Oral Presentation Society of Obstetric Medicine of Australia and New Zealand ASM 2015

Hypophosphataemia post Intravenous Ferric-carboxymaltose (FCM) in Pregnancy: A Case Series (#18)

Suet-Wan Choy 1 , Stefanie Troster 1 , Irena Idel 1 , Darren Lee 1 , Louis Huang 1 , Matthew Roberts 1 2 , Lawrence McMahon 1 2
  1. Department of Renal Medicine, Eastern Health, Box Hill, Vic, Australia
  2. Eastern Health Clinical School, Monash University, Clayton, Vic, Australia

Background: Parenteral iron is often given to pregnant women to correct iron deficiency anaemia (IDA) and iron deficiency (ID).  It is generally safe, effective and well-tolerated [1], however can cause transient hypophosphataemia [2] and may affect bone metabolism through fibroblast growth factor-23 (FGF-23).  Ferric carboxymaltose-(FCM)-related hypophosphataemia is frequent and reported to be of little clinical significance [3,4]; however, the prevalence of severe hypophosphataemia and potential clinical consequences are underreported [2].

Aim: To describe biochemical changes after a single dose of intravenous FCM in a case series of iron deficient pregnant women.

Methods: Prospective observational study; 9 pregnant women between 17-34 weeks’ gestation, (median 29 ± 6 weeks’ gestation, age 31.3 ± 4.3yrs, BMI 29.5 ± 5.8) with iron deficiency, received 1g IV FCM.  Haemoglobin, ferritin, calcium, phosphate (PO4), parathyroid hormone (PTH) and urinary fractional PO4 excretion (FEPi) were measured at baseline, D2, D7, D21 and D42 post infusion.

Results: Serum PO4 levels dropped in 9 women (nadir Day 7 post IV FCM, p<0.001) and recovered at D21 post infusion.  FEPi rose at D7 post infusion (from 5.68 ± 3.73% to 15.82 ± 8.45%, p<0.001).  There was no change in serum calcium or PTH levels.  Haemoglobin levels rose appropriately (7.78 ± 6.94g/L at D21 and 10.43 ± 6.92g/L at D42 post infusion).  One patient developed severe hypophosphataemia, PO4 0.27mmol/L [075-1.50mmol/L], 7 days after IV FCM, which required oral phosphate replacement. 

Discussion: Reduction in serum PO4 may be explained by increased urinary PO4 loss.  This could be a consequence of proximal tubular dysfunction induced by iron therapy [5] or inhibition of tubular PO4 reabsorption and 1α-hydroxylation of Vitamin-D during iron therapy [6,7].  PO4 reduction may also occur through changes in FGF-23 (to be reported). 

Conclusion: Hypophosphataemia is frequent after parenteral FCM.  This case series raises concern that severe hypophosphataemia may be underdiagnosed and untreated.  Its potential effects on maternal and fetal well-being are unknown.

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