THYROID

Thyroid

Thyroid

Introduction

Thyroid orbitopathy (TO) is most prevalent among females in the fourth and fifth decades and is usually associated with thyroid dysfunction. Clinical manifestations include soft tissue signs, lid retraction, lid lag, proptosis, restrictive myopathy, corneal exposure and optic neuropathy. Thyroid function tests are essential, while thyroid antibodies and imaging to demonstrate extraocular muscle enlargement, may also aid diagnosis. Correction of thyroid dysfunction and supportive measures are necessary in all cases. Immunosuppression is reserved for moderate to severe active orbitopathy and rehabilitative surgery is generally used once the disease is quiescent.

Pathophysiology

Despite evidence for an autoimmune aetiology, the precise pathophysiology of TO remains unknown. The inflammatory response is centred on the extraocular muscles and orbital connective tissue, and is thought to arise from autoantibody cross-reactivity between thyroid and orbital antigens6. There are two distinct stages - an active inflammatory stage followed by a quiescent stage. The inflammatory phase is characterised by lymphocytic infiltration, interstitial oedema and mucoglycoprotein deposition within the extraocular muscles and orbital fat2,3,7. Inactive disease is distinguished by fibrosis and fatty infiltration of the orbital tissues. Daniels GH, Eastman RC, Johnston HH, Kohler PO et al (1979) Cyclophosphamide in the management of advanced Graves' ophthalmopathy. A preliminary report. Ann. Intern. Med. 90: 921-923.

Clinical features

Patients often report a change in the appearance of their eyes and perusal of old photographs may be helpful. Periorbital swelling is worse in the mornings, and diplopia, retrobulbar discomfort, and pain on eye movement are other presenting. The cardinal signs are axial proptosis, eyelid retraction and lid lag. In fact, TO is the most common cause of bilateral, asymmetric and unilateral proptosis in adults3 Although progression of signs such as muscle restriction and the presence of soft tissue inflammation are suggestive of activity, the differentiation of active from inactive orbitopathy can be problematic.

Background

In many respects these thyroid hormones can be likened in their action to the speed control on a record player. They regulate the metabolic activity of all body cells and tissues. Too little thyroid hormone means that the body cells work at too slow a rate. The result is much the same as playing a 45r.p.m. record at 331/3 r.p.m.; it is slowed and sluggish. By contrast too much hormone induces the cells to work too fast, like playing a 45 r.p.m. record at 63 r.p.m. and the result is the “chipmunk” effect (Epps 1995). Although the two thyroid hormones influence the proper working of all body cells, their effect is particularly evident in certain functions. For example growth and development, both physical and mental, depend upon the presence of an adequate amount of thyroxine. Without thyroxine a tadpole will not metamorphose into a frog, and without thyroxine a newborn baby will not grow properly nor will its brain develop properly. Thyroxine regulates the rate of oxygen consumption, which is another way of saying it controls the speed of activity of body cells(Morgan 1996). The secretory activity of the thyroid gland is regulated by the pituitary gland's secretion of thyroid-stimulating ...