Assessment of Bone Density and Bone Turnover Markers in Patients With Down Syndrome and Comparison to the Ts65Dn Model

Down Syndrome Clinical Trial

Official title:

Assessment of Bone Density and Bone Turnover Markers in Patients With Down Syndrome and Comparison to the Ts65Dn Model

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01148121
• Other study ID #: 113810
• Status: Completed
• Phase: N/A
• First received: June 18, 2010
• Last updated: December 6, 2016
• Start date: June 2010
• Est. completion date: August 2015

Study information

• Verified date: December 2016
• Source: University of Arkansas
• Contact: n/a
• Is FDA regulated: No
• Health authority: United States: Institutional Review Board
• Study type: Interventional

Clinical Trial Summary

This study may provide information that may serve as the foundation for a larger research study to address issues regarding the causes, diagnosis, and treatment of osteoporosis in the Down syndrome patient population.

Description:

Osteoporosis is responsible for more than 1.5 million fractures and $14 billion in medical care costs annually (U.S Dept of Health and Human Services data, 2006). Down syndrome is an independent risk factor for osteopenia/osteoporosis. Increases in life expectancy as well as costly morbidity following fracture are reasons for further investigation of osteoporosis and prevention in this population. Etiology for low bone density is presently unknown in this population but may be related to unique genes on chromosome 21 which alter the biochemistry of bone metabolism or change the gonadal, thyroid and parathyroid function to alter bone formation and/or resorption. There are no published data on the measurement of bone turnover markers in the Down syndrome population; therefore we will measure and accrue this information and compare to our Ts65Dn data, as described later in this protocol.

This pilot study will serve as the foundation for a larger translational research grant which will address multiple issues regarding the pathogenesis, diagnosis and treatment of osteoporosis in the Down syndrome patient population and the Down syndrome mouse model (Ts65Dn). The data has the potential to improve our fundamental understanding of osteoporosis pathogenesis and treatment in the Down syndrome patient with potential applications to treatment in the general population.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 30
• Est. completion date: August 2015
• Est. primary completion date: August 2015
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• Males and Females of all races and ethnicities

• Age 18 or older and current clinical diagnosis of Down Syndrome

Exclusion Criteria:

• No legally authorized representative (if applicable) willing to provide informed consent. Any condition the investigator determines will put the subject at risk by participating in the study.

Study Design

Intervention Model: Single Group Assignment, Masking: Open Label

Related Conditions & MeSH terms

• Down Syndrome
• Syndrome

Intervention

Other:
• Skeletal Status Assessment of a Down Syndrome Population
The investigators hypothesize that the bone deficits seen in Down Syndrome patients are similar to the phenotype seen in the down syndrome mouse model (Ts65Dn).The bone turnover markers, CBC, and DXA scan results will be used to assess the skeletal status of the down syndrome patients. This data will form the basis to establish the Ts65Dn as a reasonable proxy for pathogenesis and treatment in humans.

Locations

Country	Name	City	State
United States	University of Arkansas for Medical Sciences	Little Rock	Arkansas

Sponsors (1)

Lead Sponsor	Collaborator
University of Arkansas

Country where clinical trial is conducted

United States, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Ts65DN pathogenesis proxy	The bone turnover markers, Complete Blood Count (CBC) and the Duel Energy X-ray (DXA) scan results will be used to assess the skeletal status of the Down syndrome patients. This data will form the basis to establish the Ts65Dn as a reasonable proxy for pathogenesis and treatment in humans.	1 year	No