Academic Endocrine Unit, Radcliffe Department of Medicine, University of Oxford, Oxford, UK.
Department of Clinical Research, Faculty of Health, University of Southern Denmark, Odense, Denmark.
J Bone Miner Res. 2017 Nov;32(11):2157-2170. doi: 10.1002/jbmr.3296. Epub 2017 Nov 2.
Hypercalcemia is defined as a serum calcium concentration that is greater than two standard deviations above the normal mean, which in children may vary with age and sex, reflecting changes in the normal physiology at each developmental stage. Hypercalcemic disorders in children may present with hypotonia, poor feeding, vomiting, constipation, abdominal pain, lethargy, polyuria, dehydration, failure to thrive, and seizures. In severe cases renal failure, pancreatitis and reduced consciousness may also occur and older children and adolescents may present with psychiatric symptoms. The causes of hypercalcemia in children can be classified as parathyroid hormone (PTH)-dependent or PTH-independent, and may be congenital or acquired. PTH-independent hypercalcemia, ie, hypercalcemia associated with a suppressed PTH, is commoner in children than PTH-dependent hypercalcemia. Acquired causes of PTH-independent hypercalcemia in children include hypervitaminosis; granulomatous disorders, and endocrinopathies. Congenital syndromes associated with PTH-independent hypercalcemia include idiopathic infantile hypercalcemia (IIH), William's syndrome, and inborn errors of metabolism. PTH-dependent hypercalcemia is usually caused by parathyroid tumors, which may give rise to primary hyperparathyroidism (PHPT) or tertiary hyperparathyroidism, which usually arises in association with chronic renal failure and in the treatment of hypophosphatemic rickets. Acquired causes of PTH-dependent hypercalcemia in neonates include maternal hypocalcemia and extracorporeal membrane oxygenation. PHPT usually occurs as an isolated nonsyndromic and nonhereditary endocrinopathy, but may also occur as a hereditary hypercalcemic disorder such as familial hypocalciuric hypercalcemia, neonatal severe primary hyperparathyroidism, and familial isolated primary hyperparathyroidism, and less commonly, as part of inherited complex syndromic disorders such as multiple endocrine neoplasia (MEN). Advances in identifying the genetic causes have resulted in increased understanding of the underlying biological pathways and improvements in diagnosis. The management of symptomatic hypercalcemia includes interventions such as fluids, antiresorptive medications, and parathyroid surgery. This article presents a clinical, biochemical, and genetic approach to investigating the causes of pediatric hypercalcemia. © 2017 American Society for Bone and Mineral Research.
高钙血症定义为血清钙浓度高于正常均值两个标准差以上,儿童的正常值可能随年龄和性别而变化,反映了每个发育阶段正常生理的变化。儿童高钙血症的表现可能为肌无力、喂养不良、呕吐、便秘、腹痛、嗜睡、多尿、脱水、生长不良和癫痫发作。在严重的情况下,也可能发生肾衰竭、胰腺炎和意识降低,而年龄较大的儿童和青少年可能出现精神症状。儿童高钙血症的原因可分为甲状旁腺激素(PTH)依赖性或 PTH 非依赖性,可能为先天性或后天性。PTH 非依赖性高钙血症,即与 PTH 抑制相关的高钙血症,在儿童中比 PTH 依赖性高钙血症更常见。儿童 PTH 非依赖性高钙血症的后天性病因包括维生素过量;肉芽肿性疾病和内分泌疾病。与 PTH 非依赖性高钙血症相关的先天性综合征包括特发性婴儿高钙血症(IIH)、威廉姆斯综合征和先天性代谢错误。PTH 依赖性高钙血症通常由甲状旁腺肿瘤引起,可导致原发性甲状旁腺功能亢进症(PHPT)或三发性甲状旁腺功能亢进症,后者通常与慢性肾衰竭和治疗低磷血症性佝偻病有关。新生儿 PTH 依赖性高钙血症的后天性病因包括母亲低钙血症和体外膜氧合。PHPT 通常作为一种孤立的非综合征和非遗传性内分泌疾病发生,但也可能作为遗传性高钙血症疾病发生,如家族性低钙尿性高钙血症、新生儿严重原发性甲状旁腺功能亢进症和家族性孤立性原发性甲状旁腺功能亢进症,较少见的情况下,作为多种内分泌肿瘤(MEN)等遗传性复杂综合征疾病的一部分发生。在识别遗传原因方面的进展导致对潜在生物学途径的理解加深,并改善了诊断。有症状的高钙血症的治疗包括干预措施,如补液、抗吸收药物和甲状旁腺手术。本文提出了一种临床、生化和遗传方法来调查儿童高钙血症的病因。© 2017 美国骨骼与矿物研究学会。