Correction of hypocalcemia allows optimal recruitment of FGF-23-dependent phosphaturic mechanisms in acute hyperphosphatemia post-phosphate enema
| Autor: | Laura Rodriguez-Osorio, Emilio González-Parra, Carolina Gracia-Iguacel, Mariano Rodriguez, Jesús Egido, Concepción de la Piedra, Yolanda Almaden, Alberto Ortiz, Ana Belen Sanz |
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| Rok vydání: | 2013 |
| Předmět: |
Fibroblast growth factor 23
endocrine system medicine.medical_specialty Calcitriol Endocrinology Diabetes and Metabolism medicine.medical_treatment chemistry.chemical_element Parathyroid hormone Enema Calcium urologic and male genital diseases Phosphates chemistry.chemical_compound Hyperphosphatemia Endocrinology Internal medicine medicine Humans Orthopedics and Sports Medicine Aged 80 and over Hypocalcemia business.industry nutritional and metabolic diseases General Medicine Phosphate medicine.disease Fibroblast Growth Factors Fibroblast Growth Factor-23 stomatognathic diseases chemistry Parathyroid Hormone Female business hormones hormone substitutes and hormone antagonists medicine.drug Hormone |
| Zdroj: | Journal of Bone and Mineral Metabolism. 31:703-707 |
| ISSN: | 1435-5604 0914-8779 |
| DOI: | 10.1007/s00774-013-0435-z |
| Popis: | Both parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) are phosphaturic hormones. These hormones should increase in response to phosphate excess. However, they also regulate serum calcium; PTH increases serum calcium concentration and FGF23 suppresses renal production of calcitriol, favoring hypocalcemia. We report the case of an 83-year-old woman with hyperphosphatemia and hypocalcemia resulting from phosphate-containing enemas. PTH and calcitriol increased in response to hypocalcemia, and FGF23 increased in response to hyperphosphatemia. Unexpectedly, peak FGF23 did not coincide with peak serum phosphate. Rather, peak FG23 was observed only after severe hypocalcemia was partially corrected with exogenous calcium administration, even though serum phosphate had been already decreasing for 32 h. Correction of severe hypocalcemia was thus associated with peak FGF23 values and with a precipitous decrease in PTH. Peak FGF23 was followed by an accelerated decrease in serum phosphate and significant phosphaturia. This clinical report is consistent with experimental data in rats showing a blunted FGF23 response to high phosphate in the presence of severe hypocalcemia. Thus, complementary experimental and clinical data suggest that partial correction of severe hypocalcemia is required for optimal FGF23-mediated phosphaturia, which takes place despite correction of PTH levels. We believe this the first human report suggesting blunting of the FGF23 response to high phosphate by severe hypocalcemia. |
| Databáze: | OpenAIRE |
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