Summary

A 76-year-old woman was treated with oral bisphosphonate, alendronate, for osteoporosis in an outpatient clinic. Routine blood tests 4 months after alendronate prescription surprisingly revealed severe hypophosphataemia. The patient was hospitalised and treated with intravenous and oral phosphate supplements. Alendronate was later reintroduced as treatment for osteoporosis and the patient once again presented with severe hypophosphataemia in subsequent routine blood tests. The patient had only presented with lower extremity pain, muscle weakness and difficulty walking. Blood tests in the emergency department both times reconfirmed severe hypophosphataemia. Plasma (p-)ionised calcium levels were normal or slightly elevated and p-parathyroid hormone levels were normal or slightly suppressed. The p-25-hydroxyvitamin-D and p-creatine were in the normal range. Critical illness, malabsorption, nutritional issues and genetics were reviewed as potential causes but considered unlikely. Phosphate levels were quickly restored each time on replacement therapy and the case was interpreted as bisphosphonate-induced severe hypophosphataemia.

Background

Bisphosphonates are commonly used in pharmacological treatment of osteoporosis. They have an antiresorptive effect on bone metabolism which, potentially, affects both calcium and phosphate homeostasis. Mild and transient decreases in p-calcium and p-phosphate are thus frequent side effects.1 Few cases of bisphosphonate-induced severe hypophosphataemia have been reported but only following intravenous administration of the potent bisphosphonate, zoledronic acid.2–4

Severe hypophosphataemia is defined as p-phosphate <0.3 mmol/L. It is a potentially fatal condition where symptoms include bone pain, muscle weakness, rhabdomyolysis, arrhythmias, convulsions, confusion and loss of conscious.5

We report a clinically relevant case of two consecutive episodes …