Horiuchi T, Miyachi T, Arai T, Nakamura T, Mori M, Ito H
Section of Endocrinology, Tokyo Metropolitan Geriatric Hospital, Japan.
Horm Metab Res. 1997 Sep;29(9):469-71. doi: 10.1055/s-2007-979080.
In order to clarify the pathogenesis of hypercalcemia in multiple myeloma, we measured plasma levels of parathyroid hormone related peptide (PTHrP), tumor necrosis factor alpha (TNF-alpha), tumor necrosis factor beta (TNF-beta), intact PTH and, serum 1,25-dihydroxyvitamin D in fifteen patients of multiple myeloma. We also measured serum levels of inorganic phosphorus (iP) and alkalinephosphatase activity (ALP). No significant differences in iP (3.2 +/- 0.4 vs. 4.0 +/- 2.2 mg/dl), ALP (150 +/- 28 vs. 335 +/- 305 IU/l) 1,25(OH)2 D (31.5 +/- 17.0 vs. 23.3 +/- 11.2 pg/ml) or TNF-alpha (7.8 +/- 2.1 vs. 8.0 +/- 2.0 pg/ml) were observed between normocalcemic and hypercalcemic patients. Plasma iPTH levels in hypercalcemic patients were significantly lower than those in normocalcemic patients (28.5 +/- 9.4 vs. 16.3 +/- 5.6 pg/ml, p = 0.01). Plasma levels of TNF-beta were less than 15.6 pg/ml in all subjects. On the other hand, the frequency of patients with abnormally high plasma levels of PTHrP was significantly greater (2/9 for normocalcemia vs 5/6 for hypercalcemia, chi 2 = 5.20, p = 0.02) in patients with hypercalcemia than in normocalcemic patients. Furthermore, a significant positive relationship between plasma PTHrP levels and corrected serum calcium levels (cCa) was observed using Spearman's correlation analysis by rank in fifteen myeloma cases (rs = 0.66, p = 0.013). These results suggest that PTHrP might be involved in the elevation of serum calcium levels in hypercalcemic myeloma patients. However, a few cases exhibit normocalcemia despite elevated plasma PTHrP levels or hypercalcemia without high plasma PTHrP levels. Therefore, further studies are necessary to elucidate the pathogenesis of hypercalcemia in multiple myeloma.
为了阐明多发性骨髓瘤中高钙血症的发病机制，我们检测了15例多发性骨髓瘤患者的血浆甲状旁腺激素相关肽（PTHrP）、肿瘤坏死因子α（TNF-α）、肿瘤坏死因子β（TNF-β）、完整甲状旁腺激素（iPTH）水平以及血清1,25-二羟维生素D水平。我们还检测了血清无机磷（iP）水平和碱性磷酸酶活性（ALP）。在血钙正常和高钙血症患者之间，iP（3.2±0.4 vs. 4.0±2.2mg/dl）、ALP（150±28 vs. 335±305IU/l）、1,25(OH)2D（31.5±17.0 vs. 23.3±11.2pg/ml）或TNF-α（7.8±2.1 vs. 8.0±2.0pg/ml）均未观察到显著差异。高钙血症患者的血浆iPTH水平显著低于血钙正常患者（28.5±9.4 vs. 16.3±5.6pg/ml，p = 0.01）。所有受试者的血浆TNF-β水平均低于15.6pg/ml。另一方面，高钙血症患者血浆PTHrP水平异常升高的频率显著高于血钙正常患者（血钙正常者为2/9，高钙血症者为5/6，χ2 = 5.20，p = 0.02）。此外，在15例骨髓瘤病例中，采用Spearman等级相关分析观察到血浆PTHrP水平与校正血清钙水平（cCa）之间存在显著正相关（rs = 0.66，p = 0.013）。这些结果表明，PTHrP可能与高钙血症骨髓瘤患者的血清钙水平升高有关。然而，少数病例尽管血浆PTHrP水平升高但血钙正常，或血浆PTHrP水平不高却出现高钙血症。因此，有必要进一步研究以阐明多发性骨髓瘤中高钙血症的发病机制。
