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

2014-08-27 03:12:44 | BioPortfolio

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.

Study Design

Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Health Services Research

Conditions

Down Syndrome

Intervention

Skeletal Status Assessment of a Down Syndrome Population

Location

University of AR-Medical Sciences-Genetics Clinic
Little Rock
Arkansas
United States

Status

Not yet recruiting

Source

University of Arkansas

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:12:44-0400

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A multifaceted disorder characterized by short stature, webbed neck, ptosis, skeletal malformations, hypertelorism, hormonal imbalance, CRYPTORCHIDISM, multiple cardiac abnormalities (most commonly including PULMONARY VALVE STENOSIS), and some degree of MENTAL RETARDATION. The phenotype bears similarities to that of TURNER SYNDROME that occurs only in females and has its basis in a 45, X karyotype abnormality. However, Noonan syndrome occurs in both males and females with a normal sex chromosome constitution (46,XX and 46,XY). NS1 is due to mutations at chromosome location 12q24.1, in PTPN11, a gene encoding PROTEIN TYROSINE PHOSPHATASE, NON-RECEPTOR TYPE 11. LEOPARD SYNDROME, a disorder that has clinical features overlapping those of Noonan Syndrome, is also due to mutations in PTPN11. In addition, there is a syndrome called neurofibromatosis-Noonan syndrome. Both the PTPN11 and NF1 gene products are involved in the SIGNAL TRANSDUCTION pathway of Ras (RAS PROTEINS).

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