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乳腺癌恶性高钙血症的机制

Mechanism of malignant hypercalcaemia in carcinoma of the breast.

作者信息

Percival R C, Yates A J, Gray R E, Galloway J, Rogers K, Neal F E, Kanis J A

出版信息

Br Med J (Clin Res Ed). 1985 Sep 21;291(6498):776-9. doi: 10.1136/bmj.291.6498.776.

Abstract

To investigate the mechanisms of hypercalcaemia in carcinoma of the breast, 22 patients with hypercalcaemia due to metastatic carcinoma were studied and the findings compared with those obtained in normal subjects and patients with benign and malignant breast disease without hypercalcaemia. As expected, patients with metastases of bone showed biochemical evidence of increased bone resorption. Whereas all patients with hypercalcaemia had skeletal metastases, not all patients with skeletal metastases had hypercalcaemia despite considerable degrees of bone resorption. The presence of hypercalcaemia was associated with a significant increase in renal tubular reabsorption of calcium (p less than 0.001) and decreased reabsorption of phosphate (p less than 0.001) despite adequate rehydration of patients. These studies suggest that increased renal tubular reabsorption of calcium, possibly mediated by a humoral factor with activity similar to that of parathyroid hormone, contributes appreciably to the hypercalcaemia of malignant breast disease.

摘要

为研究乳腺癌患者高钙血症的发病机制,对22例因转移性癌导致高钙血症的患者进行了研究,并将研究结果与正常受试者以及无高钙血症的良性和恶性乳腺疾病患者的结果进行了比较。正如预期的那样,骨转移患者显示出骨吸收增加的生化证据。虽然所有高钙血症患者均有骨转移,但并非所有骨转移患者尽管骨吸收程度相当高却都有高钙血症。高钙血症的存在与肾小管对钙的重吸收显著增加(p<0.001)以及磷酸盐重吸收减少(p<0.001)相关,尽管患者已充分补液。这些研究表明,肾小管对钙的重吸收增加,可能由一种活性类似于甲状旁腺激素的体液因子介导,在很大程度上导致了恶性乳腺疾病的高钙血症。

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