Development of Severe Hypophosphatemia from Acquired Fanconi Syndrome during Treatment with Abiraterone

Objectives: To report two cases of patients with metastatic, castration resistant prostate cancer who developed profound hypophosphatemia while on treatment with abiraterone. Case Summary: The first patient was a 77 year old man who had been on abiraterone for 12 months before his phosphorous was checked. At that point, it was 0.6 mg/dl, which is severely decreased. A full work up for hypophosphatemia showed normal parathyroid hormone and 25-hydroxyvitamin D. A urine study showed inappropriate excretion of phosphorous along with aminoaciduria and normoglycemic glucosuria. The phosphorous level slowly improved upon discontinuation of abiraterone and aggressive repletion of his phosphorous with elemental phosphorous and calcitriol. The second patient was a 74 year old man who had a slightly decreased phosphorous prior to abiraterone initiation. It steadily fell during abiraterone therapy down to 0.9 mg/dl. Aggressive repletion would not raise the phosphorous to normal. It only improved upon discontinuation of abiraterone. The results of the work up were similar to those of the first patient. Discussion: These two patients had profound hypophosphatemia. Phosphorous levels are not routinely checked by clinicians, and the severe hypophosphatemia in these patients demonstrates how important it is to check this level. We propose that the mechanism of phosphorous loss is through inappropriate renal wasting by Fanconi syndrome. Conclusion: Hypophosphatemia occurs in prostate cancer patients on abiraterone. It should be monitored closely in patients on this therapy.