Development of osteomalacia in a post-liver transplant patient receiving adefovir dipivoxil

Abstract

We report the case of a patient treated with living donor-related liver transplantation who suffered from osteomalacia during adefovir dipivoxil (ADV)-containing antiviral therapy for lamivudine-resistant hepatitis B virus infection. The patient had generalized bone pain, with severe hypophosphatemia after 20 mo of ADV therapy. Radiographic studies demonstrated the presence of osteomalacia. The peak plasma ADV level was 38 ng/mL after administration of ADV at 10 mg/d. It was also found that ADV affected the metabolism of tacrolimus, a calcineurin-inhibitor, and caused an increase in the plasma levels of tacrolimus. The disability was reversed with the withdrawal of ADV and with mineral supplementation. ADV can cause an elevation of plasma tacrolimus levels, which may be associated with renal dysfunction. High levels of ADV and tacrolimus can cause nephrotoxicity and osteomalacia. This case highlights the importance of considering a diagnosis of osteomalacia in liver transplantation recipients treated with both ADV and tacrolimus.

Keywords: Adefovir dipivoxil; Hepatitis B virus; Living donor-related liver transplantation; Osteomalacia; Tacrolimus.

Figure 1

Whole body bone scintigraphy shows multiple foci of increased radiotracer uptake in the thoracic spine, the sacroiliac region, the rib cage, the shoulders, the knees, and the ankles.

Figure 2

Clinical course of the present case. After switching from ADV plus LAM to ETV, serum levels of P and ALP improved, and the patient’s bone pain also decreased dramatically. ADV: adefovir dipivoxil; LAM: lamivudine; ETV: entecavir hydrate; PSL: prednisolone; P: phosphate; APL: alkaline phosphatase; γ-GTP: γ-glutamyl transferase; LDLT: living donor-related liver transplantation.