Читать книгу Graves' Orbitopathy - Группа авторов - Страница 67

The pathological processes within the orbit include:

•inflammatory infiltration of retro-ocular tissues within the orbit;

•expansion of the adipose tissue within the connective tissue located in (endomysium) and around (perimysium) the eye muscles and the fatty connective tissue which fills the intermuscular space;

•excess production by orbital fibroblasts of glycosaminoglycans (GAGs) resulting in an increase in the volume of the extraocular muscles and orbital fat/connective tissue (Fig. 1).

Orbit imaging shows a variable balance among patients between muscle enlargement (the most frequent abnormality observed) and expansion of orbital fat/connective tissue (Fig. 2). Preferential expansion of adipose tissue has been described in patients below 40 years of age, as has a predominant enlargement of extraocular muscles in older individuals with Graves’ orbitopathy (GO) [1].

Muscles may reach 2–3 times the normal volume, sometimes at the expense of the orbital fat tissue volume [2]. The inferior rectus muscle is predominantly affected, followed by the medial rectus, with the other muscles often being spared. Only the belly part of the muscles is affected, and the tendons remain unchanged, which differentiates GO from extraocular myositis. Swelling of tissues within the inextensible bony orbital cavity leads to an increase in intraorbital pressure. This has mechanical consequences which account for most of the signs and symptoms of GO.

Fig. 1. Interactions within the orbit between immune/inflammatory cells and orbit fibroblasts, and their functional consequences. The fibroblast is the central actor responsible for the deleterious effects of the upregulation of many of its functions. “Autoantibodies” refers to autoantibodies involved in the process: anti-TSH receptor and possibly anti-IGF-1 receptor antibodies. Expression of the TSH receptor occurs in preadipocytes during adipogenesis (not shown). GAG, glycosaminoglycan.