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The effect of a single large intramuscular injections of TRH (2 mg) on the thyroid 131I uptake in normal man was assessed at varying intervals following the administration of TRH. When the 131I was given simultaneously with TRH, the 3- and 5-hour 131I uptake decreased. When the 131I was administered 8 hours after TRH, the thyroid 131I increased significantly. This response in uptake is similar to that observed in the rat following TSH stimulation. The present study defines the time course of the thyroid 131I uptake response to endogenous TSH stimulation.

We have demonstrated that in patients given a single iv injection of T3, rT3, or, to a lesser extent, T4, all labeled with 125I in the outer or phenolic ring, chromatography of serum on columns of Sephadex G-25 superfine revealed the presence of a labeled material, separate from the administered hormone and from both iodide and iodoprotein. This peak has been termed pre-T3 because it elutes just before the T3 peak. Identification of the various compounds in pre-T3 was carried out by cation exchange chromatography. Pre-T3 generated from [125I]T3 consistently contained labeled compounds with the chromatographic behavior of 3,3'-diiodothyronine and 3'-monoiodothyronine, while pre-T3 generated from [125I]rT3 contained labeled products with the chromatographic mobility of 3',5'-diiodothyronine, 3,3'-diiodothyronine, and 3'-monoiodothyronine. In addition, pre-T3 also contained the glucuro- and sulfoconjugates of these several labeled products. These studies demonstrate that T3 and rT3 undergo progressive and probably sequential deiodination in the peripheral tissues, resulting in the formation of a variety of diiodothyronines and monoiodothyronine, as well as their glucuro- and sulfoconjugates.

The effect of small doses of cyclohex-imide (CH) (0.5 µg/g body wt) on the intrathyroid metabolism of carrier-free 13II and stable iodide iniodine-sufficient and iodine-deficient rats and on thyroglobulin (Tgb) maturation in iodine-deficient rats was studied. This dose of CH had no apparent toxicity but strikingly inhibited the incorporation of l4C-labeled amino acids into thyroid and plasma proteins. In iodine-sufficient rats, CH did not affect T/S (I−) ratios, but did enhance the sensitivity of the thyroid to the acute inhibitory effects of stable iodide on the organification mechanism (Wolff-Chaikoff effect). CH produced unusual effects on the intrathyroid metabolism of 131I in these iodine-sufficient rats: a decrease in 13II uptake, an increase in labeled DIT and a decrease in MIT so that MIT/DIT ratio declined, and a decrease in the proportionate synthesis of the iodothyronines T4 and T3. In iodine-deficient rats, CH also sensitized) the thyroid to the acute Wolff-Chaikoff effect but produced changes...

Disseminated aspergillosis is a major complication in immunosuprressed patients. Infiltration of the thyroid with Aspergillus organisms occurs in approximately 20% of autopsies in patients dying with disseminated disease. The present report describes Aspergillus thyroiditis, Hashimoto's thyroiditis, and possible hypothyroidism in a patient with disseminated aspergillosis.

In order to determine whether T4, TSH, or both affect hypothalamic TRH content, primary or secondary hypothyroidism was induced in the rat by thyroidectomy (Tx) or hypophysectomy (Hx), respectively. Two weeks later, rats were treated with T4, TSH, or both for 14--16 days. Tx or Hx significantly decreased hypothalamic TRH content, and T4 treatment restored hypothalamic TRH to normal in the Tx but not in the Hx rats. When TSH was administered simultaneously with T4 to Hx rats, hypothalamic TRH content was restored to normal. Whole brain TRH content was not affected by Tx, Hx, or by the various treatment regimens. Similar experiments were performed in Snell dwarf (dw/dw) mice. Hypothalamic TRH content was significantly decreased when compared to normal litter mates (dw/+). As in Hx rats, T4 administration to dw/dw mice for 16 days did not restore hypothalamic TRH content to normal. Brain TRH content was similar in both groups and was not altered by T4 treatment. It is concluded that T4 affects hypothalamic TRH content, but that TSH is required for this T4 effect. Whole brain TRH, on the other hand, is unaffected by any of these alterations in thyroid-pituitary function.

The pattern of thyrotropin secretion was analyzed in seven euthyroid women, before and after withdrawal of long-term thyroid hormone, by serial measurements of thyroid 131l uptake, serum thyroxine, tri-iodothyronine, and thyrotropin concentrations, and the response to thyrotropin-releasing hormone. During exogenous hormone administration, 131l uptake was suppressed, and serum thyrotropin concentrations before and after administration of thyrotropin-releasing hormone were undetectable. After withdrawal of exogenous hormone, thyrotropin secretory function was transiently impaired, as indicated by undetectable basal thyrotropin concentrations together with absence of response to thyrotropin-releasing hormone, and subsequently by normal values of basal thyrotropin concentration and normal responses to releasing hormone while serum thyroxine and tri-iodothyronine concentrations were subnormal. Decreased thyrotropin reserve persisted for two to five weeks. Detectable values of serum thyrotropin (less than 1.2 muU per milliliter) and a normal 131l uptake usually occurred concurrently in two to three weeks. Serum thyroxine concentration returned to normal at least four weeks after hormone withdrawal.

The daily administration of propranolol (5–20 mg/kg) to the intact male rat does not effect the serum thyroxine concentration or the peripheral metabolism of 131 I-labeled thyroxine. Except for a small decrease in 131 I-labeled triiodothyronine, propranolol did not effect the intrathyroidal metabolism of 131 I. These findings further suggest that the efficacious use of propranolol in the treatment of many of the signs and symptoms of thyrotoxicosis may not be associated with alterations in thyroid gland function or in the peripheral metabolism of thyroxine.

A simple, highly reproducible, and accurate method for the specific measurement of thyroxine in serum is described. This method depends upon the competitive protein-binding principle developed by Murphy and Pattee, but the method appears to be far simpler and more convenient than other methods based upon this principle. The results obtained by the present method and by a standard Murphy-Pattee technique in various clinical states are essentially indistinguishable, are not influenced by iodine containing compounds, accurately diagnose the presence of hyperthyroidism or hypothyroidism, and are affected in the expected manner by changes in the activity of the thyroxine-binding proteins.

The serum concentrations of triiodothyronine (T3) and thyrotropin (TSH) measured by radioimmunoassay, and that of thyroxine (T4), measured by competitive protein binding assay, were assessed in goitrous and nongoitrous subjects residing in an area of moderate iodine deficiency in Greece. Results were compared to those obtained in a group of age-matched control subjects residing in Boston, an area of adequate iodine intake. Serum T4 concentrations were within the normal range in both goitrous and non-goitrous Greek subjects, but were nevertheless significantly lower than in the Boston controls. Serum T3 concentrations in the nongoitrous Greek subjects were similar to those in the Boston group, but values in the goitrous Greek subjects were significantly increased. Serum TSH concentrations in the Greek subjects were, with one exception, within the normal range and were almost identical to those in the Boston controls. It is suggested that endemic iodine deficient goiter in Greece is the result of a...

The syndrome of iodide-induced hyperthyroidism (Jodbasedow) is not common and has been reported to occur in patients with iodine-deficient goiter after iodide replenishment. As part of a larger study to assess the effects of iodide administration on thyroid hormone synthesis in normal subjects and in patients with various underlying disorders of the thyroid, iodides (5 drops of a saturated solution of potassium iodide) were administered to eight patients with nontoxic goiter residing in Boston, an area of iodine sufficiency. Hyperthyroidism developed during and after iodide administration in four of the eight — an unexpectedly high frequency. This finding suggests that the homeostatic mechanism controlling thyroid hormone synthesis and release in these patients is not functioning normally. We recommend that large doses of iodides not be administered to patients with nontoxic goiter.

Corticosteroid therapy of acute nonsuppurative thyroiditis is often the treatment of choice. However, relapse either during or following corticosteroid withdrawal is frequent. It is suggested that steroid therapy be maintained until the thyroidal 131I uptake returns to normal or above normal.

The serum concentrations of testosterone, estradiol-17β, FSH and LH were measured in 22 male subjects addicted to heroin or methadone. Serum testosterone concentration was decreased in many of these subjects without consistent abnormalities in the other hormones. It is suggested that decreased sexual function in male addicts may be partially due to a decrease in serum testosterone concentration.

The administration of iodide to pregnant and nursing rats induces hypothyroidism in the term fetus and neonatal rat through age 10 days as indicated by an increase in the serum concentration of thyroid-stimulating hormone and a decrease in the serum of thyroxine and triiodothyronine. Thyroid function returned to normal from age 18 through 60 days in spite of continued iodide administration, strongly suggesting that resistance to the inhibitory effect of iodide on thyroid hormone synthesis is developed at approximately 18 days of age. This perinatal rat model can be used to study the mechanisms responsible for iodide-induced hypothyroidism and goiter in human newborns whose mothers received iodide-containing medications during pregnancy.

The chronic use of methadone or heroin results in various abnormalities in the transport and peripheral metabolism of thyroxine (T4). An increase in the thyroxine-binding capacity of the t...

Excerpt To the editor: Bilateral adrenal hemorrhage with resultant acute adrenal insufficiency has been recognized as a fatal complication of anticoagulant therapy (1, 2). Only rarely has this medi...

Excerpt A multitude of thyroid function tests are now available to the clinician to aid in the diagnosis of thyroid disease. Unfortunately, the laboratory test that is requested may not be appropri...