Role of Chemokines and Proinflammatory Cytokines in Rheumatoid Synovial Pathological Changes

NCT00845949 · Status: WITHDRAWN · Type: OBSERVATIONAL

Last updated 2012-05-21

No results posted yet for this study

Summary

Rheumatoid arthritis is a common chronic destructive arthritis. Major pathology change in rheumatoid arthritis is synovium hyperplasia with bone and cartilage erosion. Infiltrates in synovial tissue included type one and type two synoviocytes, B cells, T cells and fibroblasts. These cells will release many cytokines and chemokines, which will induce expression of adhesion molecules, release of variable enzyme from fibroblast and osteoclast and result in bone erosion.

Recent study revealed that fibroblast-like synoviocytes (FLS) have some role in pathogenesis of rheumatoid arthritis.We believed CXCL12/CXCR4 ligand/receptor pair is important in chronicity of rheumatoid arthritis.

CXCL12 polymorphism is studied in many disease. There is no related CXCL12 polymorphism study in rheumatoid arthritis. Our study intended to clarify the relationship between pathology, serology factor, CXCL12 polymorphism in rheumatoid arthritis in hope that new direction of therapy will be elucidated.

Conditions

Sponsors & Collaborators

  • Far Eastern Memorial Hospital

    lead OTHER

Principal Investigators

  • Chien-Sheng Wu · Division of Allergy, Autimmunity and Rheumatology, Department of Internal Medicine

Eligibility

Min Age
18 Years
Max Age
90 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2006-11-30
Primary Completion
2008-06-30
Completion
2008-06-30

Countries

  • Taiwan

Study Locations

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Entities

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 NCT00845949 on ClinicalTrials.gov