Deferasirox

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Reactions 1392 - 10 Mar 2012 S Deferasirox Hypophosphataemic osteomalacia: case report A 28-year-old woman developed hypophosphataemic osteomalacia while receiving deferasirox [route not stated; duration of treatment to reaction onset not clearly stated] for β-thalassaemia. In August 2009, the woman was referred for management of a low bone mineral density following a progressive decline in the past 3 years. She had started treatment with deferasirox 1500mg [initial frequency not stated] in November 2007 after poor compliance with deferoxamine. Her medical history was notable for diet- controlled diabetes, hepatitis C, renal caliculi, and mild transient right hip pain several months earlier following a fall, which had not required medical attention. At the time of referral, her medications included colecalciferol [vitamin D3] and deferasirox 1g daily. Biochemical analysis revealed a low serum phosphate level and an alkaline phosphatase level two to three times the upper limit of normal. Tubular reabsorption of phosphate (TRP) was abnormal, and diffuse demineralisation was apparent on thoracolumbar x-ray. A bone scan showed healing fractures of the right superior and inferior pubic rami and two older rib fractures. A urine metabolic screen demonstrated generalised aminoaciduria, glycosuria, and detectable protein. In addition, her urine β2-microglobulin level was elevated. Deferasirox was withdrawn in September 2009 and phosphorus was initiated. The woman’s abnormal serum phosphate level resolved 3 days later, and she maintained a normal TRP. A repeat urine metabolic screen showed no aminoaciduria, glycosuria, or protein urine. An improvement in her bone mineral density was observed 3 months later. Deferasirox 250mg daily was introduced in November 2009, 2-3 months after its withdrawal. Following a dose increase to 750mg daily in January 2010, the woman’s serum phosphate level and TRP decreased. Her serum phosphate level stabilised following a deferasirox dose reduction to 500mg daily in April 2010. Improvement in her bone mineral density had been maintained 6 months after reintroducing low-dose deferasirox therapy and healing of her pelvic fractures was confirmed on x-ray. However, her alkaline phosphatase level had not normalised and her serum procollagen 1 N-terminal propeptide level remained elevated. At last observation, treatment with deferiprone was being considered and her serum ferritin levels were being closely monitored while on deferasirox 500mg. Milat F, et al. A case of hypophosphatemic osteomalacia secondary to deferasirox therapy. Journal of Bone and Mineral Research 27: 219-222, No. 1, Jan 2012. Available from: URL: http://dx.doi.org/10.1002/jbmr.522 - Australia 803067697 1 Reactions 10 Mar 2012 No. 1392 0114-9954/10/1392-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved

Transcript of Deferasirox

Page 1: Deferasirox

Reactions 1392 - 10 Mar 2012

SDeferasirox

Hypophosphataemic osteomalacia: case reportA 28-year-old woman developed hypophosphataemic

osteomalacia while receiving deferasirox [route not stated;duration of treatment to reaction onset not clearly stated]for β-thalassaemia.

In August 2009, the woman was referred formanagement of a low bone mineral density following aprogressive decline in the past 3 years. She had startedtreatment with deferasirox 1500mg [initial frequency notstated] in November 2007 after poor compliance withdeferoxamine. Her medical history was notable for diet-controlled diabetes, hepatitis C, renal caliculi, and mildtransient right hip pain several months earlier following afall, which had not required medical attention. At the timeof referral, her medications included colecalciferol [vitaminD3] and deferasirox 1g daily. Biochemical analysis revealeda low serum phosphate level and an alkaline phosphataselevel two to three times the upper limit of normal. Tubularreabsorption of phosphate (TRP) was abnormal, and diffusedemineralisation was apparent on thoracolumbar x-ray. Abone scan showed healing fractures of the right superiorand inferior pubic rami and two older rib fractures. A urinemetabolic screen demonstrated generalised aminoaciduria,glycosuria, and detectable protein. In addition, her urineβ2-microglobulin level was elevated.

Deferasirox was withdrawn in September 2009 andphosphorus was initiated. The woman’s abnormal serumphosphate level resolved 3 days later, and she maintained anormal TRP. A repeat urine metabolic screen showed noaminoaciduria, glycosuria, or protein urine. Animprovement in her bone mineral density was observed3 months later.

Deferasirox 250mg daily was introduced in November2009, 2-3 months after its withdrawal. Following a doseincrease to 750mg daily in January 2010, the woman’sserum phosphate level and TRP decreased. Her serumphosphate level stabilised following a deferasirox dosereduction to 500mg daily in April 2010. Improvement inher bone mineral density had been maintained 6 monthsafter reintroducing low-dose deferasirox therapy andhealing of her pelvic fractures was confirmed on x-ray.However, her alkaline phosphatase level had notnormalised and her serum procollagen 1 N-terminalpropeptide level remained elevated. At last observation,treatment with deferiprone was being considered and herserum ferritin levels were being closely monitored while ondeferasirox 500mg.Milat F, et al. A case of hypophosphatemic osteomalacia secondary to deferasiroxtherapy. Journal of Bone and Mineral Research 27: 219-222, No. 1, Jan 2012.Available from: URL: http://dx.doi.org/10.1002/jbmr.522 - Australia 803067697

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Reactions 10 Mar 2012 No. 13920114-9954/10/1392-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved