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Biomedical subjects

R D Utiger

Publications and source records attributed to R D Utiger.

At least 109 records · Page 6Linked to original sources
PubMed1975

Augmentation of thyrotropin responses to thyrotropin-releasing hormone following small decreases in serum thyroid hormone concentrations.

To determine whether slight decreases in serum thyroid hormone concentrations resulted in augmentation of the thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH), TSH responses to TRH were determined before and after 13 days of iodide treatment in 20 normal subjects. Slight reductions in serum thyroxine (t4) and/or triiodothyronine (T3) concentrations and slight increases in basal serum TSH concentrations occurred in normal subjects treated with 50 or 250 mg iodide daily, though serum T4, T3 and TSH concentrations remained within their respective normal range. In contrast, TSH responses to TRH were significantly greater at the end of the iodide treatment period. In the subjects who received 50 mg iodide daily, mean basal serum TSH concentrations were 3.1 and 3.2 muU/ml before and 4.9 and 4.6 muU/ml after iodide. Post-TRH mean peak serum TSH concentrations were 14.2 muU/ml before and 27.4 muU/ml after iodide (P smaller than 0.01). A very similar augmentation of peak serum TSH was found in the subjects who received 250 mg iodide daily (before iodide, peak TSH 17.2 muU/ml; after iodide, peak TSH 28.7 muU/ml). No changes in serum T4, T3 or TSH concentrations or TSH responses to TRH followed iodide administration in 4 thyroxine-treated hypothyroid patients. These results indicate that slight reductions in serum T4 AND T3 concentrations result in increased pituitary sensitivity to TRH, just as small increases in serum T4 and T3 concentrations decrease sensitivity to TRH.

Adolescent↗
PubMed1975

Low serum triiodothyronine in patients with anorexia nervosa.

Patients with anorexia nervosa can demonstrate clinical and/or laboratory findings suggestive of reduced thyroid hormone secretion. In this study, the thyroxine (T4) and triiodothyronine (T3) serum concentrations, and thyrotropin (TSH) response to intravenous administration of thyrotropin releasing hormone (TRH) were determined in 6 patients (aged 9 to 15 yr) with anorexia nervosa and the results compared to those found in a group of 15 normal subjects. The mean basal TSH concentration and mean maximum increase in TSH after TRH were comparable to those in the normal subjects. The mean T4 concentration (7.2 mug/100 ml) in the anorexia nerovsa group was slightly but significantly lower than in the normal group (9.5 mug/100 ml). Five of the 6 patients had serum T3 concentrations below the lower limits of normal and the mean T3 concentrations (49.7 ng/100 ml) was significantly lower than in the normal group (106 ng/100 ml). The extremely low serum levels of T3 in these patients with anorexia nervosa suggest that peripheral conversion of T4 to T3 is impaired during chronic starvation.

Adolescent↗
PubMed1975

Hyperthyroidism in Tasmania following iodide supplementation: measurements of thyroid-stimulating autoantibodies and thyrotropin.

Serum thyroid-stimulating autoantibodies (LATS and LATS protector) and thyrotropin (TSH) concentrations were measured in the serum of 30 patients with hyperthyroidism living in Tasmania who developed their disease following correction of iodine deficiency by addition of iodate to the bread. Patients were grouped according to thyroid scan results. None of 8 patients with autonomous thyroid nodules had thyroid-stimulating autoantibodies. These were present in both of the patients with uniform thyroid scans and 14 of 20 patients (70%) with irregular scans without demonstrated localized autonomy. Serum TSH, measured by immunoassay of concentrated serum extracts, was 0.15 muU/ml or less in all patients, below the range of 0.35 to 2.60 muU/ml found in normal subjects. Only 6 (20%) of the 30 patients failed to show either localized autonomy or thyroid-stimulating autoantibodies. In most regards these patients resembled those with antonomous nodules. The findings support the conclusion that the increased incidence of phyerthyroidism in Tasmania was due to an increased supply of iodine to patients with latent hyperthyroidism whose thyroid glands, due to the presence of toxid nodule(s) or thyroid-stimulating autoantibodies, were unresponsive to control by TSH deprivation. There was no evidence for additional pathogenic mechanisms

Adult↗
PubMed1975

Lack of T-cell immune abnormalities in peripheral blood lymphocytes in patients with Graves' disease or hypothyroidism.

Lymphocytes capable of forming nonimmune (E) and immune (EAC) rosettes with sheep erythrocytes and lymphocyte reactivity to phytohemagglutinin were determined in normal subjects, in patients with hyperthyroidism due to Graves' disease and in patients with hypothyroidism with and without goiter. Neither patient group differed from the normal subjects either in regard to lymphocyte count, the proportion of thymus dependent (t) lymphocytes forming nonimmune or bone marrow-dependnet (B) lymphocytes forming immune rosettes or lymphocyte reactivity to phytohemagglutinin. These results fail to provide evidence that these disorders are associated with an immune abnormality with increased or abnormal T cells in peripheral blood.

Adult↗
PubMed1975

Serum LH and FSH responses to synthetic gonadotropin-releasing hormone in normal men.

The effects of dose and of age on the serum LH and FSH responses to synthetic gonadotropin-releasing hormone (GnRH) were determined in normal men. GnRH was given as in iv bolus in doses from 2 to 500 mug to each of nine normal men, 20-39 years old. The mean (+/- SE) maximum delta LH (maximum increment above the basal concentration) in response to each dose of GnRH was 2 mug, 7.2 +/- 1.7 mIU/ml; 10 mug, 15.7 +/- 3.4 mIU/ml; 50 mug, 37.7 +/- 9.6 mIU/ml; 250 mug, 47.8 +/- 11.2 mIU/ml; and 500 mug, 49.3 +/- 11.2 mIU/ml. The mean delta FSH in response to each dose was 2 mug, 0.5 +/- 0.2 mIU/ml; 10 mug, 0.8 +/- 0.2 mIU/ml; 50 mug, 1.2 +/- 0.3 mIU/ml; 250 mug, 2.0 +/- 0.3 mIU/ml; and 500 mug, 2.4 +/- 0.4 mIU/ml. Since both the LH and FSH responses to the 250 mug dose were significantly greater than those to smaller doses, but the responses to the 500 mug dose were not still larger, 250 mug was used as the standard test done for subsequent studies. The effect of age was tested by administering a 250 mug dose of GnRH as an iv bolus to 42 carefully selected normal men, 14 in each of three age groups, 20-39, 40-59, and 60-79 years old. Dialyzable serum testosterone levels decreased with increasing age, from 21.7 +/- 4.6 to 16.0 +/- 4.9 to 14.3 +/- 3.8 ng/dl (mean +/- SD), and the basal serum LH levels increased slightly, from 7.4 +/- 3.4 to 9.6 +/- 3.1 to 10.8 +/- 3.2 mIU/ml, suggesting that a slight degree of primary Leydig cell failure occurs with increasing age. There was no corresponding increase in mean maximum delta LH in response to GnRH with increasing age, despite the elevation in mean basal LH levels. The maximum delta LH/basal LH ratio, in fact, declined from 6.8 to 5.1 to 3.3 in the three age groups. The basal serum FSH levels did not change with increasing age, but the mean delta FSH values decreased from 3.0 +/- 0.5 to 2.9 +/- 1.1 +/- 0.3 mIU/ml. These data demonstrate decreased LH and FSH responses to synthetic GnRH, as well as some primary Leydig cell failure, in the male senescence.

Adult↗
PubMed1974

Thyrotropin-releasing hormone: regional distribution in rat brain.

A sensitive and specific radioimmnunoassay has been used to measure the distribution of thyrotropin-releasing hormone (TRH) in rat brain. All areas of brain tested, except cerebellum, contained readily measurable amounts of TRH. The hypothalamus contained only 31.2 percent of the total brain content of TRH. These results support recent suggestions of central actions for TRH in addition to its hypophysiotropic functions.

Animals↗
PubMed1974

Thyrotropin-releasing hormone in specific nuclei of rat brain.

The regional distribution of thyrotropin-releasing hormone (TRH) in rat brain was studied. The greatest concentration of TRH was found in the median eminence. High concentrations were also found in several hypothalamic nuclei. Outside the hypothalamus, relatively large amounts of TRH were found in the septal and preoptic areas.

Animals↗
PubMed1973

Metabolism and excretion of exogenous thyrotropin-releasing hormone in humans.

To study the metabolism of thyrotropin-releasing hormone (TRH) in vivo, 400 mug TRH was administered intravenously to eight normal male subjects. Multiple plasma and urine samples were obtained before and after TRH administration. Serum TSH concentrations increased after TRH administration in all subjects. Plasma TRH levels, measured by radioimmunoassay, were undetectable (< 0.4 ng/ml) before TRH administration. Plasma TRH concentrations averaged 33+/-7 ng/ml (mean +/-SEM) 2 min after TRH injection. Thereafter, they decreased rapidly so that the mean plasma TRH level was 2.9 ng/ml 20 min after TRH administration. The fall in plasma TRH levels was linear during this interval. Thereafter TRH levels declined more slowly. The mean half-life (t(1/2)) of TRH was 5.3+/-0.5 min. The mean distribution volume was 15.7+/-3.8 liters, an average of 16.5% of body weight in these subjects. In the urine, 5.5+/-0.9% of the administered TRH was recovered in the 3 h after TRH administration. Of the total urinary TRH recovered, 84.9% was excreted in the first 30 min. These results indicate that TRH is distributed in a large volume, that it is rapidly metabolized and that a significant quantity of administered TRH is excreted in the urine.

Adolescent↗
PubMed1973

Repetitive administration of thyrotropin-releasing hormone results in small elevations of serum thyroid hormones and in marked inhibition of thyrotropin response.

Repetitive administration of thyrotropin-releasing hormone (TRH) to human subjects was used to produce small elevations of endogenous serum triiodothyronine (T(3)) and thyroxine (T(4)) levels and thereby to determine the effect of these small elevations on the serum thyrotropin (TSH) response to subsequent doses of TRH. Each subject received 13 consecutive doses of 25 mug TRH at 4-h intervals. Serum T(3), T(4), and TSH levels were measured before the 1st, 7th, and 13th doses ("basal levels") and for the 4 h after each of these doses. In 10 normal subjects, the mean TSH response fell from 14.6 muU/ml after the 1st TRH dose to 6.9 and 3.0 muU/ml after the 7th, and 13th doses. These falls in TSH response were accompanied by rises in the mean basal serum T(3) levels from 81 to 115 to 114 ng/100 ml (normal range, 70-150 ng/100 ml) and rises in the mean basal serum T(4) from 6.7 to 8.6 to 9.5 mug/100 ml (normal range, 5-11 mug/100 ml). These data suggest that TRH-induced TSH release is extremely sensitive to inhibition by small elevations, not above the normal ranges, of serum T(3) and T(4) of endogenous origin. In four patients with primary hypothyroidism, the mean TSH responses were 92, 137, and 92 muU/ml after the 1st, 7th, and 13th TRH doses. The corresponding mean basal serum T(3) and T(4) levels at the times of these doses were 34, 30, and 32 ng/100 ml and 1.9, 1.9, and 1.7 mug/100 ml. These data show that repetitive administration of TRH does not result in progressively lower TSH responses in the absence of corresponding increases in serum T(3) and T(4) level. The progressive fall in TSH response observed in the normal subjects, therefore, was apparently due to the corresponding small increases in serum T(3) and T(4) levels and not to progressive depletion of pituitary TSH. In two patients with presumed TRH deficiency, the TSH responses were blunted by repetitive TRH doses but only when the serum T(3) and T(4) levels increased to within the normal ranges. TRH deficiency was thus confirmed for the first time by producing euthyroidism by replacement of TRH.

Adult↗
PubMed1973

Thyroid hormone inhibition of the prolactin response to thyrotropin-releasing hormone.

The influence of serum triiodothyronine (T(3)) and thyroxine (T(4)) concentrations on the release of prolactin in man was studied by determining the prolactin response to synthetic thyrotropin-releasing hormone (TRH) in hypothyroid and hyperthyroid patients before and after correction of their serum thyroid hormone abnormalities. The maximum increment in serum prolactin above the basal level (maximum Delta prolactin) was used as the index of response to TRH. In 12 patients with primary hypothyroidism, the maximum Delta prolactin in response to TRH fell from 100.5+/-29.1 ng/ml (mean +/-SEM) before treatment to 36.1+/-6.0 ng/ml (P < 0.01) during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily. The mean serum T(3) level increased from 57+/-8 to 138+/-10 ng/100 ml, and the mean serum T(4) level increased from 3.0+/-0.4 to 7.2+/-0.4 mug/100 ml during this treatment. In eight normal subjects the maximum Deltaprolactin in response to TRH was not significantly different during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily from the response before treatment. In 10 patients with hyperthyroidism, the maximum Deltaprolactin in response to TRH increased from 14.2+/-2.9 ng/ml before treatment to 46.9+/-6.7 ng/ml (P < 0.001) during antithyroid treatment. The mean serum T(3) level fell from 313+/-47 to 90+/-8 ng/100 ml, and the mean serum T(4) level fell from 20.8+/-2.5 to 6.8+/-0.6 mug/100 ml during this treatment. These results show that changes from normal serum levels of T(3) and T(4) are associated with changes in prolactin responses to TRH; subnormal serum levels of T(3) and T(4) increase TRH-induced prolactin release, whereas substantially higher than normal serum levels of T(3) and T(4) inhibit this release.

Adolescent↗