TY - JOUR
T1 - An Expert Perspective on Phosphate Dysregulation With a Focus on Chronic Hypophosphatemia
AU - Aljuraibah, Fahad
AU - Bacchetta, Justine
AU - Brandi, Maria Luisa
AU - Florenzano, Pablo
AU - Javaid, Muhammad K.
AU - Mäkitie, Outimaija
AU - Raimann, Adalbert
AU - Rodriguez, Mariano
AU - Siggelkow, Heide
AU - Tiosano, Dov
AU - Vervloet, Marc
AU - Wagner, Carsten A.
N1 - Funding Information: Medical writing support was provided by Afsaneh Khetrapal of ApotheCom, London, UK, and funded by Kyowa Kirin International. Funding Information: This article was based on a series of meetings organized and sponsored by Kyowa Kirin International. Medical writing support was provided by ApotheCom and funded by Kyowa Kirin International. FA consults for and has received lecture fees from KKI. JB consults for Kyowa Kirin International, Amgen, and Bayer and has received lecture fees and grants from Kyowa Kirin International. MLB was previously employed at the University of Florence, Italy, in the last 2 years. She has consulted for Alexion, Amolyt, Bruno Farmaceutici, Calcilytix, Kyowa Kirin, and UCB and has received honoraria, grants, or speaker fees from Amgen, Bruno Farmaceutici, Calcilytix, Kyowa Kirin, Abiogen, Alexion, Echolight, Eli Lilly, SPA, Theramex, and UCB. PF consults for Kyowa Kirin/Ultragenyx and has received lecture fees and a research grant from Ultragenyx. MKJ consults for UCB, Amgen, and Kyowa Kirin Hakin and previously consulted for Consilient Healthcare. He has received lecture fees from all four of these companies and received an Amgen industry grant. OM consults for Kyowa Kirin and BridgeBio. She previously consulted for Alexion, Sandoz, and Ultragenyx and received lecture fees from Kyowa Kirin. AR consults for Kyowa Kirin and has received lecture fees from Kyowa Kirin and Ipsen Pharma. He has also received support for attending meetings from Ferring and Merck. MR consults for and has received lecture fees from Viphor, Amgen, and Kyowa Kirin. He has received grant support from Amgen. HS has served as an advisory board member for Shire/Takeda, UCB, and Kyowa Kirin, and is currently one for Takeda, Kyowa Kirin. She has received speaker's fees from Shire/Takeda, UCB, Alexion, Kyowa Kirin, Merck/Serono, Biomarin, and Amgen, and has grant support from Takeda. She is spokesperson for the German network of rare bone diseases, member of the ECTS Action group of Rare Bone Diseases, member of the ESE Education committee and representative in the PARAT programme of ESE, and treasurer of the German Society of Osteology. MV consults for Astra Zeneca, Vifor Pharma, Otsuka, and Kyowa Kirin. He previously consulted for Medice and Amgen, and has received lecture fees and grant support from Amgen, Vifor, and Fresenius Medical Care. He has participated on a Data Safety Monitoring Board or Advisory Board in the OASIS and DIPAK trials. He is on the KDIGO committee on CKD‐MBD and the chair of the ERA‐EDTA working group on CKD‐MBD. CW consults for Kyowa Kirin, Ardelyx, and Medice, and previously consulted for Chugai. He has received lecture fees in the last 2 years from Kyowa Kirin, Medice, Advicenne, and Salmon Pharma and grant support from Chugai. Publisher Copyright: © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).
PY - 2022/1/1
Y1 - 2022/1/1
N2 - Because of their rarity, diseases characterized by chronic hypophosphatemia can be underrecognized and suboptimally managed, resulting in poor clinical outcomes. Moreover, serum phosphate may not be measured routinely in primary care practice. Authors participated in several working sessions to advance the understanding of phosphate homeostasis and the causes, consequences, and clinical implications of chronic hypophosphatemia. Phosphate levels are regulated from birth to adulthood. Dysregulation of phosphate homeostasis can result in hypophosphatemia, which becomes chronic if phosphate levels cannot be normalized. Chronic hypophosphatemia may be underrecognized as serum phosphate measurement is not always part of routine analysis in the primary care setting and results might be misinterpreted, for instance, due to age-specific differences not being accounted for and circadian variations. Clinical consequences of chronic hypophosphatemia involve disordered endocrine regulation, affect multiple organ systems, and vary depending on patient age and the underlying disorder. Signs and symptoms of chronic hypophosphatemic diseases that manifest during childhood or adolescence persist into adulthood if the disease is inadequately managed, resulting in an accumulation of clinical deficits and a progressive, debilitating impact on quality of life. Early identification and diagnosis of patients with chronic hypophosphatemia is crucial, and clinical management should be started as soon as possible to maximize the likelihood of improving health outcomes. Furthermore, in the absence of a universally accepted description for “chronic hypophosphatemia,” a definition is proposed here that aims to raise awareness of these diseases, facilitate diagnosis, and guide optimal phosphate management strategies by improving monitoring and assessment of patient response to treatment.
AB - Because of their rarity, diseases characterized by chronic hypophosphatemia can be underrecognized and suboptimally managed, resulting in poor clinical outcomes. Moreover, serum phosphate may not be measured routinely in primary care practice. Authors participated in several working sessions to advance the understanding of phosphate homeostasis and the causes, consequences, and clinical implications of chronic hypophosphatemia. Phosphate levels are regulated from birth to adulthood. Dysregulation of phosphate homeostasis can result in hypophosphatemia, which becomes chronic if phosphate levels cannot be normalized. Chronic hypophosphatemia may be underrecognized as serum phosphate measurement is not always part of routine analysis in the primary care setting and results might be misinterpreted, for instance, due to age-specific differences not being accounted for and circadian variations. Clinical consequences of chronic hypophosphatemia involve disordered endocrine regulation, affect multiple organ systems, and vary depending on patient age and the underlying disorder. Signs and symptoms of chronic hypophosphatemic diseases that manifest during childhood or adolescence persist into adulthood if the disease is inadequately managed, resulting in an accumulation of clinical deficits and a progressive, debilitating impact on quality of life. Early identification and diagnosis of patients with chronic hypophosphatemia is crucial, and clinical management should be started as soon as possible to maximize the likelihood of improving health outcomes. Furthermore, in the absence of a universally accepted description for “chronic hypophosphatemia,” a definition is proposed here that aims to raise awareness of these diseases, facilitate diagnosis, and guide optimal phosphate management strategies by improving monitoring and assessment of patient response to treatment.
KW - HYPOPHOSPHATEMIA
KW - OSTEOMALACIA AND RICKETS
KW - PARATHYROID HORMONE/VITAMIN D/FIBROBLAST GROWTH FACTOR 23
KW - PHOSPHATE HOMEOSTASIS
UR - http://www.scopus.com/inward/record.url?scp=85121656475&partnerID=8YFLogxK
U2 - https://doi.org/10.1002/jbmr.4486
DO - https://doi.org/10.1002/jbmr.4486
M3 - Article
C2 - 34870347
SN - 0884-0431
VL - 37
SP - 12
EP - 20
JO - Journal of bone and mineral research
JF - Journal of bone and mineral research
IS - 1
ER -