Apoptotic study in Graves disease treated with thyroid arterial embolization

Endocr J. 2009;56(2):201-11. doi: 10.1507/endocrj.k08e-232. Epub 2008 Nov 14.

Abstract

Objective: To investigate apoptosis in the thyroid of Graves disease (GD) induced by thyroid arterial embolization.

Materials and methods: Forty one patients with clinically and laboratorily ascertained GD were treated with thyroid arterial embolization and followed up for 3-54 months following embolization. Prior to embolization and at 1, 3, 6, 12 and 36 months following embolization, thyroid autoimmunue antibodies were tested respectively, including thyroid stimulating antibody (TSAb), thyroglobulin antibody (TGAb) and thyroid microsomal antibody (TMAb). Thyroid biopsy was performed under the guidance of computed tomography for immunohistochemistry examination using semi-quantity analysis.

Results: The positive staining of Fas and FasL was mostly in the cytoplasma and cell membrane, the positive expression of Bax was mainly in the cytoplasma, and no positive expression of P53 was detected in the thyroid cells before embolization. After arterial embolziation, the positive cell number and staining degree of these genes were both greater than before embolization.

Conclusion: The treatment method of thyroid arterial embolization can effectively enhance the positive expression of pro-apoptotic genes of Fas, FasL, Bax, Bcl-2 and P53 in GD thyroid, thus promoting apoptosis of GD thyroid and helping restore the thyroid size and function to normal conditions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Apoptosis / immunology*
  • Arteries
  • Autoantibodies / blood
  • Embolization, Therapeutic*
  • Fas Ligand Protein / biosynthesis
  • Female
  • Gene Expression
  • Graves Disease / immunology*
  • Graves Disease / physiopathology
  • Graves Disease / therapy
  • Humans
  • Male
  • Middle Aged
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Thyroid Gland / blood supply
  • Thyroid Gland / immunology*
  • Thyroid Hormones / blood
  • Tumor Suppressor Protein p53 / biosynthesis
  • bcl-2-Associated X Protein / biosynthesis
  • fas Receptor / biosynthesis

Substances

  • Autoantibodies
  • FASLG protein, human
  • Fas Ligand Protein
  • Proto-Oncogene Proteins c-bcl-2
  • Thyroid Hormones
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • fas Receptor