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Graves' Orbitopathy


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of fat has recently been reported to be more abundant in adult humans than previously anticipated, especially in smokers [37], and, as discussed below, smoking is a major risk factor for the development of GO.

      Other factors that could contribute to the association of thyroid and orbit pathologies:

      Upon infiltrating the orbit, inflammatory cells, T and B lymphocytes, macrophages and mast cells interact with orbital fibroblasts through a whole array of cytokines. This interplay amplifies and perpetuates inflammatory/autoimmune reactions and activation of fibroblasts. However, as shown by the Rundle curve, evolution of GO is monophasic and appears as self-limited, and fibrosis ultimately develops, notably in the extraocular muscles.

      •increase the expression of HLA class 2 molecules, heat shock protein 72 and ICAM-1;

      •stimulate the production of prostaglandin E2, a modulator of the immune response;

      •stimulate the production of chemoattractants (IL-16, RANTES) as well as IL-6;

      •enhance the synthesis of GAGs;

      •stimulate adipocyte differentiation (TGF-β, IFN-γ and IL-1, but not IFN-α);

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      Fig. 4. Exacerbation of the production of glycosaminoglycans, notably of hyaluronan, by the fibroblasts is central to the swelling of retro-orbital tissues. Since orbital fibroblasts do not express hyaluronidase, hyaluronan accumulates. Also, the turnover of the extracellular matrix is modified by the increased expression of proteinase inhibitors which leads to changes in the structure of the adipoconnective tissue.

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