Alexandre C, Chappard D, Vergnon J M, Emonot A, Riffat G
Rev Rhum Mal Osteoartic. 1987 Feb;54(2):159-62.
The sarcoidosis granuloma secretes 1-25 dihydroxyvitamin D (1-25(OH)2 D) at the origin of the hypercalcemia found in about 20 p. cent of sarcoidoses. Its mechanism was considered exclusively of a digestive nature, but the activity of osteoclastic stimulation of 1-25(OH)2 D must consider an associated bony origin. Nine patients with bouts of non-steroid sarcoidosis were studied by osseous histomorphometric analysis. In a patient with hypercalcemia and radiographic manifestations, a high degree of bone remodelling is demonstrated, with stimulation of osteoclastic and osteoblastic activity. In eight patients with normocalcemia, two subgroups are individualized: two patients present intramedullary sarcoidosis granulomas with increased contact resorption; six patients present a normal marrow: the total areas of resorption remain increased. It is concluded that the activity of osteoclastic resorption is increased in sarcoidosis, which may explain partially the hypercalcemia. The absence of titration of 1-25(OH)2 D in our study does not permit to precise the role of this enzyme in the genesis of hyperosteoclastosis, although this seems quite plausible.
结节病肉芽肿分泌1,25 - 二羟维生素D(1,25(OH)₂D),这是约20%结节病患者出现高钙血症的原因。其机制曾被认为完全是消化性的,但1,25(OH)₂D对破骨细胞的刺激作用必须考虑到相关的骨源性因素。对9例非类固醇性结节病发作患者进行了骨组织形态计量学分析。在1例高钙血症且有影像学表现的患者中,显示出高度的骨重塑,伴有破骨细胞和成骨细胞活性增强。在8例血钙正常的患者中,可分为两个亚组:2例患者存在骨髓内结节病肉芽肿且接触性吸收增加;6例患者骨髓正常,但吸收总面积仍增加。结论是结节病中破骨细胞吸收活性增加,这可能部分解释了高钙血症。在我们的研究中未检测到1,25(OH)₂D的水平,尽管其在破骨细胞增多症发生中的作用似乎相当合理,但这使得我们无法精确确定该酶的作用。