Adalimumab-induced hypophosphataemia: an unknown adverse effect

Tanya Chopra; Florika Radia; Jeremy Cox; Tannaz Vakilgilani

doi:10.1530/endoabs.117.P268

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Endocrine Abstracts (2026) 117 P268 | DOI: 10.1530/endoabs.117.P268

SFEBES2026 Poster Presentations Late Breaking (54 abstracts)

Adalimumab-induced hypophosphataemia: an unknown adverse effect

Tanya Chopra ¹ , Florika Radia ¹ , Jeremy Cox ¹ & Tannaz Vakilgilani ²

Author affiliations

¹St Mary’s Hospital, Imperial College Healthcare NHS Trust, London, United Kingdom; ²St Mary’s Hospital, Imperial College Healthcare NHS Trust, Ruislip, United Kingdom

We report a case of recurrent, treatment-resistant hypophosphataemia associated with Adalimumab, resolving after drug cessation. A 59-year-old woman with rheumatoid arthritis, type 2 diabetes, chronic kidney disease, cirrhosis and hypertension was admitted in May 2025 with severe hypophosphataemia (0.26mmol/l) and hypomagnesaemia (0.46mmol/l). She had multiple similar admissions since 2023. She denied gastrointestinal losses, alcohol use, or antacid intake. Her medications included adalimumab, hydroxychloroquine, insulin, metformin, amlodipine and omeprazole (subsequently changed to famotidine). Despite treatment with intravenous phosphate, magnesium and high dose Vitamin D, hypophosphataemia persisted. Investigations:


	Normal range	Jul-24	May-25
Phosphate(mmol/l	0.8-1.5	0.23↓	<0.2↓
Calcium(mmol/l)	2.2-2.6	2.87↑	2.41
Magnesium(mmol/l)	0.7-1	0.57↓	0.46↓
PTH(pmol/l)	2.2-14	0.8↓	4
Vitamin D(nmol/l)	> 50	58.8	30↓

• eGFR: 30ml/min (>90)

• FGF-23: 112RU/mL (<100)

• 1,25 Vit D: 144pmol/l (55–139)

• 24-hr urine phosphate: <2.13mmol/day (13-42)

• 24-hr urine calcium: 5.27mmol/day (2.5-7.5)

• Urinary protein: 13g/l

• PET CT 2024: breast and pulmonary nodule (intraductal breast papilloma and necrotising granulomatous inflammatory pulmonary nodule resected via video-assisted thoracoscopic surgery)

• DEXA 2024: normal bone density

Although FGF-23 was mildly elevated, low urinary phosphate and normal acid-base status made tumour-induced osteomalacia and renal tubular disorders unlikely. Notably, the onset of hypophosphataemia coincided with the initiation of Adalimumab for rheumatoid arthritis. As her rheumatoid arthritis was stable, Adalimumab was withheld following Rheumatology discussion. This resulted in a normalisation of her biochemistry and symptoms, which remain stable four months following Adalimumab discontinuation. Although the underlying mechanism remains unclear, TNF-α inhibition may influence renal phosphate handling. Additionally, cirrhosis may exacerbate hypophosphataemia, as chronic liver disease can impair gluconeogenesis and ATP turnover, promoting an intracellular phosphate shift. This case describes an unusual case of recurrent hypophosphataemia in an Adalimumab-treated patient. With the rising use of biologic therapies, clinicians should remain alert for unknown adverse effects.