Use of a rapid, sensitive immunoradiometric assay for thyrotropin to distinguish normal from hyperthyroid subjects.

Using a new three-site immunoradiometric assay for thyrotropin (TSH), we measured concentration of this hormone in the serum of 47 patients with hyperthyroidism and 46 controls. The mean and range of serum TSH concentration was significantly lower in thyrotoxic than in control subjects, and it was possible to correctly identify 96% of thyrotoxic patients on the basis of a serum TSH concentration less than 0.5 milli-int. unit/L. We conclude that such measurement is highly sensitive for distinguishing hyperthyroid from normal subjects, and that the lower limit of normal for TSH in serum is about 0.5 milli-int. unit/L.

Growth hormone secretory status is a determinant of the thyrotropin response to thyrotropin-releasing hormone in euthyroid patients with hypothalamic-pituitary disease.

To assess the influence of endogenous GH secretion on the TSH and T3 responses to TRH administration in patients with hypothalamic-pituitary disease, we analyzed tests in a selected group of 26 euthyroid patients with hypothalamic-pituitary disease and in 15 normal controls. Basal TSH levels and the TSH response to TRH were significantly greater in GH-deficient patients (group 1) than in patients with normal anterior pituitary function and unimpaired GH reserve (group II). However, the T3 response to TRH was significantly less in group 1 than in group II patients. In acromegaly (group III), the TSH response to TRH was blunted, while basal and stimulated T3 levels were no different compared to control levels. These findings suggest that endogenous GH depresses the TSH response to TRH while enhancing the thyroid secretion of T3 in response to the evoked TSH released.

Neurogenic diabetes insipidus: management with dDAVP (1-desamino-8-D arginine vasopressin).

We used dDAVP, the 1-desamino-8-D arginine analogue of arginine vasopressin with high antidiuretic and low vasopressor potency, to treat 29 patients with neurogenic diabetes insipidus for up to 22 months. Intranasal dDAVP, 2.5 to 15 microgram twice daily, provided excellent control in most patients. Individual responses were independent of age, weight, and severity of diabetes insipidus. Resistance to dDAVP may be a rare complication of prolonged therapy. Two patients with acute postoperative diabetes insipidus were effectively treated with 5 microgram of dDAVP every 14 to 18 h. Compared to previous therapy, side effects of dDAVP were minimal (headaches in two patients), and control of symptoms and urine volume was as good as with vasopressin tannate in oil or better than chlorpropamide and lysine vasopressin nasal spray. We conclude that intranasal dDAVP, because of efficacy, long duration of action, and infrequent side effects, is the preferred treatment of neurogenic diabetes insipidus in children and adults.

Why does anyone still use desiccated thyroid USP?

The effect on thyroid status of changing from thyroid USP to sodium L-thyroxine was evaluated in 40 patients. With thyroid, abnormally high triiodothyronine (T3) levels were seen in 36 of 38 patients receiving doses of 90 to 240 mg; compared to sodium L-thyroxine, 0.15 to 0.2 mg, the serum T3 was higher (289 +/- 15 ng/dl versus 176 +/- 9 ng/dl, p less than 0.0005) and the thyroxine (T4) lower (7.4 +/- 0.3 microgram/dl versus 11.6 +/- 0.5 microgram/dl, P less than 0.01). Thyrotoxic symptoms occurred in six patients and diminished or disappeared after the change to sodium L-thyroxine, suggesting that the raised T3 level with thyroid may have undesirable effects in some patients. The T4 level, because it is low whether symptoms are present or not, may inadvertently suggest the need for higher dosage of desiccated thyroid in patients who have already received adequate replacement. The dose of sodium L-thyroxine was adequately assessed by measurement of both T4 and T3 levels. Thyroid USP should be discontinued as thyroid medication since it produces thyroid hormone levels that are misleading estimates of thyroid function and can cause thyrotoxic symptoms.

Drug therapy reviews: management of hypothyroidism.

The therapeutic management of hypothyroidism caused by deficient thyroid hormone production is discussed. The therapeutic use of the following thyroid agents is reviewed: levothyroxine sodium, Thyroid USP, thyroglobulin, liotrix, and liothyronine sodium. Myxedema coma, neonatal hypothyroidism, primary hypothyroidism, and secondary and tertiary hypothyroidism are specific hypothyroid states for which drug therapy is discussed. Levothyroxine sodium is the preferred agent because of consistent potency, restoration of normal, constant serum levels of thyroxine (T4) and triiodothyronine (T3) and ease of interpretation of thyroid hormone levels. Other agents, because they contain T3, result in postabsorptive elevated T3 serum concentrations that may cause thyrotoxic symptoms and reduction of T4 levels. This, in turn, may give rise to misleading estimates of thyroid dosage. Patients with the sick euthyroid or low T3 syndromes are not candidates for thyroid hormone therapy.