Thyroid Eye Disease

1. Front Matter

   Pages i-xii

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2. Pathogenesis

   1. Orbital Autoantigens

      • Anthony P. Weetman, E. Helen Kemp, Jonathan N. Ridgway, Philip F. Watson

      Pages 1-20

   2. Orbital Autoimmunity in Graves’ Disease

      • Armin E. Heufelder, Werner Joba

      Pages 21-36

   3. Adipogenesis and TSH Receptor Expression

      • Natee Munsakul, Rebecca S. Bahn

      Pages 37-44

   4. Role of Cytokines in the Pathogenesis of Graves’ Ophthalmopathy

      • Yuji Hiromatsu, Tomasz Bednarczukt

      Pages 45-65

   5. Animal Models of Graves’ Ophthalmopathy

      • Marian Ludgate, Glynn Baker

      Pages 67-81

   6. Participation of Orbital Fibroblasts in the Inflammation of Graves’ Ophthalmopathy

      • Terry J. Smith

      Pages 83-98

   7. Genetic and Environmental Contributions to Pathogenesis

      • Wilmar M. Wiersinga

      Pages 99-118

3. Disease Evaluation

   1. Clinical Presentation and Natural History of Graves’ Ophthalmopathy

      • P. Perros, A. J. Dickinson, P. Kendall-Taylor

      Pages 119-136

   2. Imaging in Graves’ Ophthalmopathy

      • George J. Kahaly, Wibke Müller-Forell, Gregor J. Förster, Susanne Pitz, Hans Peter Rösier, Wolf J. Mann

      Pages 137-162

   3. Quality of Life Measurement in Patients with Graves’ Ophthalmopathy

      • C. B. Terwee, Martin Gerding

      Pages 163-183

   4. Assessment of Disease Activity

      • Maarten P. Mourits

      Pages 185-200

4. Treatment

   1. Immunosuppressive Therapy

      • Mark F. Prummel

      Pages 201-218

   2. Surgical Management of Graves’ Ophthalmopathy

      • Elizabeth A. Bradley, George B. Bartley, James A. Garrity

      Pages 219-233

   3. Orbital Radiotherapy: An Update

      • Henry B. Burch

      Pages 235-248

5. Back Matter

   Pages 249-253

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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.

• Antigen
• autoimmunity
• cytokine
• eye
• pathogenesis
• diabetes

`Of interest to general endocrinologists, pediatric endocrinologists and ophthalmologists '
Journal of Pediatric Endocrinology and Metabolism, 15:4 (2002)

• Division of Endocrinology, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, USA

  Rebecca S. Bahn

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