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      Potentially Life-Threatening Phosphate Diabetes Induced by Ferric Carboxymaltose Injection: A Case Report and Review of the Literature

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      1 , * , 2
      Case Reports in Endocrinology
      Hindawi Publishing Corporation

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          Abstract

          We report the case of a 45-year-old female patient who developed phosphate diabetes after administration of ferric carboxymaltose. Ten days after the second dose, she complained of intense fatigue and blood analysis showed a phosphate plasma level of 0.93 mg/dL with phosphate excretion rate of 23%. She received phosphate supplementation which resulted in phosphate clearance improvement which persisted for two months. We reviewed other cases described in the literature and would draw attention to this rare but potentially life-threatening side effect.

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          Most cited references23

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          Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism.

          The metabolically active and perpetually remodeling calcium phosphate-based endoskeleton in terrestrial vertebrates sets the demands on whole-organism calcium and phosphate homeostasis that involves multiple organs in terms of mineral flux and endocrine cross talk. The fibroblast growth factor (FGF)-Klotho endocrine networks epitomize the complexity of systems biology, and specifically, the FGF23-αKlotho axis highlights the concept of the skeleton holding the master switch of homeostasis rather than a passive target organ as hitherto conceived. Other than serving as a coreceptor for FGF23, αKlotho circulates as an endocrine substance with a multitude of effects. This review covers recent data on the physiological regulation and function of the complex FGF23-αKlotho network. Chronic kidney disease is a common pathophysiological state in which FGF23-αKlotho, a multiorgan endocrine network, is deranged in a self-amplifying vortex resulting in organ dysfunction of the utmost severity that contributes to its morbidity and mortality.
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            Effects of iron deficiency anemia and its treatment on fibroblast growth factor 23 and phosphate homeostasis in women.

            Fibroblast growth factor 23 (FGF23) is an osteocyte-derived hormone that regulates phosphate and vitamin D homeostasis. Through unknown mechanisms, certain intravenous iron preparations induce acute, reversible increases in circulating FGF23 levels that lower serum phosphate in association with inappropriately low levels of calcitriol, similar to genetic diseases of primary FGF23 excess. In contrast, studies in wild-type mice suggest that iron deficiency stimulates fgf23 transcription but does not result in hypophosphatemia because FGF23 is cleaved within osteocytes by an unknown catabolic system. We tested the association of iron deficiency anemia with C-terminal FGF23 (cFGF23) and intact FGF23 (iFGF23) levels in 55 women with a history of heavy uterine bleeding, and assessed the longitudinal biochemical response over 35 days to equivalent doses of randomly-assigned, intravenous elemental iron in the form of ferric carboxymaltose (FCM) or iron dextran. Iron deficiency was associated with markedly elevated cFGF23 (807.8 ± 123.9 relative units [RU]/mL) but normal iFGF23 (28.5 ± 1.1 pg/mL) levels at baseline. Within 24 hours of iron administration, cFGF23 levels fell by approximately 80% in both groups. In contrast, iFGF23 transiently increased in the FCM group alone, and was followed by a transient, asymptomatic reduction in serum phosphate <2.0 mg/dL in 10 women in the FCM group compared to none in the iron dextran group. Reduced serum phosphate was accompanied by increased urinary fractional excretion of phosphate, decreased calcitriol levels, and increased parathyroid hormone levels. These findings suggest that iron deficiency increases cFGF23 levels, and that certain iron preparations temporarily increase iFGF23 levels. We propose that intravenous iron lowers cFGF23 in humans by reducing fgf23 transcription as it does in mice, whereas carbohydrate moieties in certain iron preparations may simultaneously inhibit FGF23 degradation in osteocytes leading to transient increases in iFGF23 and reduced serum phosphate. Copyright © 2013 American Society for Bone and Mineral Research.
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              Prevalence of iron deficiency in the United States.

              To determine the prevalence of iron deficiency and iron deficiency anemia in the US population. Nationally representative cross-sectional health examination survey that included venous blood measurements of iron status. Iron deficiency, defined as having an abnormal value for at least 2 of 3 laboratory tests of iron status (erythrocyte protoporphyrin, transferrin saturation, or serum ferritin); and iron deficiency anemia, defined as iron deficiency plus low hemoglobin. A total of 24,894 persons aged 1 year and older examined in the third National Health and Nutrition Examination Survey (1988-1994). Nine percent of toddlers aged 1 to 2 years and 9% to 11% of adolescent girls and women of childbearing age were iron deficient; of these, iron deficiency anemia was found in 3% and 2% to 5%, respectively. These prevalences correspond to approximately 700,000 toddlers and 7.8 million women with iron deficiency; of these, approximately 240,000 toddlers and 3.3 million women have iron deficiency anemia. Iron deficiency occurred in no more than 7% of older children or those older than 50 years, and in no more than 1% of teenage boys and young men. Among women of childbearing age, iron deficiency was more likely in those who are minority, low income, and multiparous. Iron deficiency and iron deficiency anemia are still relatively common in toddlers, adolescent girls, and women of childbearing age.
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                Author and article information

                Journal
                Case Rep Endocrinol
                Case Rep Endocrinol
                CRIE
                Case Reports in Endocrinology
                Hindawi Publishing Corporation
                2090-6501
                2090-651X
                2014
                13 November 2014
                : 2014
                : 843689
                Affiliations
                1Department of General Internal Medicine, Centres Hospitaliers Jolimont, 1400 Nivelles, Belgium
                2Department of General Internal Medicine, Hopital Erasme, 1070 Bruxelles, Belgium
                Author notes

                Academic Editor: Najmul Islam

                Article
                10.1155/2014/843689
                4247964
                25478250
                a456def4-56e6-4824-a25d-22c81d89970a
                Copyright © 2014 X. Vandemergel and F. Vandergheynst.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 15 July 2014
                : 24 October 2014
                : 27 October 2014
                Categories
                Case Report

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