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Case Reports
Journal Article
Pathologic femoral fracture due to tenofovir-induced Fanconi syndrome in patient with chronic hepatitis B: A case report.
Medicine (Baltimore) 2017 November
RATIONALE: We report a case of a hepatitis B virus (HBV)-positive patient with preexisting bone disease who developed tenofovir-induced Fanconi syndrome and subsequently sustained pathologic fracture. To our best knowledge, this is the first report in the English literature about pathologic femoral fracture due to tenofovir-induced Fanconi syndrome in patient with chronic hepatitis B (CHB). The present report describes detailed our experience with the diagnosis of pathologic femoral fracture due to tenofovir-induced Fanconi syndrome and treatment.
PATIENT CONCERNS: A 45-year-old man visited our hospital with pain in the right thigh region and gait disturbance which had started 3 months ago and worsened 1 week before admission. The patient was diagnosed with CHB in 2004. He was on lamivudine medication for 2 years. Medication for the patient was subsequently changed to adefovir in 2009 and tenofovir disoproxil fumarate (TDF) in 2013. He was on TDF since 2013.
DIAGNOSIS: His hip joint magnetic resonance imaging (MRI) revealed hypointensity lesions and cortical bone destruction in fat-saturated MR image at the iliopsoas muscle attachment site of the lesser trochanter of both femur. On blood test showed 25-OH vitamin D level at 6.42 ng/mL (normal range, >20 ng/mL) and U-deoxypyridinoline level at 7.60 nM/mMcr (normal range, 2.30-5.40 nM mMcr). However, osteocalcin and parathyroid hormone levels were within normal range. Based on these findings, the present case was concluded as tenoforvir-induced Fanconi syndrome.
INTERVENTIONS: TDF treatment was discontinued. After cooperation with internal medicine department, in order to prevent further fractures of the right lesser trochanter, internal fixation was performed under spinal anesthesia using compression hip nails (APIS, TDM, Korea).
OUTCOMES: Positive outcome by medication and operation demonstrates that his phosphorus and serum calcium levels were maintained within normal range and pain in the right thigh region was improved from visual analogue pain score (VAS) 7 before surgery to VAS 2 after surgery.
LESSONS: Physicians need to regularly monitor bone metabolism in patients with take in tenofovir for early diagnosis before its progression to pathologic fractures.
PATIENT CONCERNS: A 45-year-old man visited our hospital with pain in the right thigh region and gait disturbance which had started 3 months ago and worsened 1 week before admission. The patient was diagnosed with CHB in 2004. He was on lamivudine medication for 2 years. Medication for the patient was subsequently changed to adefovir in 2009 and tenofovir disoproxil fumarate (TDF) in 2013. He was on TDF since 2013.
DIAGNOSIS: His hip joint magnetic resonance imaging (MRI) revealed hypointensity lesions and cortical bone destruction in fat-saturated MR image at the iliopsoas muscle attachment site of the lesser trochanter of both femur. On blood test showed 25-OH vitamin D level at 6.42 ng/mL (normal range, >20 ng/mL) and U-deoxypyridinoline level at 7.60 nM/mMcr (normal range, 2.30-5.40 nM mMcr). However, osteocalcin and parathyroid hormone levels were within normal range. Based on these findings, the present case was concluded as tenoforvir-induced Fanconi syndrome.
INTERVENTIONS: TDF treatment was discontinued. After cooperation with internal medicine department, in order to prevent further fractures of the right lesser trochanter, internal fixation was performed under spinal anesthesia using compression hip nails (APIS, TDM, Korea).
OUTCOMES: Positive outcome by medication and operation demonstrates that his phosphorus and serum calcium levels were maintained within normal range and pain in the right thigh region was improved from visual analogue pain score (VAS) 7 before surgery to VAS 2 after surgery.
LESSONS: Physicians need to regularly monitor bone metabolism in patients with take in tenofovir for early diagnosis before its progression to pathologic fractures.
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