Sloand James A, Shelly Mark A
University of Rochester School of Medicine, Department of Medicine, Nephrology and Infectious Disease Division, Rochester, NY, USA.
Am J Kidney Dis. 2006 Nov;48(5):832-7. doi: 10.1053/j.ajkd.2006.07.019.
An underrecognized side effect of long-term lithium carbonate therapy is hyperparathyroidism with associated hypercalcemia and hypocalciuria. Because cessation of lithium carbonate therapy usually does not correct the hyperparathyroidism and associated hypercalcemia, parathyroidectomy frequently is necessary. This is the initial report of 2 patients with lithium carbonate-induced hyperparathyroidism treated with cinacalcet hydrochloride (HCl), which normalized serum calcium levels and reduced intact parathyroid hormone (iPTH) secretion. The patients, both with bipolar disease and a 15- to 30-year history of lithium carbonate therapy, were evaluated for stage 3 chronic kidney disease, persistent hypercalcemia, and hyperparathyroidism. A 67-year-old woman was administered cinacalcet HCl, 30 mg/d, for 11 months. Mean serum calcium level decreased from 10.8 +/- 0.4 mg/dL (2.69 +/- 0.10 mmol/L) to 9.9 +/- 0.4 mg/dL (2.47 +/- 0.10 mmol/L; P < 0.001), and iPTH level decreased from 139 +/- 31 pg/mL (139 +/- 31 ng/L) to 114 +/- 39 pg/mL (114 +/- 39 ng/L; P = not significant). A 63-year-old man was administered 30 mg/d of cinacalcet HCl for 8 months, then 60 mg/d for another 2 months. Mean serum calcium and iPTH levels decreased from 11.0 +/- 0.5 mg/dL (2.74 +/- 0.12 mmol/L) to 10.3 +/- 0.4 mg/dL (2.57 +/- 0.10 mmol/L; P < 0.001) and 138 +/- 10 pg/mL (138 +/- 10 ng/L) to 73 +/- 7 pg/mL (73 +/- 7 ng/L; P = 0.03), respectively. Urinary fractional excretion of calcium was low for both patients before (<0.026 and <0.015) and after (0.026 and 0.008) treatment with cinacalcet HCl. These findings suggest that cinacalcet HCl can provide an alternative nonsurgical means to control this disorder in patients with hypercalcemia of variable severity for whom surgical treatment is not a consideration because of perceived mildness of disease or unsuitability of the patient for surgical intervention.
长期碳酸锂治疗一个未得到充分认识的副作用是甲状旁腺功能亢进,伴有高钙血症和低钙尿症。由于停用碳酸锂治疗通常不能纠正甲状旁腺功能亢进和相关的高钙血症,甲状旁腺切除术常常是必要的。本文首次报告了2例碳酸锂诱导的甲状旁腺功能亢进患者接受盐酸西那卡塞治疗,该治疗使血清钙水平恢复正常,并减少了甲状旁腺激素(iPTH)分泌。这两名患者均患有双相情感障碍,有15至30年的碳酸锂治疗史,因慢性肾脏病3期、持续性高钙血症和甲状旁腺功能亢进接受评估。一名67岁女性接受盐酸西那卡塞30mg/d治疗11个月。平均血清钙水平从10.8±0.4mg/dL(2.69±0.10mmol/L)降至9.9±0.4mg/dL(2.47±0.10mmol/L;P<0.001),iPTH水平从139±31pg/mL(139±31ng/L)降至114±39pg/mL(114±39ng/L;P无统计学意义)。一名63岁男性接受盐酸西那卡塞30mg/d治疗8个月,然后60mg/d再治疗2个月。平均血清钙和iPTH水平分别从11.0±0.5mg/dL(2.74±0.12mmol/L)降至10.3±0.4mg/dL(2.57±0.10mmol/L;P<0.001)和138±10pg/mL(138±10ng/L)降至73±7pg/mL(73±7ng/L;P=0.03)。两名患者在接受盐酸西那卡塞治疗前(<0.026和<0.015)和治疗后(0.026和0.008)的尿钙分数排泄均较低。这些发现表明,对于因疾病较轻或患者不适合手术干预而不考虑手术治疗的不同严重程度高钙血症患者,盐酸西那卡塞可提供一种替代的非手术方法来控制这种疾病。