Normal calcium homeostasis depends on the interaction of 3 organ systems: the skeleton, small intestine, and kidney. Bone contains 99% of total body calcium and less than 1% is found in the extracellular fluid (ECF) at a concentration of 9-10 mg/dl. Several players interact to maintain normocalcemia. Parathyroid hormone (PTH) causes calcium resorption from bones; active vitamin D (calcitriol) facilitates calcium absorption from the small intestine; and calcitonin plays a minor role in calcium metabolism by its anti-PTH effect. The kidney plays a major role in calcium metabolism via 2 mechanisms: a) 1-alpha hydroxylation of vitamin D and b) as a target organ for PTH which decreases phosphate reabsorption in the proximal tubular cells and enhances calcium reabsorption in the distal tubules. Hypocalcemia and hypercalcemia, resulting from imbalances in the above mechanisms, present challenging diagnostic and therapeutic issues to the pediatrician. Both acute and chronic, syndromic and non-syndromic, and hereditary and acquired forms are recognized.
The aim of this research topic is to provide an update on the latest developments related to the etiology, pathophysiology, molecular basis, and treatment of hypocalcemic and hypercalcemic syndromes encountered in pediatric practice.
Hypocalcemia may occur in the neonatal period, both early and late, and the mechanisms involved are only partially understood. Hypocalcemia in infants and older children is usually related to hypoparathyroidism or inactive PTH, severe vitamin D deficiency or inactivating mutations in the vitamin D nuclear receptor. A rare cause is the activating mutations in calcium sensing receptor (CaSR) which leads to autosomal dominant familial hypercalciuric hypocalcemia.
Hypercalcemia may be due to increased intestinal absorption (vitamin D excess, granulomatous diseases), increased bone resorption (hyperparathyroidism, acidosis, malignancies, immobilization), William’s syndrome, thyroid disease, and pheochromocytoma.
We are interested in submissions of Original basic and clinical research in the general themes of hypocalcemia and hypercalcemia in children.
Hypocalcemia secondary includes but is not limited to:
• Gastrointestinal malabsorption , Severe vitamin D deficiency;
• Impaired vitamin D metabolism (vit dependent rickets types 1 and 2);
• Chronic kidney disease, Acute kidney injury;
• Hypoparathyroidism, Hypomagnesemia, CaSR mutations.
Hypercalcemia secondary includes but is not limited to:
• Hypervitaminosis D;
• Hyperparathyroidism;
• Granulomatous diseases (sarcoidosis and more), Malignancies;
• William’s syndrome, Idiopathic hypercalcemia of infancy;
• Familial hypocalciuric hypercalcemia.
Manuscripts should address the above items as to:
• Etiology and pathophysiologic aspects;
• New developments in the field, Molecular basis when appropriate;
• Therapeutic novelties that may improve patient outcomes.
The types of manuscripts for the research topic:
• Original, basic and clinical articles;;
• Case studies;
• Prospective studies;
• Mini review articles
Normal calcium homeostasis depends on the interaction of 3 organ systems: the skeleton, small intestine, and kidney. Bone contains 99% of total body calcium and less than 1% is found in the extracellular fluid (ECF) at a concentration of 9-10 mg/dl. Several players interact to maintain normocalcemia. Parathyroid hormone (PTH) causes calcium resorption from bones; active vitamin D (calcitriol) facilitates calcium absorption from the small intestine; and calcitonin plays a minor role in calcium metabolism by its anti-PTH effect. The kidney plays a major role in calcium metabolism via 2 mechanisms: a) 1-alpha hydroxylation of vitamin D and b) as a target organ for PTH which decreases phosphate reabsorption in the proximal tubular cells and enhances calcium reabsorption in the distal tubules. Hypocalcemia and hypercalcemia, resulting from imbalances in the above mechanisms, present challenging diagnostic and therapeutic issues to the pediatrician. Both acute and chronic, syndromic and non-syndromic, and hereditary and acquired forms are recognized.
The aim of this research topic is to provide an update on the latest developments related to the etiology, pathophysiology, molecular basis, and treatment of hypocalcemic and hypercalcemic syndromes encountered in pediatric practice.
Hypocalcemia may occur in the neonatal period, both early and late, and the mechanisms involved are only partially understood. Hypocalcemia in infants and older children is usually related to hypoparathyroidism or inactive PTH, severe vitamin D deficiency or inactivating mutations in the vitamin D nuclear receptor. A rare cause is the activating mutations in calcium sensing receptor (CaSR) which leads to autosomal dominant familial hypercalciuric hypocalcemia.
Hypercalcemia may be due to increased intestinal absorption (vitamin D excess, granulomatous diseases), increased bone resorption (hyperparathyroidism, acidosis, malignancies, immobilization), William’s syndrome, thyroid disease, and pheochromocytoma.
We are interested in submissions of Original basic and clinical research in the general themes of hypocalcemia and hypercalcemia in children.
Hypocalcemia secondary includes but is not limited to:
• Gastrointestinal malabsorption , Severe vitamin D deficiency;
• Impaired vitamin D metabolism (vit dependent rickets types 1 and 2);
• Chronic kidney disease, Acute kidney injury;
• Hypoparathyroidism, Hypomagnesemia, CaSR mutations.
Hypercalcemia secondary includes but is not limited to:
• Hypervitaminosis D;
• Hyperparathyroidism;
• Granulomatous diseases (sarcoidosis and more), Malignancies;
• William’s syndrome, Idiopathic hypercalcemia of infancy;
• Familial hypocalciuric hypercalcemia.
Manuscripts should address the above items as to:
• Etiology and pathophysiologic aspects;
• New developments in the field, Molecular basis when appropriate;
• Therapeutic novelties that may improve patient outcomes.
The types of manuscripts for the research topic:
• Original, basic and clinical articles;;
• Case studies;
• Prospective studies;
• Mini review articles
