PTH-137 Phosphare studies: important changes in phosphate homeostasis and bone metabolism after IV iron

Introduction Iron deficiency anaemia (IDA) is the most common extraintestinal complication of inflammatory bowel disease (IBD), and IV iron is commonly used to treat IDA in IBD. Of the two commonly used IV iron preparations, ferric carboxymaltose (FCM) and iron isomaltoside IIM, there is evidence that FCM can cause hypophosphatemia due to FGF23 mediated renal phosphate wasting, which has been associated with osteomalacia; the comparative effects of IIM are unknown. Methods In two identical, open-label trials, 245 adults with IDA randomly received (1:1) IIM (1×1000 mg) or FCM (2×750 mg; 1 week apart). We compared the incidence, severity and duration of hypophosphatemia, and effects on fractional phosphate urinary excretion (FEPO4), FGF23, parathyroid hormone (PTH), vitamin D (VitD), and bone turnover biomarkers in blood and urine. Results In a pooled analysis, the incidence of hypophosphatemia Conclusion Compared to IIM, FCM-induced high rates of FGF23-mediated hypophosphatemia, which was frequently severe and often persisted for >35 days. FCM, but not IIM, induced changes in vitD and calcium homeostasis that triggered secondary hyperparathyroidism, which likely contributed to persistence of hypophosphatemia. Alteration of bone metabolism after FCM administration may be of great clinical significance particularly for IBD patients who often have low vit D and regularly receive iv iron.