Abstract
The advent of new insights into phosphate metabolism must urge the endocrinologist to rethink the pathophysiology of widespread disorders, such as primary hyperparathyroidism, and also of rarer endocrine metabolic bone diseases, such as hypoparathyroidism and tumor-induced hypophosphatemia. These rare diseases of mineral metabolism have been and will be a precious source of new information about phosphate and other minerals in the coming years. The parathyroid glands, the kidneys, and the intestine are the main organs affecting phosphate levels in the blood and urine. Parathyroid disorders, renal tubule defects, or phosphatonin-producing tumors might be unveiled from alterations of such a simple and inexpensive mineral as serum phosphate. This review will present all these disorders from a ‘phosphate perspective’.
Highlights
The interpretation of serum calcium abnormalities might not be straightforward for the endocrinologist, phosphate metabolism alterations are always challenging.Understanding calcium–phosphate metabolism alterations requires deep knowledge of both bone metabolism and kidney physiology and pathology
The advent of new insights into phosphate metabolism must urge the endocrinologist to rethink the pathophysiology of widespread disorders, such as primary hyperparathyroidism, or rarer endocrine disorders known to deeply affect quality of life, such as hypoparathyroidism and tumor-induced osteomalacia (TIO)
These increase postprandial serum phosphate levels and to stimulate the release of the findings suggested that fibroblast growth factor 23 (FGF-23) does not rapidly contribute to phosphate homeostasis, with parathyroid hormone, in spite of unchanged concentrations of FGF-23 in up to eight hours
Summary
The interpretation of serum calcium abnormalities might not be straightforward for the endocrinologist, phosphate metabolism alterations are always challenging. The advent of new insights into phosphate metabolism must urge the endocrinologist to rethink the pathophysiology of widespread disorders, such as primary hyperparathyroidism, or rarer endocrine disorders known to deeply affect quality of life, such as hypoparathyroidism and tumor-induced osteomalacia (TIO). The review will briefly deal with phosphatonin-secreting tumors, in which circulating molecules can lead to the well-known TIO syndrome. These topics will be preceded by a brief review of phosphate physiology and by a few practical suggestions on how to quickly interpret phosphate metabolism in everyday clinical practice
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