IN VITRO TEST FOR EVALUATION OF THYROID FUNCTION.
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Secondary thyroid function tests were compared in 41 mildly thyrotoxic and 36 euthyroid patients with an elevated free thyroxine index (FT4I). A serum TSH measurement 20 minutes after intravenous TRH (delta TSH) most reliably separates these two groups. A significant delta TSH response (greater than 0.5 microU/ml) is also helpful in excluding clinical thyrotoxicosis in patients with nodular goitre. The free T3 index was normal in one-third of mildly thyrotoxic patients and in all euthyroid patients with a falsely elevated FT4I. Blunted delta TSH responses to TRH in elderly New Zealand women were associated with nodular goitre or occult thyroid nodularity revealed only by thyroid scan. The reduced TRH responses are more likely due to partial thyroid autonomy than reduced synthetic capacity of thyrotrophs in old age.
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After administration of the dopamine-receptor-blocking drug, metoclopramide (10 mg orally), there is significant release of thyrotrophin (T.S.H.) in hypothyroid patients which is not evident in euthyroid subjects. This is not due to spontaneous fluctuation in basal T.S.H. levels, and it indicates inhibitory dopaminergic control of T.S.H. release in man. The lack of significant T.S.H. release in euthyroid subjects may be due to the inhibitory effects of normal circulating levels of T3 and T4 on T.S.H. release. The T.S.H. response in hypothyroidism is significantly correlated with both T3 and T4 levels, suggesting suppression of this inhibitory pathway in increasingly severe hypothyroidism.
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A study of 1167 children (age: 7-15 years) inhabiting districts contaminated with radionuclide due to Chernobyl atomic station accident indicates that children with thyroid hyperplasia revealed high requirement and intensity of the peripheral metabolism of thyroid hormones that results finally in relative hormonal deficit (subclinical hypothyroidism) and thyroid hyperplasia. This is a sequel of maximum functional tension of the thyroid with impending breakdown of adaptation and this should be considered as a pathological process requiring correction, i.e. presence of subclinical hypothyroidism in children with thyroid hyperplasia requires substitution therapy with thyroid hormones.
A study was made of pituitary-thyroid function in patients with different forms of schizophrenia. Radioimmunoassay was used. All the patients with schizophrenia showed impairment of interrelations within the pituitary-thyroid system, which manifested by accumulation in the peripheral blood of metabolically active T3 due to enhanced degradation of T4 in the peripheral tissues. The rise of TTH concentration represents one of the mechanisms of correction, aimed at the attainment of the physiological content of T4 at the expense of its additional output for its level in the blood serum is appreciably reduced.
We studied 10 patients with subacute thyroiditis. All had an increase in free thyroxine index, PBI, T4 and PBI/T4 ratio, an absence of thyroidal radioiodine uptake and no increase in plasma TSH after TRH injection. Exogenous TSH increased the uptake in 6/9 patients. The three patients who did not respond to TSH had higher PBI/T4 ratio than others. After treatment for one month there was either a normalization of laboratory tests either a subnormal thyroid function associated with an absence of response to TRH. All tests became normal two months later.
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The effects of treatment with L-thyroxine (1 mg/m2 of body surface/d, PO, for 8 weeks) on the thyroxine (T4) and triiodothyronine (T3) responses to thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) administration were determined in 10 euthyroid Beagles; 4 other dogs acted as controls. The TSH response test was performed before treatment and at weeks 2, 4, and 8 of treatment in all dogs and at 2 and 4 weeks after cessation of treatment in 6 dogs. The TRH response test was performed before treatment and at week 6 of treatment in all dogs and at 5 weeks after cessation of treatment in 6 dogs. Suppression of the T3 response to TSH was evident at treatment week 2, whereas the T4 response was suppressed at week 4 and remained suppressed for the duration of the study. Four weeks after stopping treatment, T4 and T3 responses to TSH in 2 dogs were within the hypothyroid range. The T4 response to TRH was completely suppressed after 6 weeks of thyroxine treatment, but returned to pretreatment values by 5 weeks after cessation of treatment. Suppression of thyroid and pituitary function is evident after administration of a replacement dose of L-thyroxine to euthyroid dogs.