Abstract

Studies with laboratory animals have shown that pertechnetate ion is selectively concentrated in the thyroid gland, salivary glands and stomach, and selectively excluded from the cerebrospinal fluid almost to the same extent as inorganic iodide. Since the radionuclide technetium-99m gives extremely low energy dissipation in tissue, human studies were undertaken to evaluate pertechnetate-99m as a clinical tracer material. After intravenous administration, approximately 30% of the technetium-99m is excreted in the urine over the first 24 hr. The pertechnetate remaining in the body is evidently slowly metabolized, since the urinary excretion decreases markedly while fecal excretion increases progressively to a total of about 20% of the injected dose at 72 hr. In normal subjects, up to 2 % of the radioactivity from intravenously injected pertechnetate-99m is accumulated by the ion-concentrating mechanism of the thyroid at 1 hr, which corresponds closely to the accumulation of radioiodide in the gland blocked with methimazole. Both iodide and pertechnetate “trapping” are greatly increased (10–20 times) in diffuse toxic goiter. The ion-concentrating mechanism may thus be studied using pertechnetate-99m, without perturbing the gland with blocking agents. Such studies indicate that the ionconcentrating mechanism is under the control of thyroid-stimulating hormone in normal glands, but is autonomous in hyperactive thyroid nodules and Graves' disease. Thirty min after administering 1 me of pertechnetate-99m intravenously, good scans of the thyroid are obtainable with unmodified equipment, and the gland receives a radiation dosage of only 100 millirads, or 1/1000 of the dosage from 50 μc of 131I.

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