Article Text
Abstract
Background Anaemia is the most common extra intestinal manifestation in paediatric Inflammatory Bowel Disease (pIBD) needing monitoring and supplementation. Intravenous iron is often needed in moderate to severe disease or intolerance to oral iron. Ferric Carboxymaltose (FCM) infusion has been used in our centre. While the risk of hypophosphatemia (HP) associated with FCM is known, (Medicines and Healthcare Products Regulation Agency alert), it is not been quantified in clinical practice.
Aims and Objectives Primary objectives’ to report incidence and severity of HP after infusion of FCM in pIBD. Assess time to recovery from HP with interventions. Secondary objectives’ to review patient characteristics and biochemical markers to identify risk factors for FCM infusions associated HP.
Design study We conducted a retrospective electronic records review of pIBD patients who received FCM infusion from November 19-November 20.
Results 24 patients (13 M) received 26 infusions in the period reviewed. The median age was 14.5(12.6–15.9). From all the children, 7(29.2%) were diagnosed with Ulcerative Colitis (UC), 16(66.7%) with Crohn’s Disease and 1(4.2%) with IBD-Unclassified (IBDU). The timing of infusion coincided with: admitted with new diagnosis of pIBD, [10(41.7%)], flare of disease [9(37.5%)] and elective admission [5(20.8%)] for correction.
Median dose for the 26 infusions was 1000(500–1000)mg. Pre-infusion median (IQR) haemoglobin 107.5 (92.7–119.2), MCV 81(74.7–83.2), iron 3.4(2.1–5.5), ferritin 73.1(33.2–115.7) and transferrin saturation 4.85(3.6–10.0)%. All had normal renal function; median(IQR) urea 2.9(2.32–3.35) and creatinine, 50.5(37–61.7). Pre-transfusion Vitamin D (n=19) median was 38.5(27.5–53.5), with levels being deficient in 13(68.3%) with no association to recovery time.
The biochemical markers are shown in table 1 below, with the change shown as delta change. The delta change was found to be statistically significant for serum phosphate levels. There were no statistically significant association, on univariate analysis, between the delta change in serum phosphate levels and the features of patient demographics or biochemical markers.
All 24 patients had reduction in phosphate level post FCM infusion. In 14/26(53%), phosphate levels dropped to moderate-severe range; 10/14(71.4%) HP was moderate (< 0.65 mmol/L) and in 4/14(28.5%) HP was severe (< 0.32 mmol/L). The median time of recovery from hypophosphatemia was 14(4–26) days. Those that took longer than 14 days to normalise phosphate (9,37.5%) had no features attributable to it.
No serious sequelae of hypophosphatemia were seen. Treatment included a combination of IV phosphate infusion (6,25%), oral phosphate supplements (12,50%), oral calcium supplements (15,62.5%) and vitamin D supplements (17,70.8%).
Conclusion HP is frequently seen with FCM infusion. The fall in phosphate post FCM infusion was found to be clinically and statistically significant; though none of the patient demographic features or serological markers were found to be associated with the delta change in phosphate to predict high risk patients. The median recovery time of 14 days is less than what is reported in adult reviews. FCM infusions need pre-assessment, counselling and post infusion monitoring to assess effectiveness and recovery.