Seyberth H W
Klin Wochenschr. 1978 Apr 15;56(8):373-87. doi: 10.1007/BF01477292.
Evidence has been presented for prostaglandin-mediated hypercalcemia and bone resorption in malignancies of both, experimental animals and man. Occurence of hypercalcemia in cancer patients is known for a long time, but its pathogenesis has been poorly understood so far. Besides ectopic parathyroid hormone secretion by tumors, an osteoclast-activating factor released from leukocytes and direct bone destruction by tumor cells, prostaglandins of the E series have to be considered as one of the candicates involved in the pathomechanism of hypercalcemia and osteoclastic osteolysis in cancer patients. This new concept on the pathophysiology of cancer-associated hypercalcemia has implications for the diagnosis and management of this common complication of neoplastic disease.
在实验动物和人类的恶性肿瘤中,已有证据表明前列腺素介导了高钙血症和骨吸收。癌症患者中高钙血症的发生由来已久,但迄今为止其发病机制仍知之甚少。除了肿瘤异位分泌甲状旁腺激素、白细胞释放的破骨细胞激活因子以及肿瘤细胞对骨的直接破坏外,E系列前列腺素必须被视为参与癌症患者高钙血症和破骨细胞性骨溶解发病机制的候选因素之一。这种关于癌症相关性高钙血症病理生理学的新概念对这种肿瘤疾病常见并发症的诊断和管理具有重要意义。