Adefovir dipivoxil
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Reactions 1451 - 11 May 2013 S Adefovir dipivoxil Fanconi’s syndrome: case report A 61-year-old man developed Fanconi’s syndrome during treatment with adefovir dipivoxil. The man presented with pain in both lower legs in year "X". He had been diagnosed with chronic hepatitis B at "X-17" years, and had started lamivudine treatment in October "X-10" years. Lamivudine resistance developed, and internal adefovir dipivoxil 10 mg/day was added in September "X-7" years [route not clearly stated]. In August "X-6" years, his serum creatinine level had gradually increased; from October, his serum uric acid level had decreased. From September "X-4" years, his serum alkaline phosphatase level had increased (548 U/L). In January of "X-2" years, his urinal sugar was 2+ and his uric protein was 2+. In February, renal physical results revealed interstitial inflammatory cell infiltrate and atrophy of his renal tubule, diagnosed as benign glomerulosclerosis. From January "X-1" years, he became aware of discomfort in both lower legs, and began walking with crutches due to the gradual progression of pain. In June of year "X", stress fractures were diagnosed in both his tibias and fibulas. In October, his alkaline phosphatase level was 1836 IU/L; he was hospitalised in November. At hospitalisation, his bone mineral density had decreased, and examination confirmed slight kidney damage and renal glycosuria. His alkaline phosphatase level was 1751 U/L, his serum uric acid level was 2.1 mg/dL, and his serum phosphate level was 1.8 mg/dL. Bone scintigraphy revealed multiple fractures in his ribs, and a build up of metaphyseal fractures in the distal end of his femurs, tibias and fibulas. He was diagnosed with hypophosphataemia and osteomalacia from image examination results. Calcium and phosphorus in the urine, increased uric acid excretion, generalised aminoaciduria, renal glycosuria, high chloride metabolic acidosis, and a high level of β-2 microglobulin in the urine were confirmed. From investigation findings, it was determined that he had osteomalacia from hypophosphatemia resulting from proximal tubule defects, and he was diagnosed with Fanconi’s syndrome. The man was switched to entecavir; he was treated with vitamin D, and subsequently with vitamin K and bisphosphonate. In December, his alkaline phosphatase level decreased, and he was discharged. After about 8 months, his alkaline phosphatase level was 912 U/L and his serum phosphate level was 3.1 mg/dL. His bone density improved, his pain resolved, and he was able to walk again. Author comment: In this case, the serum Cr [creatinine] value increased from 11 months after starting internal administration of ADV [adefovir dipivoxil], and the serum ALP [alkaline phosphatase] value increased from 2 years and 3 months after starting. This case is therefore thought to be Fanconi’s syndrome caused by long-term administration of ADV. Kumade E, et al. A case of Fanconi’s syndrome caused by long-term administration of adefovir by a patient with chronic hepatitis B. Kanzo 54: 187-193, No. 3, 2013. Available from: URL: http://dx.doi.org/10.2957/ kanzo.54.187 [Japanese; summarised from a translation] - Japan 803086477 1 Reactions 11 May 2013 No. 1451 0114-9954/10/1451-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
Transcript of Adefovir dipivoxil
Reactions 1451 - 11 May 2013
SAdefovir dipivoxil
Fanconi’s syndrome: case reportA 61-year-old man developed Fanconi’s syndrome during
treatment with adefovir dipivoxil.The man presented with pain in both lower legs in year "X".
He had been diagnosed with chronic hepatitis B at"X-17" years, and had started lamivudine treatment in October"X-10" years. Lamivudine resistance developed, and internaladefovir dipivoxil 10 mg/day was added in September"X-7" years [route not clearly stated]. In August "X-6" years, hisserum creatinine level had gradually increased; from October,his serum uric acid level had decreased. From September"X-4" years, his serum alkaline phosphatase level had increased(548 U/L). In January of "X-2" years, his urinal sugar was 2+ andhis uric protein was 2+. In February, renal physical resultsrevealed interstitial inflammatory cell infiltrate and atrophy ofhis renal tubule, diagnosed as benign glomerulosclerosis.From January "X-1" years, he became aware of discomfort inboth lower legs, and began walking with crutches due to thegradual progression of pain. In June of year "X", stress fractureswere diagnosed in both his tibias and fibulas. In October, hisalkaline phosphatase level was 1836 IU/L; he was hospitalisedin November. At hospitalisation, his bone mineral density haddecreased, and examination confirmed slight kidney damageand renal glycosuria. His alkaline phosphatase level was1751 U/L, his serum uric acid level was 2.1 mg/dL, and hisserum phosphate level was 1.8 mg/dL. Bone scintigraphyrevealed multiple fractures in his ribs, and a build up ofmetaphyseal fractures in the distal end of his femurs, tibias andfibulas. He was diagnosed with hypophosphataemia andosteomalacia from image examination results. Calcium andphosphorus in the urine, increased uric acid excretion,generalised aminoaciduria, renal glycosuria, high chloridemetabolic acidosis, and a high level of β-2 microglobulin in theurine were confirmed. From investigation findings, it wasdetermined that he had osteomalacia from hypophosphatemiaresulting from proximal tubule defects, and he was diagnosedwith Fanconi’s syndrome.
The man was switched to entecavir; he was treated withvitamin D, and subsequently with vitamin K andbisphosphonate. In December, his alkaline phosphatase leveldecreased, and he was discharged. After about 8 months, hisalkaline phosphatase level was 912 U/L and his serumphosphate level was 3.1 mg/dL. His bone density improved,his pain resolved, and he was able to walk again.
Author comment: In this case, the serum Cr [creatinine]value increased from 11 months after starting internaladministration of ADV [adefovir dipivoxil], and the serum ALP[alkaline phosphatase] value increased from 2 years and3 months after starting. This case is therefore thought to beFanconi’s syndrome caused by long-term administration ofADV.Kumade E, et al. A case of Fanconi’s syndrome caused by long-termadministration of adefovir by a patient with chronic hepatitis B. Kanzo 54:187-193, No. 3, 2013. Available from: URL: http://dx.doi.org/10.2957/kanzo.54.187 [Japanese; summarised from a translation] - Japan 803086477
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Reactions 11 May 2013 No. 14510114-9954/10/1451-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved
