Measurements of serum triiodothyronine (T3) concentrations were made in 46 patients who had thyroid ablation for thyroid cancer and who were receiving T3 three times a day as suppressive treatment. In all patients thyrotropin (TSH) suppression was confirmed by the inhibition of TSH response to thyrotropin releasing hormone (TRH). The suppressive dose of T3 varied from 40 to 100 micrograms/day (mean +/- SD 72.39 +/- 13.07 micrograms/day). Related to body weight the dose varied from 0.95 to 1.35 micrograms/kg/day (mean +/- SD 1.13 +/- 0.13 micrograms/kg/day). In ten hospitalized patients serum T3 levels were measured at hourly intervals from 08:00 to 23:00. Before the first dose of T3, serum T3 levels were 153 +/- 43 mg/100 ml; after T3 the levels increased promptly reaching after 4 h a peak of 264 +/- 90 ng/100 ml. Afterwards T3 levels showed a similar peak after each dose: 262 +/- 77 and 266 +/- 78 ng/100 ml, slightly decreasing in the intervals between the doses: 227 +/- 63 and 255 +/- 69 ng/100 ml. After the last peak T3 levels showed a slow decline during the night. TSH response to TRH was completely inhibited both at 08:00 and at 16:00. In 36 outpatients T3 levels were measured twice a day and T3 levels were found similar to the ones of the first group. In these patients also TSH response to TRH evaluated at 08:00 was completely inhibited. No important side effect was noted in both groups of patients.

Circadian Rhythm↗

PubMedDate not supplied

Carcinoembryonic antigen in thyroid cancer.

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Carcinoembryonic Antigen↗

PubMedDate not supplied

Clinical role of TSH binding inhibiting antibodies (TBIAb) assay.

Anti TSH-receptor antibodies (TBIAb) were measured by a radioreceptor assay in 277 patients with Graves' disease, 101 with autoimmune thyroiditis, 43 with autonomous adenoma, 15 with subacute thyroiditis, 15 with euthyroid ophthalmopathy, 155 with euthyroid multinodular goiter, 10 with amiodarone-induced hyperthyroidism and 2 with tumoral TSH hypersecretion. TBIAb were present at high titers in 74% of patients with untreated or relapsed Graves' disease and, at lower titers, in only 10% of patients who had recovered from Graves' disease, in 8% of patients with autoimmune thyroiditis and in 4% of patients with euthyroid goiter. TBIAb were absent in normal subjects as well as in the other groups studied. These findings suggest that TBIAb represent a specific marker of Graves' disease, particularly of the untreated form. Their presence in non Graves' patients may be considered expression of inactive or inhibiting antibodies.

Antibodies↗