Study of the Inappropriate Secretion of FGF23 in Patients Followed in Hospital in a Context of Hypophosphatemia
NCT04846647 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 260
Last updated 2023-05-11
Summary
The discovery of FGF23, the missing link in the long researched and finally found phosphate metabolism, marked a turning point in the understanding and physiopathology of specific hypophosphatemia. By inhibiting the renal reabsorption of phosphate and the production of calcitriol, FGF23 behaves like a hypophosphatemia hormone.
Hypersecretion of FGF23 can occur in the case of genetic abnormalities (X-linked hypophosphatemic vitamin-resistant rickets, recessive or dominant hypophosphatemic rickets, McCune-Albright syndrome ...) or acquired abnormalities (oncogenic osteomalacia). Oncogenic osteomalacia can be induced by hyperproduction of FGF23 by benign tumours of mesenchymal origin. But more recently, several cases of malignant tumours secreting FGF23 have also been described (prostate, colon, breast, ovarian and lung cancers, pulmonary carcinoma, etc.)
Conditions
- Hypophosphatemia Without Immediate Anteriority
- Unexplained Hypophosphatemia
Interventions
- BEHAVIORAL
-
unexplained hypophoshatemia
Collection of additional blood volume (approximately 10 mL) during blood tests provided as part of the usual medical care.
Sponsors & Collaborators
-
DiaSorin ; Saluggia, Italia
collaborator UNKNOWN -
University Hospital, Clermont-Ferrand
lead OTHER
Principal Investigators
-
Damien BOUVIER · University Hospital, Clermont-Ferrand
Eligibility
- Min Age
- 18 Years
- Sex
- ALL
- Healthy Volunteers
- Yes
Timeline & Regulatory
- Start
- 2021-10-05
- Primary Completion
- 2022-04-25
- Completion
- 2022-04-25
Countries
- France
Study Locations
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