Caravaca F, Cubero J J, de Francisco A L, Arrobas M, Pizarro J L, Sánchez-Casado E
Servicio de Nefrología, Hospital Infanta Cristina, Badajoz.
Med Clin (Barc). 1991 May 4;96(17):659-61.
We describe the case of a 42-year-old woman diagnosed of chronic renal failure secondary to sarcoidosis. Since the beginning of the dialysis treatment she presented episodes of symptomatic hypercalcemia which did not response to calcium restriction diet and a lower calcium concentration in the dialysate. Secondary hyperparathyroidism and aluminium intoxication were biochemically ruled out. Hypercalcemic crisis were associated to 1.25-dihydroxy-vitamin D (1.25-D) serum levels abnormally raised and they responded quickly to low doses of corticosteroids. Subsequently, this treatment had to be withdrawn because of upper gastrointestinal bleeding, and hypercalcemia recurred. Chloroquine phosphate was prescribed with a rapid response to normalize the serum calcium levels. No side effects was recorded. Twelve months later of chloroquine therapy, the patient remained normocalcemic. A bone biopsy showed an active osteopenia without aluminium deposits, hyperparathyroidism signs or granuloma. We discuss about the pathogenesis of hypercalcemia in this case and its relation with abnormal high serum levels of 1.25-D in hemodialysis patients and sarcoidosis.
我们描述了一例42岁女性患者,诊断为结节病继发慢性肾衰竭。自开始透析治疗以来,她出现了有症状的高钙血症发作,对钙限制饮食和透析液中较低的钙浓度均无反应。生化检查排除了继发性甲状旁腺功能亢进和铝中毒。高钙血症危象与血清1,25-二羟维生素D(1,25-D)水平异常升高有关,且对低剂量皮质类固醇迅速起效。随后,由于上消化道出血,该治疗不得不停用,高钙血症复发。给予磷酸氯喹后,血清钙水平迅速恢复正常,未记录到副作用。氯喹治疗12个月后,患者血钙维持正常。骨活检显示为活动性骨质减少,无铝沉积、甲状旁腺功能亢进体征或肉芽肿。我们讨论了该病例中高钙血症的发病机制及其与血液透析患者和结节病患者血清1,25-D异常高水平的关系。