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
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 April 15, 2014