Davies M, Mawer E B, Hayes M E, Lumb G A
Lancet. 1985 May 25;1(8439):1186-8. doi: 10.1016/s0140-6736(85)92864-8.
In the autumn of 1984 there was spontaneous correction of hypercalcaemia in a patient with Hodgkin's lymphoma. Hypercalcaemia recurred when ultraviolet radiation (UVR) was given and this abnormality was associated with high serum concentrations of 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) although concentrations of precursor 25-hydroxyvitamin D3 were normal. Chemotherapy of Hodgkin's lymphoma corrected the hypercalcaemia and subsequent exposure to UVR did not produce either hypercalcaemia or a high serum 1,25(OH)2D3. Rigorous tests were applied to the putative 1,25(OH)2D3 produced during hypercalcaemia and it was not possible to separate this metabolite from 1,25(OH)2D3 itself. It is concluded that the hypercalcaemia was caused by abnormal vitamin D metabolism which was a result of the Hodgkin's lymphoma. Hodgkin's tissue may have been the site of excessive synthesis of 1,25(OH)2D3.
1984年秋，一名霍奇金淋巴瘤患者的高钙血症自发得到纠正。给予紫外线辐射（UVR）时，高钙血症复发，且这种异常与血清中高浓度的1,25 - 二羟维生素D3（1,25[OH]2D3）相关，尽管前体25 - 羟维生素D3的浓度正常。霍奇金淋巴瘤的化疗纠正了高钙血症，随后暴露于UVR既未产生高钙血症，血清1,25(OH)2D3也未升高。对高钙血症期间产生的假定1,25(OH)2D3进行了严格检测，无法将该代谢产物与1,25(OH)2D3本身区分开来。结论是，高钙血症是由异常的维生素D代谢引起的，这是霍奇金淋巴瘤的结果。霍奇金组织可能是1,25(OH)2D3过度合成的部位。
