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[一例暂时性严重失衡性高钙血症]

[A case of temporary severe disequilibrium hypercalcemia].

作者信息

Kogawa K, Inaba M, Okuno Y, Miki T, Nishizawa Y, Morii H

机构信息

Second Department of Internal Medicine, Osaka City University Medical School.

出版信息

Nihon Ronen Igakkai Zasshi. 1994 Feb;31(2):142-6. doi: 10.3143/geriatrics.31.142.

Abstract

The patient, a 69-year-old woman, was admitted to Osaka City University Hospital on July 25, 1992, for severe hypercalcemia. Laboratory data on admission revealed severe hypercalcemia of 14.9 mg/dl and renal dysfunction with serum creatinine of 2.9 mg/dl. As reflected by increased urinary excretions of pyridinoline and deoxypyridinoline and suppressed serum levels of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D, increased bone resorption seemed to be a main factor for the development of hypercalcemia. The development of hypercalcemia seemed to be acute because of (i) her severe symptoms caused by hypercalcemia and (ii) impaired renal function which improved after normalization of serum calcium. Following combination therapy of saline infusion and furosemide, there was a gradual decrease and later normalization of serum calcium together with serum creatinine. Even 8 months after discontinuation of the therapy for hypercalcemia, the serum calcium level has remained within the normal range. Measurement of serum factors which have hypercalcemia effects such as PTH, parathyroid hormone-related peptide and cytokines (interleukin-1 alpha, interleukin-1 beta, interleukin-2, interleukin-6 and tumor necrosis factor-alpha) were all within the normal range. In summary, hypercalcemia in this patient was regarded as a kind of disequilibrium hypercalcemia due to a combination of increased bone resorption and decreased renal capacity to excrete calcium. Furthermore, since it was temporary and has not recurred despite no treatment, her hypercalcemia developed due to imbalance in calcium regulation but not due to any organic disease.

摘要

该患者为一名69岁女性,于1992年7月25日因严重高钙血症入住大阪市立大学医院。入院时的实验室检查数据显示,血钙严重升高至14.9mg/dl,伴有肾功能不全,血清肌酐为2.9mg/dl。吡啶啉和脱氧吡啶啉尿排泄增加,甲状旁腺激素(PTH)和1,25-二羟维生素D血清水平降低,提示骨吸收增加似乎是高钙血症发生的主要因素。高钙血症的发生似乎是急性的,原因如下:(i)高钙血症引起的严重症状;(ii)肾功能损害,血钙正常后肾功能改善。经生理盐水输注和呋塞米联合治疗后,血钙及血清肌酐逐渐下降,随后恢复正常。即使在停止高钙血症治疗8个月后,血钙水平仍保持在正常范围内。对具有高钙血症作用的血清因子进行检测,如PTH、甲状旁腺激素相关肽和细胞因子(白细胞介素-1α、白细胞介素-1β、白细胞介素-2、白细胞介素-6和肿瘤坏死因子-α),结果均在正常范围内。综上所述,该患者的高钙血症被认为是一种由于骨吸收增加和肾脏排钙能力下降共同作用导致的失衡性高钙血症。此外,由于其为暂时性且未经治疗未复发,她的高钙血症是由于钙调节失衡而非任何器质性疾病所致。

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