немного по диагностике этого осложнения:
In symptomatic patients a test panel including ionized calcium, total and bone-specific alkaline phosphatase, PTH, 25 (OH) vitamin D and 1,25 (OH)2 vitamin D is recommended. Typical findings in patients with intravenous iron-induced hypophosphatemia include mild hypocalcemia, normal or mildly reduced 25 (OH) vitamin D and markedly reduced 1,25 (OH)2 vitamin D with hyperparathyroidism and elevated total and bone-specific alkaline phosphatase. These changes can persist beyond the resolution of hypophosphatemia...
по ведению-профилактике:
Delay further intravenous iron doses and switch to iron formulations with lower hypophosphatemia risk in patients with hypophosphatemia.
It is unknown if vitamin D supplementation before FCM administration reduces hypophosphatemia and fracture risk.
...treatment was started in the majority of patients including oral (n = 36) or intravenous (n = 20) phosphate, activated vitamin D (n = 21),vitamin D (n = 9) or calcium (n = 10). Treatment outcome was highly variable and inconsistently reported. Considering the underlying pathogenesis driven by elevated intact FGF23, phosphate supplementation would not sustainably correct hypophosphatemia, but increase urinary phosphate excretion [[39], [40], [41]]. As clinical and biochemical changes apparently persist up to several months after the last FCM infusion, rational treatment approaches would include mitigation of secondary hyperparathyroidism with activated vitamin D, which was successfully used in some patients [40,42,43].
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Hypophosphatemia after intravenous iron therapy: Comprehensive review of clinical findings and recommendations for management. 2022
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