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Atger M et
al., Lyon, France, devised an ELISA test using the native
purified TSH-receptor (TSHR) to study anti-TSHR autoantibodies in
48 subjects with untreated Graves’ disease and 47 healthy
volunteers. Positive results were found in 45/48 and 26/47
respectively. The affinity of the antibodies to the receptor was
similar in both groups, but the concentration was significantly
higher in the patients with Graves’ disease. The authors
conclude that autoantibodies against the TSHR occur in a great
number of normal subjects and are not pathogenic per se. However
in some individuals a sub-population of the autoantibodies
(<10% of total TSHR antibodies) is present that specifically
bind to receptor-activating regions, as was confirmed by their
cAMP stimulating activity. (Comment: It seems thus that only
binding of TSHR antibodies to specific epitopes on the TSHR, that
have cAMP stimulating activity, may be pathogenic in the
development of Graves’ disease).
Santos et al., Lisbon, Portugal, evaluated stressful life events (SLE) in the genesis of Graves’ disease and toxic goitre in 31 patients with Graves’ disease (22 females, mean age 38.48 years), 31 patients with toxic goitre (22 females, mean age 48.3 years), and 31 controls (22 females, mean age 41.1 years). SLE evaluation (number and impact) was reported from the 12 months preceding the onset of symptoms in both patient groups. SLE measurement was done using Life Experiences Survey-LES from Saranson et al. SLE were significantly greater in number in Graves’ disease versus toxic goitre and healthy controls (p<0.01). Impact of negative SLE was significantly higher in Graves’ disease as compared to toxic goitre and controls (p<0.01). Graves’ disease had more positive SLE than toxic goitre (p<0.05). No differences were present between toxic goitre and controls with regard to negative and positive SLE. Neutral SLE were similar in the three groups. The authors suggest SLE as a precipitating factor in Graves’ disease. (Comment: the number of reports suggesting stressful life events as a precipitating factor in the development of Graves’ disease is increasing in recent years). Paschke et al., Leipzig, Germany, studied thyrotropin binding inhibiting immunoglobulins (TBII), thyroid stimulating antibodies (TSAB), and thyrotropin stimulating blocking antibodies (TSBAB) in 63 patients with Graves’ disease, at the time antithyroid drug treatment (given for 2 years) was stopped and 1 year later. Twenty-seven patients stayed in remission, whereas 36 patients were in a relapse. In patients in remission, there was a significant decrease in TSAB whereas TBII and TSBAB were not changed one year after discontinuation of drug treatment. Combined measurement of TSAB and TSBAB (loss of TSAB and transition of TSAB to TSBAB and vice versa) showed a higher prognostic significance for remission prediction (P = 0.0001) than measurement of TSAB alone. In relapsed patients no significant changes were seen in activities of the three parameters. Kawar et al., Newcastle, UK, evaluated the effect of a fixed dose (400 MBq) (38 patients) or a graded dose related to thyroid mass (mean dose 185 MBq) (111–259 MBq) of 131I in patients with Graves’ disease. Percentage hypothyroidism one year after treatment was 68% vs 41% (p <0.05) respectively, euthyroidism 26% vs 41% (NS), hyperthyroidism 5% vs 17% (NS). The authors conclude that the relative benefits of the two treatment modalities needs to be assessed in the context of the relative morbidity and mortality of persistent hyperthyroidism vs T4 substituted post-RAJ hypothyroidism. (Comment: My personal feeling is that for the time being early hypothyroidism is preferred over a high rate of relapse, if only on a cost benefit basis). Duntas et al., Athens, Greece, measured urinary thyocyanates (TCN) as a parameter for smoking and urinary iodide, and serum TSH and thyroid hormone concentrations in patients with hyperthyroidism who were smokers (n = 23) or non-smokers (n = 16) and in 60 controls of whom 29 were smokers and 31 non-smokers. They found increased TCN and iodide in hyperthyroids as compared to controls. In hyperthyroid smokers TCN levels were highest whereas iodide excretion was highest in non-smoking hyperthyroids. No correlation was found between TCN and thyroid eye disease (TED), either measured with NOSPECS or Clinical Activity Score (CAS). The marginally but statistically increased TCN levels in hyperthyroid non-smokers as compared to controls me be caused by altered clearance and/or accelerated conversion of cyanide to TCN. Furthermore, TCN apparently lowers iodide excretion in the urine. (Comment: Remarkable is that in this study no association was found between TCN and TED contrary to other reports in the literature.) |
