Hepatic hemochromatosis and hypophosphatemic osteomalacia caused by the continuous intravenous administration of saccharated ferric oxide

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 199-237-Disorders of Parathyroid Hormone & Calcium Homeostasis
Translational
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-212
Keiji Iida*, Anna Tamagawa, Yasuhisa Hino, Takeshi Ohara, Seitetsu Yoon, Masayo Fujimoto and Kazuo Chihara
Hyogo Prefectural Kakogawa Medical Center, Kakogawa, Japan
Background: Transfusional iron overload can sometimes cause secondary hemochromatosis, and saccharated ferric oxide (SFO) is known to cause hypophosphatemic osteomalacia. We report a patient who developed both hemochromatosis and hypophosphatemic osteomalacia caused by the repeated and prolonged intravenous administration of SFO for anemia treatment.

Clinical case: A 48-year-old man developed progressive bilateral lower limbs pain and weakness over 2 years. He had a history of anemia of unknown cause for which his family physician prescribed intravenous SFO administration 3 times a week. He was presented at our hospital for further evaluation of his bone pain. At the hospital, his serum ferritin level was found to be extremely elevated at 3879 ng/mL(reference range, 39.4–340 pg/mL). Computed tomography (CT) scan revealed that his liver density increased by 85–95 Hounsfield Unit (HU), whereas liver magnetic resonance imaging revealed low intensity T1- and T2- weighted images. Histological evaluation of a liver biopsy specimen confirmed hemochromatosis. Laboratory test results indicated a low serum phosphate level of 1.6 mg/dL (reference range, 2.5–4.5 mg/L) and an elevated alkaline phosphatase level of 1259 U/L (reference range, 100–350 U/L).The patient’s 1,25-dihydroxyvitamin D (1,25(OH)2D) level was below normal at 24.4 pg/mL (reference range, 20–60 pg/mL). Urinary tubular reabsorption of phosphate (TRP) was 76% (reference range, >82%), and the ratio of the maximum rate of renal tubular reabsorption of phosphate to glomerular filtration rate (TmPO4/GFR) was 1.24 (reference range, 2.5–4.2), indicating renal phosphate wasting. The patient’s serum fibroblast growth factor 23 (FGF-23) level was at the upper normal at 43 pg/mL (reference range, 10–60 pg/mL). Iron infusions were discontinued, and subsequently his serum phosphate level, 1,25 (OH)2D level, %TRP, TmPO4/GFR, and FGF-23 level normalized. Subsequently, his bone pain resolved. This clinical course confirmed SFO-induced osteomalacia.

Conclusion: We report a patient who developed both hemochromatosis and hypophosphatemic osteomalacia caused by intravenous administrations of SFO. We should consider the possibility that the continuous intravenous administration of SFO may cause hemochromatosis and hypophosphatemic osteomalacia.

Nothing to Disclose: KI, AT, YH, TO, SY, MF, KC

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