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ABSTRACT
A screen of a range of bacteria normally found in gut flora identified eight with the ability to bind TSH specifically. These included the previously reported Yersinia enterocolitica, Gram-positive, Gramnegative, pathogenic and commensal organisms. Eleven preparations of TSH-receptor autoantibodies strongly able to displace 125I-labelled TSH from the mammalian TSH receptor differed in their ability to displace the tracer from binding to bacterial extracts. None could displace the tracer from E. coli 06–1, four displaced 125I-labelled TSH from E. coli V21/1 and five displaced the tracer from Y. enterocolitica. Of those immunoglobulin preparations which did react with the bacterial protein, their apparent potency compared with that of TSH in displacing tracer from bacterial binders was an order of magnitude greater than with the mammalian receptor. This is consistent with the autoantibodies having a relatively better fit with the bacterial antigen than with the receptor when compared with TSH. The bacterial-binding activity and mammalian receptor-binding activities in each of two samples co-chromatographed on a Remazol yellow GGL–Sepharose affinity column strongly indicated that the same immunoglobulin species reacts with both antigens. These results are consistent with the proposal that a bacterial protein is the primary immunogen for the TSH-receptor antibodies in at least some patients with Graves' disease.
Journal of Endocrinology (1989) 121, 571–577
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ABSTRACT
Turnover studies of thyroxine (T4), 3,5,3′-tri-iodothyronine (T3) and 3,3′,5′-tri-iodothyronine (rT3) have been performed in the rabbit. A novel modification of a conventional radioimmunoassay has been used to measure specific 125I-labelled iodothyronines in small volumes of plasma in the presence of other 125I-labelled metabolites. Kinetic analysis of plasma disappearance of tracer was performed by a new theoretical approach. For T4 the mean (±s.d.) plasma concentration, clearance and production rates were 34±12 nmol/l, 109±19 ml/kg per day and 3·7±1·4 nmol/kg per day respectively (n = 9). For T3 the corresponding values were 2·04±0·42 nmol/l, 1·52±0·29 litres/kg per day and 3·07±0·76 nmol/kg per day (n = 8), and for rT3 0·12±0·04 nmol/l, 5·7±1·7 litres/kg per day and 0·69±0·23 nmol/kg per day (n = 8). The combination of these two new methodologies affords a simple and convenient means of studying iodothyronine metabolism under normal and abnormal conditions. The techniques employed may be generally applied to turnover studies of other compounds of physiological interest which can be measured by radioimmunoassay.
J. Endocr. (1985) 106, 87–94
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Samples of cord blood derived from 105 normal babies after uncomplicated deliveries were assayed for thyroxine (T4), tri-iodothyronine (T3), reverse tri-iodothyronine (rT3), throxinebinding globulin (TBG) and thyrotrophin (TSH). The values for T3, rT3 and TSH were log-normally distributed (geometric means 0·62 nmol/l, 3·28 nmol/l and 10·9 mu./l respectively) and those for T4 and TBG were normally distributed (means 126 nmol/l and 13·7 mg/1). The data were systematically analysed and no evidence was obtained to suggest that the concentration of TSH, which varied widely, was regulated by any of the thyroid hormones alone or in combination. There was a direct relation between the concentrations of T4 and T3 in the cord blood at birth but not between either of these and rT3. There is thus no evidence of a functional interdependence of the hypothalamic-pituitary-thyroid system in man at birth.
