Graves' disease
	Brix et al., Odense, Denmark, studied genetic factors in Danish twin pairs with Graves' disease (18 monozygotic and 33 dizygotic). In the monozygotic twins the probandwise concordance rate was 0.36, whereas this figure was 0.0 in the dizygotic twins. The authors conclude that genetic factors are certainly important in the etiology of Graves' disease, however, not as powerful as previously thought. They indicate that in the past concordance rates were reported between 0.66 and 0.86 but that no serious effort was made to distinguish between Graves' disease and other types of hyperthyroidism. Poertl et al., Essen, Germany, tested whole (unfractionated) sera for thyroid stimulating antibodies (TSAb) activity, based on cyclic AMP stimulation in CHO cells transfected with the human TSH receptor. They tested sera of 162 patients with Graves' disease (38 untreated, 78 during medication and 46 in remission) and of 85 normal controls. The diagnostic sensitivity of this assay in active Graves' disease was 97% and the test was positive in 77% taking all patients together. The correlation with TBII (TSH binding inhibiting immunoglobulins) activity was poor and the results of the two assays may dissociate under therapy. The authors suggest further investiga-tions to evaluate the test for its prognostic significance. Michelangeli et al., Melbourne, Australia, measured thyroid immunoreactivity in 244 patients (206 females) who attended a large teaching and referral hospital in Papua New Guinea for signs and symptoms of thyrotoxicosis between April '94 and December '96. Serum measurements included antibodies against TG (TGAb), thyroperoxidase (TPOAb), the TSH-receptor measured as thyroid stimulating antibodies (TSAb), and as TSH-binding inhibition immunoglobulins (TBII). TPOAb, TGAb, TBII, and TSAb were elevated in 96%, 43%, 58%, and 34% of patients respectively. In 98% of patients, at least one antibody was present. TPOAb was markedly elevated in 82% of patients with levels above 2 SD, 58% had elevated levels of TPOAb and TBII, 42% of TPOAb and TGAb, and 27% of all antibodies. The authors conclude that autoimmune thyroid disease is by far the commonest cause of thyrotoxicosis in this area. Romaldini et al., Sao Paulo, Brazil, followed 139 patients with Graves' disease who were treated with propylthiouracil (PTU) or methimazole (MMI) without any period of recurrence after discontinuation of medication. 13/139 Patients with a median age of 41 years developed spontaneous hypothyroidism. The incidence of hypothyroidism was 2.3% per year. The development of hypothyroidism occurred between 4 and 144 months after medication withdrawl. Patients were treated with antithyroid drugs for a median period of 15.5 months. TPOAb were higher in those patients who developed hypothyroidism than in those who remained euthyroid. Gupta et al., Cleveland, OH, USA, and Halifax, Nova Scotia, measured TSAb and TBAb (= blocking antibodies) using CHO cells transfected with the human TSH receptor and TBII before and 2 and 6 months post 131 therapy in 17 newly diagnosed patients with Graves' disease, and compared results with 20 patients with Graves' disease treated with methimazole. They found a significant decrease of TSAb with a concomitant increase of TBII at 2 and 6 months after 131 therapy. TBAb was only increased 2 months post 131 therapy. In the methimazole treated group a small decrease of TSAb and increase of TBAb was seen, but no change in TBII. Apparently 131 therapy has a selected effect on TBII levels, the significance of which is not known so far.