DOI: 10.12890/2025_005824
Treatment-resistant hypophosphataemia after ferric carboxymaltose: expanding the spectrum of 6H syndrome (hypophosphataemia, hyperphosphaturia, hypovitaminosis D, hypocalcaemia, secondary hyperparathyroidism, high fibroblast growth factor-23)
Authors
luqy225@gmail.com
Keywords
Ferric carboxymaltose, hypophosphatemia, fibroblast growth factor-23, coeliac diseaseAbstract
Background: Ferric carboxymaltose (FCM) is widely used to treat iron deficiency anaemia (IDA), particularly in patients with gastrointestinal disease who are intolerant of oral iron. While generally well tolerated, FCM is increasingly recognised to cause hypophosphatemia. Most cases are mild and transient, but severe and prolonged episodes remain uncommon.
Case report: A 40-year-old woman with newly diagnosed coeliac disease and severe IDA, received two intravenous FCM infusions (total 1.5 g). Within 1 week she developed profound symptomatic hypophosphatemia (0.34 mmol/l), presenting with escalating fatigue, exertional dyspnoea and arthralgia. Investigations revealed renal phosphate wasting (109.4 mmol/day) and secondary hyperparathyroidism, consistent with FCM-induced fibroblast growth factor-23 phosphaturia; also described as “6H syndrome”. Coexistent coeliac-related malabsorption further compounded the condition and rendered oral phosphate supplementation ineffective. The patient required continuous intravenous phosphate infusions via a peripherally inserted central catheter for 5.5 weeks, in addition to dietary optimisation and calcitriol. Gradual recovery was achieved 8.5 weeks after onset, with stabilisation of serum phosphate at 0.9 mmol/l and resolution of symptoms.
Conclusion: This case highlights an uncommon, severe and resource-intensive manifestation of FCM-associated hypophosphatemia. It reinforces the clinical utility of the 6H syndrome framework in recognising the biochemical pattern of FCM-induced phosphate wasting and underlines the importance of considering coexistent malabsorptive disorders, such as coeliac disease, which can magnify severity. Clinicians should remain vigilant, monitor phosphate in at-risk patients, and provide clear safety-netting to enable early detection and intervention.
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