Sasidharan Pillai Sabitha, Robilliard Renee, Fredette Meghan E, Serrano-Gonzalez Monica, Scully Kevin J
Division of Pediatric Endocrinology, Hasbro Children's Hospital, Providence, USA.
Department of Pediatrics, The Warren Alpert Medical School of Brown University, Providence, USA.
J Pediatr Endocrinol Metab. 2023 Oct 5;36(11):1109-1113. doi: 10.1515/jpem-2023-0304. Print 2023 Nov 27.
Hypercalcemia has been reported as an uncommon complication of the ketogenic diet (KD). Here we present a toddler whose hypercalcemia persisted for 2 months after stopping the KD.
A 2 year 11-month-old child with global developmental delay, infantile spasms, neuromuscular weakness with limited mobility, tracheostomy and ventilator dependence, and oropharyngeal dysphagia with G-tube dependence presented with hypercalcemia in the setting of recurrent vomiting. At presentation, the patient was adherent to a KD and taking topiramate since infancy for intractable seizures. His laboratory parameters at presentation showed hypercalcemia (11.9 mg/dL), hypercalciuria, acute renal failure, low alkaline phosphatase (76 IU/L [110-302 IU/L]), parathyroid hormone (PTH) <6 pg/mL (18-80 pg/mL), normal thyroid function, cortisol and vitamin D level. The patient's hypercalcemia persisted post-discontinuation of the KD and topiramate. PTH-related protein was mildly elevated at 15.3 pmol/L. Follow-up laboratory and imaging studies ruled out malignancy. He was managed with calcitonin 4 u/kg/dose Q12H × 1 day and 8 u/kg/dose Q8H × 1 day, hydration and low-calcium formula. Post-discontinuation of the KD, normalization of alkaline phosphatase levels preceded the normalization of calcium on day 55 and PTH on day 85.
Hypercalcemia may persist for an extended period after weaning from a KD; lab parameters may mimic that of hypophosphatasia as previously described in the literature. Normalization of alkaline phosphatase, a marker of bone turnover, indicates recovery from the adynamic state induced by the KD and typically precedes the normalization of calcium and PTH.
高钙血症已被报道为生酮饮食（KD）的一种罕见并发症。在此，我们报告一名幼儿，其高钙血症在停用KD后持续了2个月。
一名2岁11个月大的儿童，有全面发育迟缓、婴儿痉挛、神经肌肉无力且活动受限、气管切开并依赖呼吸机，以及口咽吞咽困难且依赖胃造瘘管，在反复呕吐的情况下出现高钙血症。就诊时，该患者坚持KD饮食，自婴儿期起因难治性癫痫服用托吡酯。其就诊时的实验室检查参数显示高钙血症（11.9mg/dL）、高钙尿症、急性肾衰竭、碱性磷酸酶水平低（76IU/L[110 - 302IU/L]）、甲状旁腺激素（PTH）<6pg/mL（18 - 80pg/mL）、甲状腺功能、皮质醇和维生素D水平正常。停用KD和托吡酯后，患者的高钙血症仍持续。PTH相关蛋白轻度升高至15.3pmol/L。后续的实验室和影像学检查排除了恶性肿瘤。给予降钙素4u/kg/剂量，每12小时一次，共1天，然后8u/kg/剂量，每8小时一次，共1天，同时进行补液和低钙配方饮食治疗。停用KD后，碱性磷酸酶水平在第55天恢复正常，钙水平在第85天恢复正常，PTH水平在第85天恢复正常。
停用KD后，高钙血症可能会持续较长时间；实验室检查参数可能类似于文献中先前描述的低磷酸酯酶症。骨转换标志物碱性磷酸酶的正常化表明从KD诱导的骨动力不足状态中恢复，通常先于钙和PTH的正常化。
