We read with interest the recent article by Bartko and colleagues.(1) In this article the authors report a case of hypophosphatemia and fatigue fractures occurring after iron substitution in a patient with inflammatory bowel disease. Their hypothesis is that chronic iron supplementation had induced fibroblast growth factor 23 (FGF23)-mediated phosphaturic osteomalacia, but they did not have the opportunity to confirm their hypothesis because plasma FGF23 levels were not available for their patient. We recently observed a very similar case and had the opportunity to monitor FGF23 serum levels, confirming Bartko and colleaguesL (1) hypothesis. The patient was a 38-year-old man with severe CrohnLs disease, referred to our rheumatology department for pain in both hips. He received infliximab for 4 years. He also received monthly 1-g infusions of ferric carboxymaltose for 8 months for recurrent iron deficiency induced anemia. He presented for 2 months with bilateral hip pain, with recent worsening resulting in an inability to walk. He also reported costal and sternal pain. Clinical examination revealed severe pain and limitation of both hips in every direction, but spine and sacroiliac joint examination was normal.

Biological tests showed major hypophosphatemia at 0.34 mmol/L (normal, 0.8 to 1.45 mmol/L), with a low calcium level of 1.97 mmol/L (normal, 2.20 to 2.55 mmol/L), low 25-OH-vitamin D level at 18ng/mL (normal, 30 to 100ng/mL), but a particularly low 1-25-OH-vitamin D level at 8 pg/mL (normal, 20 to 70 pg/mL), with normal parathyroid hormone (PTH) level at 52 ng/mL (normal, 14 to 74 ng/mL). Urine analysis showed high phosphaturia at 19.4 mmol/mmol of creatininuria with a low phosphate reabsorption rate (60%; normal> 80%) and normal calciuria (0.66 mmol/mmol; normal, 0.35-0.75 mmol/mmol). MRI of the hips showed multiples fractures of both femoral heads with diffuse edema but with no sign of osteonecrosis (Fig. 1A, a and b). The bone mineral density (BMD) assessment by dual-energy X-ray absorptiometry (DXA) revealed a T-score of-2.9 SD at the femoral neck and-2.1 SD at the lumbar spine. Serum FGF23 level was elevated at 226ng/L (normal, 25 to 50 ng/L), leading to the diagnosis of FGF23-mediated