Abstract
BackgroundIntravenous iron replacement is recommended for iron-deficient patients with inflammatory bowel disease (IBD), but may be associated with hypophosphataemia, predisposing to osteomalacia and fractures. This study aimed to evaluate the incidence and risk factors for hypophosphataemia following intravenous ferric carboxymaltose (FCM) in patients with IBD.MethodsThis prospective observational study of patients with and without IBD evaluated serum phosphate for 28 days following intravenous FCM, and assessed associations with symptoms, markers of inflammation and vitamin D status.ResultsTwenty-four patients with IBD (11 with Crohn’s disease [CD], 13 with ulcerative colitis [UC], mean age 45 years [range 19–90], 7 female), and 20 patients without IBD (mean age 56 [22–88] y, 11 female), were included. Overall, serum phosphate declined by a mean of 36% at Day 7, with a mean fall of 42% (SD 19%) at some time point over 28 days (p < 0.001). Twenty-four of 44 (55%) patients developed moderate to severe hypophosphataemia (serum phosphate < 0.6 mmol/L). No differences between patients with and without IBD were seen, but patients with CD had greater decline in phosphate than those with UC. There was no association between hypophosphataemia and symptomatic adverse events, faecal calprotectin, C-reactive protein, albumin, platelet count, 25(OH) vitamin D, or 1,25(di-OH) vitamin D. Serum phosphate < 1.05 mmol/L on Day 2 predicted susceptibility to moderate-severe hypophosphataemia (OR 7.0).ConclusionsHypophosphataemia following FCM is common, unrelated to symptomatic adverse events, baseline intestinal or systemic inflammation, or vitamin D status.
Highlights
Intravenous iron replacement is recommended for iron-deficient patients with inflammatory bowel disease (IBD), but may be associated with hypophosphataemia, predisposing to osteomalacia and fractures
Recognition and correction of iron deficiency independent of IBD activity is associated with an improvement in these parameters [7, 8], and intravenous iron is recommended for patients with moderate to severe anaemia or intolerance to oral iron formulations [2, 4, 5, 9]
Hypophosphataemia following intravenous iron, especially following ferric carboxymaltose (FCM), is increasingly recognised, likely mediated by a transient increase in intact fibroblast growth factor-23 due to inhibition of its cleavage, which results in phosphaturia [15,16,17]
Summary
Intravenous iron replacement is recommended for iron-deficient patients with inflammatory bowel disease (IBD), but may be associated with hypophosphataemia, predisposing to osteomalacia and fractures. This study aimed to evaluate the incidence and risk factors for hypophosphataemia following intravenous ferric carboxymaltose (FCM) in patients with IBD. Iron deficiency anaemia in patients with IBD is considered a marker of disease activity, and is associated with a reduced quality of life, impaired cognition and social functioning, and an increased risk of hospitalisation [5,6,7]. Hypophosphataemia following intravenous iron, especially following ferric carboxymaltose (FCM), is increasingly recognised, likely mediated by a transient increase in intact fibroblast growth factor-23 (iFGF-23) due to inhibition of its cleavage, which results in phosphaturia [15,16,17]. This may result in osteomalacia and fractures [16, 18]
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