Graves' disease
	Coles et al., Cambridge, Oxford, and Sheffield, UK, reported in 12/34 patients, who were depleted of 95% of circulating lymphocytes (by using anti- lymphocyte monoclonal antibody) for multiple sclerosis, unexpected development of carbimazole-responsive Graves' disease, 6-31 months after treatment. In these 12 patients, biochemical hyperthyroidism, increased thyroidal RAI uptake and antibodies to the TSH receptor were present. Prevalence of HLA DR3 and/or DR7 was significantly increased. The authors report that similar treatment of other diseases does not seem to cause autoimmune thyroid disorders. Pratt et al., Sutton, UK, studied factors that influenced the response to 50 Gy 131I for active Graves' disease in 50 patients. At 12 months 26/50 patients still required antithyroid drugs, 20/50 patients were euthyroid, and 4/50 patients used T4 supplements. There were no differences between these groups with regard to pretreatment thyroid 131I uptake and effective thyroidal half-life of 131I. The mean functional thyroid volume was slightly higher in the patients still on antithyroid drugs than in the euthyroid patients (19 vs 15 ml). By 18 months only 2/50 patients were still requiring antithyroid drug treatment and 44/50 patients were euthyroid (3 requiring a second dose 131I). The authors conclude that in the majority of cases euthyroidism can be achieved after a single dose of radioactive iodine, but euthyroidism may appear later in those patients with a higher thyroid volume. (Comment: This study is one of the so many that have been reported on the outcome of thyroid function after treatment with radioactive iodine in patients with Graves' disease. The results have so far limited value in that follow-up time is really very short.) Daumerie et al., Brussels, Belgium, studied the etiology of pretibial myxedema in 2 patients with this entity in combination with Graves' disease and thyroid associated ophthalmopathy (TAO). The TSH receptor (TSH-R) is considered to be responsible for thyroidal hyperfunction in Graves' disease and maybe also for TAO as reports have suggested expression of this peptide in orbital tissue. In the present report, positive staining, using two monoclonal antibodies against TSH-R, was found in the dermis of 2 patients with pretibial myxedema and not in the dermis of 2 controls. (Comment: Although only 2 patients were studied, the importance of this report lies in the fact that the end product of gene expression i.e. the TSH-R protein was identified. One should realize that in studies where the presence of the mRNA is found, this does not mean that the protein is always expressed.) Evans et al., Cardiff and Cambridge, UK, report the development of a bioluminescent assay potentially suitable for routine measurement of TSH-R antibodies. As a target cell responsive to measure TSH-R stimulation by TSH, a Chinese Hamster Ovary cell line expressing TSH-R was used and that was stably cotransfected with the cAMP responsive luciferase reporter construct. Preliminary results show 11-24 fold stimulation using a range of 1-10 mU/mL bovine TSH. (Comment: This bioassay has a nice sensitivity. Preliminary results for detection of TSH-R antibodies are promising.) Morgenthaler et al., Berlin, Germany, and Brussels, Belgium, also developed an assay to measure TSH-R antibodies. They use a system in which circulating TSH-R antibodies compete with labeled TSH for binding to affinity immobilized human recombinant TSH-R. In 94/100 patients with Graves' disease serum was positive for inhibition of TSH binding. The authors state that the human origin of the antigen (TSH-R) and reduced non-specific binding in the solid fase assay, increase clinical sensitivity. (Comment: This assay seems promising for routine use with a high sensitivity. Further clinical studies should show this.)