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

Hypophosphatemia Clinical Trial

Official title:

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

Clinical Trial Details — Status: Recruiting

Administrative data

• NCT number: NCT01660308
• Other study ID #: 201105045RC
• Status: Recruiting
• Phase: N/A
• First received: August 5, 2012
• Last updated: July 4, 2016
• Start date: June 2011
• Est. completion date: August 2016

Study information

• Verified date: July 2016
• Source: National Taiwan University Hospital
• Contact: Shyang-Rong Shih, PhD
• Email: srshih[@]ntu.edu.tw
• Is FDA regulated: No
• Health authority: Taiwan: Ministry of Health and Welfare
• Study type: Observational

Clinical Trial Summary

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.

Recruitment information / eligibility

• Status: Recruiting
• Enrollment: 40
• Est. completion date: August 2016
• Est. primary completion date: August 2016
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Both
• Age group: 20 Years to 85 Years

Eligibility

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.

Study Design

Observational Model: Case Control, Time Perspective: Prospective

Related Conditions & MeSH terms

• Hypophosphatemia
• Neoplasms, Connective Tissue
• Osteomalacia

Locations

Country	Name	City	State
Taiwan	National Taiwan University Hospital	Taipei

Sponsors (1)

Lead Sponsor	Collaborator
National Taiwan University Hospital

Country where clinical trial is conducted

Taiwan, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	FGF23, P		at the time TIO is diagnosed	No