生酮饮食可以导致儿童高钙血症?
创作:orchid 审核:兵兵 2020年11月08日
  • 长期生酮饮食可能因成骨细胞活性降低和骨形成受损导致高钙血症;
  • 生酮饮食2.1(0.2至12岁)年后,14名患者(均龄6.3(0.9至18)岁)发生高钙血症;
  • 除了1个例外,所有患者甲状旁腺激素和1,25-二羟基维生素D水平均较低;
  • 除了2个年龄最大的,其他患者碱性磷酸酶水平降低, 7名患者的肾功能受损;
  • 随访9.8年,仅2名患者高钙血症复发,且有1名患者在达到正常血钙之前、4名患者在高钙血症消退后停止了生酮饮食;
  • 具体作用机制尚不清楚。
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兵兵
文章采用多中心研究手段,探究了生酮饮食与儿童高钙血症的相关性。研究结果显示,生酮饮食或影响患者的激素分泌、酶水平等,进而干预血钙浓度。这可能与成骨细胞活性或受损的骨形成有关,但具体机制尚不清楚。
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Hypercalcemia in Children Using the Ketogenic Diet: A Multicenter Study

采用生酮饮食的儿童高钙血症:一项多中心研究

10.1210/clinem/dgaa759

2020-10-30, Article

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Context: The ketogenic diet is associated with progressive skeletal demineralization, hypercalciuria and nephrolithiasis. Acute hypercalcemia has been described as a newly recognized complication of this treatment.
Objective: To describe the clinical characteristics of acute hypercalcemia in children on the ketogenic diet through analysis of the presentation, response to treatment, and natural history in a large cohort of patients.
Design: A multicenter case series was performed including children who developed acute hypercalcemia while treated with the ketogenic diet. Information on clinical presentation, treatment and course of this complication was collated centrally.
Results: There were 14 patients (median (range) age 6.3 (0.9 to 18) years) who developed hypercalcemia 2.1 (range 0.2 to 12) years after starting the ketogenic diet. All had low levels of parathyroid hormone and levels of 1,25-dihydroxyvitamin D were low in all except one. Seven (50%) had impaired renal function at presentation. All except the two oldest had low alkaline phosphatase levels for age. Once normocalcemia was achieved, hypercalcemia recurred in only two of these patients over observation of up to 9.8 years. One patient discontinued the ketogenic diet prior to achieving normocalcemia while four more stopped the diet during follow-up after resolution of hypercalcemia.
Conclusions: Ketotic hypercalcemia can occur years after starting the ketogenic diet, especially in the setting of renal impairment. The mechanism is unknown, but appears to be due to reduced osteoblast activity and impaired bone formation. We recommend close attention to optimizing bone health in these children, and screening for the development of ketotic hypercalcemia.

First Authors:
Colin P Hawkes

Correspondence Authors:
Michael A Levine

All Authors:
Colin P Hawkes,Sani M Roy,Bassem Dekelbab,Britney Frazier,Monica Grover,Jaime Haidet,James Listman,Sarianne Madsen,Marian Roan,Celia Rodd,Aviva Sopher,Peter Tebben,Michael A Levine

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