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Role of the Protein Osteoprotegerin in the Bone Health of Women With Congenital Adrenal Hyperplasia

NCT00694525 · Status: UNKNOWN · Type: OBSERVATIONAL · Enrollment: 40

Last updated 2009-06-02

No results posted yet for this study

Summary

21-hydroxylase deficiency (21-OHD) is an inherited disorder that results from a mutation on the CYP21A2 gene. It affects the adrenal glands and is the most common cause of congenital adrenal hyperplasia (CAH). 21-OHD CAH causes the body to produce an insufficient amount of cortisol and an excess of androgen, the type of hormone that produces male characteristics. The primary treatment for 21-OHD CAH, glucocorticoid replacement therapy, has been shown to cause bone loss. However, the elevated hormone levels caused by 21-OHD CAH may increase production of the protein osteoprotegerin (OPG), which in turn may protect against bone loss. This study will compare bone density and OPG levels in women who have 21-OHD CAH and have undergone a lifetime of glucocorticoid replacement therapy to that in women who have neither of these criteria. In doing so, the study will aim to determine the relationship between OPG and bone loss.

Conditions

  • Adrenal Hyperplasia, Congenital

Sponsors & Collaborators

  • Office of Rare Diseases (ORD)

    lead NIH

Principal Investigators

  • Karen Lin Su, MD · Icahn School of Medicine at Mount Sinai

Eligibility

Min Age
20 Years
Max Age
35 Years
Sex
FEMALE
Healthy Volunteers
Yes

Timeline & Regulatory

Start
2008-04-30
Primary Completion
2009-06-30
Completion
2009-06-30

Countries

  • United States

Study Locations

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Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT00694525 on ClinicalTrials.gov