腺功能亢进“保护”骨骼免受铝的有害影响,而甲状旁腺切除术后骨中的铝沉积会增加。低甲状旁腺激素水平和铝沉积在再生障碍性骨病变中各自所起的作用难以确定,因为甲状旁腺功能减退本身可能会导致再生障碍性骨病。现在甲状旁腺激素的作用更加明显,因为在透析患者中骨铝超载已明显降低。许多再生障碍性骨病患者(最初在铝中毒中描述)骨中无铝沉积,但由于某些未知原因,甲状旁腺激素水平正常甚至降低。这种类型骨病的临床病程仍有待确定,但似乎无需担忧,因为许多患者并无症状。在避免使用氢氧化铝的同时预防继发性甲状旁腺功能亢进是血液透析患者骨营养不良的主要治疗目标。

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