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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.
List of contents
Pathogenesis.- 1. Orbital Autoantigens.- 2. Orbital Autoimmunity in Graves' Disease..- 3. Adipogenesis and TSH Receptor Expression.- 4. Role of Cytokines in the Pathogenesis of Graves' Ophthalmopathy.- 5. Animal Models of Graves' Ophthalmopathy.- 6. Participation of Orbital Fibroblasts in the Inflammation of Graves' Ophthalmopathy.- 7. Genetic and Environmental Contributions to Pathogenesis.- 8. Clinical Presentation and Natural History of Graves' Ophthalmopathy.- 9. Imaging in Graves' Ophthalmopathy.- 10. Quality of Life Measurement in Patients with Graves' Ophthalmopathy.- 11. Assessment of Disease Activity.- 12. Immunosuppressive Therapy.- 13. Surgical Management of Graves' Ophthalmopathy 219 Elizabeth A..- 14. Orbital Radiotherapy: An Update.
Summary
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.
Additional text
`Of interest to general endocrinologists, pediatric endocrinologists and ophthalmologists '
Journal of Pediatric Endocrinology and Metabolism, 15:4 (2002)
Report
`Of interest to general endocrinologists, pediatric endocrinologists and ophthalmologists '
Journal of Pediatric Endocrinology and Metabolism, 15:4 (2002)
