L'utilisation du radio-iode dans l'étude de la fonction thyroïdienne a permis de mettre en évidence le rôle important du foie dans l'élimination et la destruction des hormones thyroïdiennes. En effet, après l'injection de thyroxine marquée à l'131I on constate que cette hormone passe rapidement du sang dans les différents organes et surtout dans le foie où elle subit les processus d'inactivation, de dégradation et enfin d'élimination. Les travaux de Gross & Leblond (1947) nous indiquent que deux heures après l'injection, le 65 % de la radioactivité se trouve fixé dans les principaux organes pour tomber à 46% 24 heures après. L'organe le plus riche en radioactivité est le foie. Celui-ci contient, en effet, 9 à 24 % de composés organiques de radio-iode deux heures aprés l'injection de doses physiologiques de thyroxine marquée et seulement 4 à 8 % 24 heures aprés l'injection. L'injection d'iodures radioactifs donne des résultats similaires; dans ce
Th. Béraud, B.-R. Scazziga and A. Vannotti
Th. Lemarchand-Béraud, B. R. Scazziga and A. Vannotti
A radioimmunoassay has been developed and was applied in a first study to the determinations of human plasma TSH in normal subjects. In the present work a systematic study was made of the relation between the pituitary and the thyroid gland in thyroid disease, and on the effect of various forms of treatment in 750 patients. Normal values for adults of both sexes were found to be 0.19 mU/ml, referred to the international bovine TSH standard (USP).
No TSH was found in pituitary hypothyroidism. Elevated levels, up to fifteen times those of normal subjects, were found in myxoedema. The low initial values in all forms of thyrotoxicosis were followed by modifications during treatment depending on the kind of treatment used. Every qualitative or quantitative deficiency of thyroid hormone secretion was accompanied by an elevation of TSH (euthyroid nodular goitre, thyroid carcinoma, subacute thyroiditis and Hashimoto's disease) and treatment with thyroid hormones induced a rapid fall in plasma TSH. The action of lysine vasopressin was also studied.
Th. Lemarchand-Béraud, A.-Ch. Holm and B. R. Scazziga
In an investigation of thyroxine (T4) and triiodothyronine (T3) receptors in humans, the lymphocyte was chosen as the target cell. This study was performed to elucidate whether T3 and T4 bind to different receptors, if T4 is bound only after conversion into T3, and whether there is any modification of the receptors in hyper- and hypothyroidism. Lymphocytes were found to possess a high-affinity, limited-capacity binding sites for both T4 and T3. The mean equilibrium affinity constant (Ka) was 2.28 · 1010 ± 0.21 m −1 for T3, and 0.98 · 1010 ± 0.16 m −1 for T4. The mean number of saturable binding sites was 115 for T3, and 102 for T4. The binding capacities and affinities also determined in the lymphocyte nuclei isolated after incubation of the intact cell, were similar to those observed in the intact cells. In competition experiments, labelled T4 was as readily displaced by T3 as by T4 itself, whereas labelled T3 was displaced only by a 40 times higher concentration of T4 than T3. These observations suggest identical receptors for the two hormones and a binding of T4 as such, provided it is not in competition with T3. In lymphocytes from hyperthyroid patients, receptor affinities and numbers remained unchanged. In lymphocytes from hypothyroid patients, the affinity was normal, but the mean number of T3 binding sites was increased to 310 (P < 0.001), to return to normal after a few months of treatment.
U. Bürgi, B. R. Scazziga, P. O. Rosselet, H. Bürgi and H. Studer
Abstract. Serum thyroglobulin and goitre size were followed in 22 patients with simple goitre or single thyroid nodules during 9 months of thyroxine therapy, to see whether alterations in serum thyroglobulin correlated with changes in goitre size. In the case of such a correlation serum thyroglobulin could be used to predict which goitres respond to thyroxine therapy and which require surgery. Pretreatment serum thyroglobulin was elevated in 11 patients. It normalized in one of 7 patients whose goitre did not shrink and in none of the 4 patients whose goitre shrank during thyroxine treatment. Thus no simple correlation exists between alterations in serum thyroglobulin and goitre size during short-term thyroxine therapy. Since other studies suggest that increased serum thyroglobulin indicates ongoing goitre growth, thyroxine treatment might have been unsuccessful in all patients with persistently elevated serum thyroglobulin with a longer follow-up. The presence of predominantly thyroxine responsive tissue together with some autonomously growing, thyroglobulin-releasing areas in the same goitre could explain the failure of serum thyroglobulin to normalize in patients whose goitre shrank during therapy. The study shows that after eradication of iodine deficiency, thyroxine treatment is rarely successful in the Swiss goitre population and that surgical treatment is usually required.