Summary Background Iron deficiency and iron deficiency anaemia are common complications in inflammatory bowel disease (IBD). In patients with moderate‐to‐severe anaemia, oral iron intolerance or ineffectiveness of oral iron, ferric carboxymaltose and iron isomaltoside are widely used. Hypophosphatemia is a side effect of both preparations. Aims To investigate the occurrence of hypophosphatemia in IBD patients with iron deficiency/iron deficiency anaemia treated with high‐dose intravenous iron. Methods A prospective observational study of adult IBD patients with iron deficiency/iron deficiency anaemia was conducted at two study sites where patients received 1000 mg of ferric carboxymaltose or iron isomaltoside. At baseline, weeks 2 and 6, blood and faecal samples were collected. The primary endpoint was to determine the incidence of moderate‐to‐severe hypophosphatemia. Secondary endpoints included the total incidence of hypophosphatemia, possible risk factors for hypophosphatemia, and response to single‐dose intravenous iron. Results One hundred and thirty patients were included. In the per‐protocol set, 52 patients received ferric carboxymaltose and 54 patients received iron isomaltoside. Ferric carboxymaltose treatment had a significantly higher incidence of moderate‐to‐severe hypophosphatemia compared with iron isomaltoside at week 2 (56.9% vs 5.7%, P < 0.001) and a higher incidence at week 6 (13.7% vs 1.9%, P = 0.054).The overall incidence of hypophosphatemia was significantly higher with ferric carboxymaltose compared with iron isomaltoside treatment at weeks 2 (72.5% vs 11.3%, P < 0.001) and 6 (21.6% vs 3.7%, P = 0.013). Conclusions In IBD patients with iron deficiency/iron deficiency anaemia, ferric carboxymaltose was associated with higher incidence, severity and persistence of hypophosphatemia compared with iron isomaltoside. The presence of moderate‐to‐severe hypophosphatemia beyond 6 weeks is a clinical concern that requires further investigation.

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BACKGROUND High-dose intravenous iron is an effective 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. AIM To investigate mechanisms behind the development of hypophosphatemia after intravenous iron treatment, and disclose symptoms and clinical manifestations related to hypophosphatemia short-term. METHODS 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 received one dose of 1000 mg of either FCM or ferric derisomaltose (FDI) and were followed for an observation period of at least 7 wk. Blood and urine samples were collected for relevant analyses at baseline, week 2 and at week 6. Clinical symptoms were assessed at the same timepoints using a respiratory function test, a visual analogue scale, and a health-related quality of life questionnaire. RESULTS A total of 106 patients was available for analysis in this study. The FCM treatment group consisted of 52 patients and hypophosphatemia was present in 72.5% of the patients at week 2, and in 21.6% at week 6. In comparison, the FDI treatment group consisted of 54 patients and 11.3% of the patients had hypophosphatemia at week 2, and 3.7% at week 6. The difference in incidence was highly significant at both week 2 and 6 ( P < 0.001 and P < 0.013, respectively). We observed a significantly higher mean concentration of intact fibroblast growth factor 23 ( P < 0.001), a significant rise in mean urine fractional excretion of phosphate ( P = 0.004), a significant decrease of 1,25-dihydroxyvitamin D ( P < 0.001) and of ionised calcium levels ( P < 0.012) in the FCM-treated patients compared with patients who received FDI. No clinical symptoms could with certainty be related to hypophosphatemia, since neither the respiratory function test, SF-36 (36-item short form health survey) or the visual analogue scale scores resulted in significant differences between patients who developed hypophosphatemia or not. CONCLUSION Fibroblast growth factor 23 has a key role in FCM induced hypophosphatemia, probably by inducing loss of phosphate in the urine. Short-term clinical impact of hypophosphatemia was not demonstrated.

Objectives: Acute upper gastrointestinal bleeding is a well-recognized complication of peptic ulcers and erosions. The aim of this study was to assess the incidence rate and identify risk factors for this complication in southeastern Norway. Materials and methods: Between March 2015 and December 2017, a prospective observational study was conducted at two Norwegian hospitals with a total catchment area of approximately 800,000 inhabitants. Information regarding patient characteristics, comorbidities, drug use, H. pylori status and 30-day mortality was recorded. Results: A total of 543 adult patients were included. The incidence was 30/100,000 inhabitants per year. Altogether, 434 (80%) of the study patients used risk medication. Only 46 patients (8.5%) used proton pump inhibitors (PPIs) for more than 2 weeks before the bleeding episode. H. pylori testing was performed in 527 (97%) patients, of whom 195 (37%) were H. pylori-positive. The main comorbidity was cardiovascular disease. Gastric and duodenal ulcers were found in 183 (34%) and 275 (51%) patients, respectively. Simultaneous ulcerations at both locations were present in 58 (10%) patients, and 27 (5%) had only erosions. Overall, the 30-day mortality rate was 7.6%. Conclusions: The incidence of upper gastrointestinal bleeding due to peptic ulcers and erosions was found to be lower than previously demonstrated in comparable studies, but the overall mortality rate was unchanged. The consumption of risk medication was high, and only a few patients had used prophylactic PPIs. Concurrent H. pylori infection was present in only one-third of the patients. Clinical trial registration: Bleeding Ulcer and Erosions Study 'BLUE Study', ClinicalTrials.gov Identifier. NCT03367897.

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