Endocrine Abstracts

Osteomalacia is most commonly caused by vitamin D deficiency. This typically results in features of secondary hyperparathyroidism and hypophosphataemia. PTH secretion is however dependant on normal serum magnesium levels. Hypomagnesaemia due to malabsorption, diuretic or laxative abuse may lead to functional hypoparathyroidism despite typical features of osteomalacia.

A 24-year old Afro-Caribbean woman presented with bilateral knee and upper back pain with associated leg weakness. Her symptoms were worse during the winter. She had complained of frequent loose motions and vomiting over the preceding two months, but denied purging or binge eating. She had a history of depression and abnormal perception of being overweight despite a normal BMI of 18.7 kg/m² and regularly taken laxatives in the past. She claimed never to have taken diuretics.

Biochemistry demonstrated a corrected calcium of 2.0 mmol/l (2.15–2.65), phosphate 0.71 mmol/l (0.80–1.40), 25-OH vitamin D 15 nmol/l (25–120), potassium 3.5 mmol/l (3.8–5.5), PTH<5 mg/l (1.1–6.8), magnesium 0.41 mmol/l (0.7–1.0), alkaline phosphatase 1279 IU/l (30–130), remaining liver function was normal. A macrocytosis but normal haemoglobin was identified. Coeliac screen and stool culture proved negative, haematinics were also normal. X-ray of her right knee demonstrated a Looser’s zone.

Her symptoms were consistent with osteomalacia due to vitamin D deficiency most likely due to her racial origin, poor oral intake and suspected continued laxative abuse. Follow-up demonstrated serum magnesium had returned to normal, corrected calcium remained low at 1.99 mmol/l but PTH had risen to 179 mg/l, more consistent with her osteomalacia. She failed to take vitamin D or magnesium supplements and did not attend follow-up.

Functional hypoparathyroidism secondary to hypomagnesaemia may be seen in patients with an eating disorder or malabsorption. Appropriate treatment may unmask the typical biochemical features seen in osteomalacia.