The Association of Costimulatory Molecules and PPAR-polymorphisms With Autoimmune Thyroid Disease in Taiwan

This study is enrolling participants by invitation only.
Sponsor:
Information provided by:
Taipei Medical University WanFang Hospital
ClinicalTrials.gov Identifier:
NCT01260532
First received: December 13, 2010
Last updated: NA
Last verified: December 2010
History: No changes posted
  Purpose

Autoimmune thyroid disease is the most common organ-specific autoimmune disease. AITD include Graves' disease and Hashimoto's thyroiditis. Although the pathogenesis of AITD remains unclear, it is generally thought that the mechanisms of the disease is a complex disease in which susceptibility genes and environmental triggers act in concert to initiate the autoimmune response to the thyroid.

The initial step of thyroid autoimmunity is the activation of T cells. The activation of T cell requires two signals: firstly, thyroid follicular cells or antigen presenting cells binds to T cell receptor through antigenic HLA complex. Secondly, the activation of T cells is also required the interaction of costimulatory molecules between thyroid follicular cells and immune cells, including CTLA-4, CD 40, CD28, ICOS. PPAR- is a kind of intranuclear transcription factor, associated with adipogenesis and inflammation. Some reports showed that PPAR- polymorphism may have a protective effect from Graves' ophthalmopathy.

The goal of the study is to investigate the relationship among SNP and mRNA of costimulatory molecules and PPAR- , serum cytokine including TNF- and sIL-2R, and clinical characteristics in AITD patients. From the study, we hope to clarify the role of costimulatory molecules and PPAR- polymorphism in AITD.


Condition
AITd Patients With Different Polymorphisms

Study Type: Observational
Study Design: Observational Model: Cohort
Time Perspective: Prospective
Official Title: The Association of Costimulatory Molecules and PPAR-polymorphisms With Autoimmune Thyroid Disease in Taiwan

Resource links provided by NLM:


Further study details as provided by Taipei Medical University WanFang Hospital:

Estimated Enrollment: 300
Study Start Date: July 2009
Estimated Study Completion Date: June 2019
Groups/Cohorts
Graves' disease
no intervention
Hashimoto's thyroiditis
no intervention
Healthy subjects
no intervention

Detailed Description:

Autoimmune thyroid disease is the most common organ-specific autoimmune disease. AITD include Graves' disease and Hashimoto's thyroiditis. Although the pathogenesis of AITD remains unclear, it is generally thought that the mechanisms of the disease is a complex disease in which susceptibility genes and environmental triggers act in concert to initiate the autoimmune response to the thyroid.

The initial step of thyroid autoimmunity is the activation of T cells. The activation of T cell requires two signals: firstly, thyroid follicular cells or antigen presenting cells binds to T cell receptor through antigenic HLA complex. Secondly, the activation of T cells is also required the interaction of costimulatory molecules between thyroid follicular cells and immune cells, including CTLA-4, CD 40, CD28, ICOS. PPAR- is a kind of intranuclear transcription factor, associated with adipogenesis and inflammation. Some reports showed that PPAR- polymorphism may have a protective effect from Graves' ophthalmopathy.

The goal of the study is to investigate the relationship among SNP and mRNA of costimulatory molecules and PPAR- , serum cytokine including TNF- and sIL-2R, and clinical characteristics in AITD patients. From the study, we hope to clarify the role of costimulatory molecules and PPAR- polymorphism in AITD.

  Eligibility

Ages Eligible for Study:   20 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Sampling Method:   Probability Sample
Study Population

Autoimmune thyroid patients

Criteria

Inclusion Criteria:

  • Autoimmune thyroid patients
  • patients who cut Nodular Goiter in Wanfang Hospital

Exclusion Criteria:

  • none
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01260532

Locations
Taiwan
Taipei Medical University - WanFang Hospital
Taipei, Taiwan
Sponsors and Collaborators
Taipei Medical University WanFang Hospital
Investigators
Principal Investigator: Jiunn-Diann Lin Taipei Medical University WanFang Hospital
  More Information

No publications provided

Responsible Party: Jiunn-Diann Lin, Division of Endocrinology and Metabolism
ClinicalTrials.gov Identifier: NCT01260532     History of Changes
Other Study ID Numbers: 98049
Study First Received: December 13, 2010
Last Updated: December 13, 2010
Health Authority: Taiwan: Department of Health

Keywords provided by Taipei Medical University WanFang Hospital:
Autoimmune thyroid disease

Additional relevant MeSH terms:
Thyroid Diseases
Hashimoto Disease
Endocrine System Diseases
Thyroiditis, Autoimmune
Thyroiditis

ClinicalTrials.gov processed this record on July 23, 2014