Graves' ophthalmopathy (GO)
  Isozaki et al., Tokyo, Japan, studied the effects of somatostatin and its analogue octreotide on the proliferation of fibroblasts taken from retro-orbital tissue of patients operated for Graves' ophthalmopathy. They performed this study because Graves' ophthalmopathy patients have been successfully treated with octreotide showing a decrease in proptosis. Proptosis in Graves' ophthalmopathy is, at least in part, caused by proliferation of fibroblasts leading to increased synthesis of glycosaminoglycans. Their studies showed that both somatostatin and octreotide have a potent inhibitory activity on proliferation of these fibroblasts and the effect was not signaled via the TSH receptor. Szucs-Farkas et al., Debrecen, Hungary, measured muscle volume and connective tissue volume in 50 orbits of 25 patients with Graves' ophthalmopathy and in 20 orbits of 10 healthy controls using magnetic resonance imaging. They found that the major contributor to eye protrusion in Graves' ophthalmopathy is muscle enlargement while contribution of connective tissue expansion is less marked. (Comment: an important common factor for volume expansion of retro-orbital connective tissue and extra-ocular muscles is the proliferation of fibroblasts with secondary water retention by produced glycosaminoglycans.) Lisi et al., Pisa, Italy, studied the distribution of thyroglobulin in orbital tissues from patients with GO. They did this because several decades ago Kriss et al. hypothesized that retrograde transported Tg via the lymphatics could move to retro-orbital tissues and in this way act as an autoantigen in the pathogenesis of the ophthalmopathy. The authors found Tg, using immunoprecipitation, in 3/7 patients and, using ELISA, in 4/7 cases in retrobulbar fibroadipose tissue and in inflamed palpebral skin. In addition, ELISA Tg was also detected in extra-ocular muscles. The results support the previously forwarded hypothesis by Kriss, in that Tg may act as a co-antigen in the pathogenesis of GO.