Published online May 7, 2021. doi: 10.3748/wjg.v27.i17.2039
Peer-review started: January 28, 2021
First decision: March 6, 2021
Revised: March 19, 2021
Accepted: April 21, 2021
Article in press: April 21, 2021
Published online: May 7, 2021
High-dose intravenous iron is an effective and frequently used treatment option for iron deficiency (ID) or ID anaemia (IDA) in inflammatory bowel disease (IBD). However, treatment with ferric carboxymaltose (FCM) has been associated with the development of hypophosphatemia.
We aimed to investigate the occurrence of hypophosphatemia after treatment with either FCM and ferric derisomaltose (FDI) for ID or IDA in patients with IBD.
In this part of the study, we aimed to disclose underlying mechanism behind the development of hypophosphatemia after treatment with high dose intravenous iron and whether hypophosphatemia had a clinical impact on these patients.
A prospective observational study of adult IBD patients with ID or IDA was conducted between February 1, 2017 and July 1, 2018 at two separate university hospitals in the southeast region of Norway. Patients were recruited consecutively and received one dose of 1000 mg of either FCM or FDI, and were followed for an observation period of at least 7 wk at three timepoints; baseline, week 2 and week 6. Blood and urine samples were collected for relevant analyses at all three visits in addition to assessment of clinical symptoms using a respiratory function test, a visual analogue scale, and a health-related quality of life questionnaire.
Our study results demonstrate an association between FCM treatment and the development of hypophosphatemia by increasing the level of intact Fibroblast Growth Factor 23 (iFGF23) and phosphate wasting in the urine. Moreover, we observed a significant decline in active Vitamin D and ionised calcium. No clinical impact was detected by applying Short Form-36 questionnaire, visual analogue scale score and real-time position management breathing test in an observation period of 6 wk.
FCM treatment is associated with the development of hypophosphatemia in patients with IBD. This is due to increased formation of iFGF23 which in turn probably results in an increase of urinary phosphate output. No clinical impact was detected nor excluded. Assumably our study is underpowered together with a too short observation period to provide solid information with regard to clinical impact of hypophosphatemia.
Based on our results we encourage clinicians to be aware of the risk of developing hypophosphatemia after treatment with FCM. Larger studies with a longer observation period to detect possible clinical impact of hypophosphatemia is desirable.