Observing the Changes of Fibroblast Growth Factor 23 in Patients of Tumor Induced Osteomalacia

NCT ID: NCT01660308

Last Updated: 2016-07-06

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

40 participants

Study Classification

OBSERVATIONAL

Study Start Date

2011-06-30

Study Completion Date

2016-08-31

Brief Summary

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Fibroblast froth factors (FGFs) are humoral factors identified by their ability to stimulate cell proliferation1. They play different roles in the regulation of cell proliferation, differentiation and function. Most FGF family members act as paracrine factors. But FGF19(FGF19) subfamily members, including FGF19, 21, and 23, work as endocrine factors to regulate bile acid, carbohydrate and phosphate metabolism2. Of these, FGF23 plays an important role in phosphate and bone metabolism3. FGF23 gene encodes 251 amino acids, including a 24-amino acid signal peptide4. The secreted FGF23 is a protein consisted of 227 amino acids. It works by binding to a Klotho-FGF receptor 1c (FGF1c) complex5. FGF suppresses the expression of type 2a and 2c sodium-phosphate cotransporters, which mediate phosphate reabsorption in proximal tubules.6 FGF23 decreases 25-hydroxyvitamin D-1α-hydroxylase expression and enhances 25-hydroxyvitamin D-24-hydroxylase expression6. Therefore, FGF23 reduces serum 1,25-dihydroxyvitamin D〔1,25(OH)2D〕, which stimulates intestinal calcium and phosphate absorption. FGF23 decreases serum phosphate through the above mechanisms FGF23 over-expression might result in hypophosphatemic rickets and osteomalacia.

Tumor induced osteomalacia (TIO) is a paraneoplastic syndrome usually caused by benign phosphaturic mesenchymal tumors. Symptoms are nonspecific, such as general weakness, fatigue, and bone pain. Sometimes fracture may occurs. The responsible tumors are sometimes small and difficult to detect. Tumors secrete FGF23. FGF23 reduced phosphate reabsorption in the proximal tubules and decrease 1,25(OH)2D levels, which result in hypophosphatemia and then osteomalacia.

The investigators would like to observe the changes of FGF23 in patients who receive operation or medical treatment and hope this will benefit future treatment.

Detailed Description

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Conditions

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Hypophosphatemia

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

PROSPECTIVE

Study Groups

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Tumor induced osteomalcia

No interventions assigned to this group

Eligibility Criteria

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Inclusion Criteria

* patients with tumor induced osteomalacia.
* people without osteomalacia such as healthy people,
* people under dialysis,
* people with poor nutrition.

Exclusion Criteria

* people younger than 20 years old or older than 85 years old.
* people who are pregnant.
Minimum Eligible Age

20 Years

Maximum Eligible Age

85 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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National Taiwan University Hospital

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Principal Investigators

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Shyang-Rong Shih, PhD

Role: PRINCIPAL_INVESTIGATOR

National Taiwan University Hospital

Locations

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National Taiwan University Hospital

Taipei, Taiwan, Taiwan

Site Status RECRUITING

Countries

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Taiwan

Central Contacts

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Shyang-Rong Shih, PhD

Role: CONTACT

Facility Contacts

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Shyang-Rong Shih, PhD

Role: primary

886-972653337

References

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Lin CH, Chang CK, Shih CW, Li HY, Chen KY, Yang WS, Tsai KS, Wang CY, Shih SR. Serum fibroblast growth factor 23 and mineral metabolism in patients with euthyroid Graves' diseases: a case-control study. Osteoporos Int. 2019 Nov;30(11):2289-2297. doi: 10.1007/s00198-019-05116-1. Epub 2019 Aug 5.

Reference Type DERIVED
PMID: 31384956 (View on PubMed)

Lin HA, Shih SR, Tseng YT, Chen CH, Chiu WY, Hsu CY, Tsai KS. Ovarian cancer-related hypophosphatemic osteomalacia--a case report. J Clin Endocrinol Metab. 2014 Dec;99(12):4403-7. doi: 10.1210/jc.2014-2120.

Reference Type DERIVED
PMID: 25181387 (View on PubMed)

Other Identifiers

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201105045RC

Identifier Type: -

Identifier Source: org_study_id

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