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Journal of Clinical and Molecular Endocrinology
ISSN: 2572-5432
August 09-10, 2018
Madrid, Spain
Endocrinology 2018
Page 18
11th International Conference on
Endocrinology and
Diabetology
Chronichypophosphatemiadevelopsricketsandosteomalacia
characterized by impaired mineralization of bone matrix.
Rickets, such as X-linked hypophsohatemic rickets (XLH),
occurs in childhood before the closure of epiphyseal plate and
results in growth retardation and bone deformities. On the other
hand, osteomalacia occurs in adulthood with severe muscle
weakness and bone pain. Tumor-induced osteomalacia (TIO) is
an underrecognized paraneoplastic syndrome presenting with
hypophosphatemic osteomalacia, which is one of causes of
adult onset osteomalacia. Recently elevated circulated levels of
fibroblast growth factor 23 (FGF23) was identified as a cause of
hypophosphatemic rickets/osteomalacia such as XLH and TIO.
FGF23 is a bone-derived hormone, which regulate phosphate
and vitamin D metabolism. Chronic elevation of circulated
FGF23 causes hypophosphatemia by urinary phosphate wasting
and attenuate activation of vitamin D, resulted in rickets and
osteomalacia. Circulating FGF23 measurement is required to
obtain proper diagnosis in rickets and osteomalacia. In familial
rickets, genetic testing such as PHEX gene is recommended.
In TIO, it is difficult to identify the causative tumor, which
secrete FGF23. Recently, somatostatin receptor scintigraphy
was reported to be useful for the diagnosis and localization of
causative tumors. Conventional therapies for these FGF23-
induced rickets and osteomalacia are active vitamin D and/
or inorganic phosphate, however, the clinical efficacy of these
therapies are limited. Burosumab, a monoclonal antibody that
targets FGF-23, improved renal tubular phosphate reabsorption,
serum phosphate levels, linear growth, physical function and
reducedpain inchildrenwithXLH.This newantibody ispromising
treatments not only for XLH but also for TIO.
Biography
Yasuo Imanishi graduated from Kagawa Medical School (MD), Japan. He
has completed his PhD from Osaka City University, and Postdoctoral Fel-
lowships fromMassachusetts General Hospital in Harvard Medical School
and University of Connecticut Health Center. He is an Associate Professor
of Osaka City University Graduate School of Medicine. His major interests
are calcium and phosphate homeostasis in the clinical filed of osteoporo-
sis, rickets & osteomalacia, and chronic kidney disease-mineral and bone
disorder (CKD-MBD). He has been working as an Endocrinologist/Nephrol-
ogist at Osaka City University Graduate School of Medicine from 2000.
Hypophosphatemic rickets and osteomalacia:
pathogenesis, diagnosis and treatments
Yasuo Imanishi
Osaka City University, Japan
Yasuo Imanishi, J Clin Mol Endocrinol 2018, Volume 3
DOI: 10.21767/2572-5432-C2-004