Transient neonatal hyperparathyroidism secondary to maternal pseudohypoparathyroidism.

Glass, E J; Barr, D. G. D.

doi:10.1136/adc.56.7.565

Cited by 50 publications

(19 citation statements)

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“…These findings have been observed in babies born of mothers whose hypercalcemia during pregnancy was caused by primary hyperparathyroidism (79,149,304,393,609,718), inactivating mutations of Casr (529), or hypercalcemia of malignancy (9,131,278,454,529,673,674,700). Conversely, maternal hypocalcemia caused by hypoparathyroidism (11,76,389,586,652,710) or pseudohypoparathyroidism (226,710) has been associated with fetal parathyroid gland hyperplasia, normal cord blood calcium, increased PTH, and effects on the fetal skeleton that include increased resorption, demineralization, and fractures occurring in utero or during delivery (see sect. XII, C and D).…”

Section: Pthmentioning

confidence: 99%

“…Maternal hypercalcemia likely increases the flow of calcium across the placenta, thereby suppressing the fetal parathyroids. Conversely, maternal hypocalcemia caused by hypoparathyroidism or pseudohypoparathyroidism has been associated with intrauterine fetal hyperparathyroidism, skeletal demineralization, intrauterine fractures, and bowing of the long bones (226,389,652,710). This is compatible with reduced placental calcium transfer that prompts secondary hyperparathyroidism to develop in the fetus.…”

Section: Maternal Regulation Of Placental Mineral Transportmentioning

confidence: 99%

“…In women, hypocalcemia due to maternal pseudohypoparathyroidism during pregnancy can lead to the same fetal outcomes that have been associated with maternal hypoparathyroidism, including parathyroid hyperplasia, skeletal demineralization, and fractures (226,710). Postnatally, the relatively autonomous parathyroid function can cause neonatal hypercalcemia before the parathyroids involute.…”

Section: Human Datamentioning

confidence: 99%

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Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

197

188

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Mineral and bone metabolism are regulated differently in utero compared with the adult. The fetal kidneys, intestines, and skeleton are not dominant sources of mineral supply for the fetus. Instead, the placenta meets the fetal need for mineral by actively transporting calcium, phosphorus, and magnesium from the maternal circulation. These minerals are maintained in the fetal circulation at higher concentrations than in the mother and normal adult, and such high levels appear necessary for the developing skeleton to accrete a normal amount of mineral by term. Parathyroid hormone (PTH) and calcitriol circulate at low concentrations in the fetal circulation. Fetal bone development and the regulation of serum minerals are critically dependent on PTH and PTH-related protein, but not vitamin D/calcitriol, fibroblast growth factor-23, calcitonin, or the sex steroids. After birth, the serum calcium falls and phosphorus rises before gradually reaching adult values over the subsequent 24 -48 h. The intestines are the main source of mineral for the neonate, while the kidneys reabsorb mineral, and bone turnover contributes mineral to the circulation. This switch in the regulation of mineral homeostasis is triggered by loss of the placenta and a postnatal fall in serum calcium, and is followed in sequence by a rise in PTH and then an increase in calcitriol. Intestinal calcium absorption is initially a passive process facilitated by lactose, but later becomes active and calcitriol-dependent. However, calcitriol's role can be bypassed by increasing the calcium content of the diet, or by parenteral administration of calcium.

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Section: Pthmentioning

confidence: 99%

Section: Maternal Regulation Of Placental Mineral Transportmentioning

confidence: 99%

Section: Human Datamentioning

confidence: 99%

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Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Kovacs

2014

Physiological Reviews

197

188

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“…Typically, mothers of babies with congenital rickets have osteomalacia with severe vitamin D deficiency, low calcium intake, and hypocalcemia at delivery and had not taken vitamin D supplementation during pregnancy [83,[183][184][185][186][187][188][189][190][191][192][193][194][195][196][197] . In rare cases, congenital rickets can occur when mothers have had severe prolonged hypocalcemia not primarily caused by vitamin D deficiency such as poorly treated hypoparathyroidism [198][199][200][201] , renal failure [202][203][204][205][206] , received phosphate-containing enemas [207] , or iatrogenic hypermagnesemia [208] .…”

Section: Evidencementioning

confidence: 99%

Global Consensus Recommendations on Prevention and Management of Nutritional Rickets

Munns¹,

Shaw²,

Kiely³

et al. 2016

Horm Res Paediatr

346

477

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Background: Vitamin D and calcium deficiencies are common worldwide, causing nutritional rickets and osteomalacia, which have a major impact on health, growth, and development of infants, children, and adolescents; the consequences can be lethal or can last into adulthood. The goals of this evidence-based consensus document are to provide health care professionals with guidance for prevention, diagnosis, and management of nutritional rickets and to provide policy makers with a framework to work toward its eradication. Evidence: A systematic literature search examining the definition, diagnosis, treatment, and prevention of nutritional rickets in children was conducted. Evidence-based recommendations were developed using the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) system that describes the strength of the recommendation and the quality of supporting evidence. Process: Thirty-three nominated experts in pediatric endocrinology, pediatrics, nutrition, epidemiology, public health, and health economics evaluated the evidence on specific questions within five working groups. The consensus group, representing 11 international scientific organizations, participated in a multiday conference in May 2014 to reach a global evidence-based consensus. Results: This consensus document defines nutritional rickets and its diagnostic criteria and describes the clinical management of rickets and osteomalacia. Risk factors, particularly in mothers and infants, are ranked, and specific prevention recommendations including food fortification and supplementation are offered for both the clinical and public health contexts. Conclusion: Rickets, osteomalacia, and vitamin D and calcium deficiencies are preventable global public health problems in infants, children, and adolescents. Implementation of international rickets prevention programs, including supplementation and food fortification, is urgently required. nology, pediatrics, nutrition, epidemiology, public health, and health economics evaluated the evidence on specific questions within five working groups. The consensus group, representing 11 international scientific organizations, participated in a multiday conference in May 2014 to reach a global evidence-based consensus. Results: This consensus document defines nutritional rickets and its diagnostic criteria and describes the clinical management of rickets and osteomalacia. Risk factors, particularly in mothers and infants, are ranked, and specific prevention recommendations including food fortification and supplementation are offered for both the clinical and public health contexts. Conclusion: Rickets, osteomalacia, and vitamin D and calcium deficiencies are preventable global public health problems in infants, children, and adolescents. Implementation of international rickets prevention programs, including supplementation and food fortification, is urgently required. Key WordsRickets · Nutrition · Vitamin D · Calcium · Consensus recommendations Abstract Background: Vitamin D and ca...

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“…Tertiary hyperparathyroidism occurs in patients with long-standing secondary hyperparathyroidism who develop autonomous PTH production with hypercalcemia. The most common situation resulting in tertiary hyperparathyroidism is the patient with secondary hyperparathyroidism with renal failure who then receives a renal allograft [14,15].…”

Section: Discussionmentioning

confidence: 99%

Severe Hypercalcemia Due to Primary Neonatal Hyperparathyroidism in an 8-Day-Old Neonate: A Case Report

Naseri

2014

Int J Clin Pediatr

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An 8-day-old boy was referred to our hospital because of poor feeding and hypotonia from the second day of his life. Investigations in our hospital showed marked hypercalcemia due to primary hyperparathyroidism (PHPT). Intensive medical treatment was unsuccessful and he was cured after total parathyroidectomy had been performed. It seems that total parathyroidectomy is the treatment of choice in cases of neonatal PHPT.

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Transient neonatal hyperparathyroidism secondary to maternal pseudohypoparathyroidism.

Cited by 50 publications

References 5 publications

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Bone Development and Mineral Homeostasis in the Fetus and Neonate: Roles of the Calciotropic and Phosphotropic Hormones

Global Consensus Recommendations on Prevention and Management of Nutritional Rickets

Severe Hypercalcemia Due to Primary Neonatal Hyperparathyroidism in an 8-Day-Old Neonate: A Case Report

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