Thyroid Eye Disease

  • Rebecca S. Bahn

Part of the Endocrine Updates book series (ENDO, volume 14)

Table of contents

  1. Front Matter
    Pages i-xii
  2. Pathogenesis

    1. Anthony P. Weetman, E. Helen Kemp, Jonathan N. Ridgway, Philip F. Watson
      Pages 1-20
    2. Armin E. Heufelder, Werner Joba
      Pages 21-36
    3. Natee Munsakul, Rebecca S. Bahn
      Pages 37-44
    4. Yuji Hiromatsu, Tomasz Bednarczukt
      Pages 45-65
    5. Marian Ludgate, Glynn Baker
      Pages 67-81
  3. Disease Evaluation

    1. P. Perros, A. J. Dickinson, P. Kendall-Taylor
      Pages 119-136
    2. George J. Kahaly, Wibke Müller-Forell, Gregor J. Förster, Susanne Pitz, Hans Peter Rösier, Wolf J. Mann
      Pages 137-162
    3. Maarten P. Mourits
      Pages 185-200
  4. Treatment

    1. Mark F. Prummel
      Pages 201-218
    2. Elizabeth A. Bradley, George B. Bartley, James A. Garrity
      Pages 219-233
    3. Henry B. Burch
      Pages 235-248
  5. Back Matter
    Pages 249-253

About this book

Introduction

Patients aftlicted with thyroid eye disease or Graves' ophthamopathy (GO) may experience not only pain and visual loss, but also disfigurement. Full understanding of pathogenesis has been elusive, and treatment modalities are imperfect. As with other conditions, more effective intervention will follow only after a better understanding of pathogenesis is reached. The goal of this volume is to give an overview by leaders in the field of the present state of the art both in pathogenesis and clinical aspects of GO. Much attention has been directed towards determining which cells within the orbit are targets of the autoimmune process, and how these and other cells might participate in the local inflammatory process. It is now generally agreed that orbital fibroblasts, preadipocyte fibroblasts, and adipocytes are the targeted and activated cells in GO and that full-length TSH receptor (TSHr) is expressed in these cells. Further, there is growing consensus that this receptor is up-regulated in the orbit in GO, residing primarily in newly differentiated adipocytes. However, it is also evident, given a sufficiently sensitive assay, that TSHr is detectable in fibroblasts and adipocytes from the normal orbit and other anatomic sites, as well. It will be important to determine whether the observed increase in orbital TSHr expression itself initiates the orbital autoimmune process. Also to be decided is whether orbital lymphocytes from GO patients specifically recognize this receptor, and what factor or factors unique to Graves' dIsease might stimulate TSHr expression in orbital cells.

Keywords

Antigen autoimmunity cytokine eye pathogenesis

Editors and affiliations

  • Rebecca S. Bahn
    • 1
  1. 1.Division of Endocrinology, Department of Internal MedicineMayo Clinic and FoundationRochesterUSA

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4615-1447-3
  • Copyright Information Kluwer Academic Publishers 2001
  • Publisher Name Springer, Boston, MA
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4613-5558-8
  • Online ISBN 978-1-4615-1447-3
  • Series Print ISSN 1566-0729
  • About this book