Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness

1994 ◽  
Vol 130 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Nicola Custro ◽  
Vincenza Scafidi ◽  
Salvatore Gallo ◽  
Alberto Notarbartolo
Keyword(s):  
Thyroid Hormone ◽  
Healthy Subjects ◽  
Normal Subjects ◽  
Healthy Individuals ◽  
Circadian Variations ◽  
Tsh Secretion ◽  
Thyroid Hormone Levels ◽  
Rhythmic Change ◽  
Serum Tsh ◽  
Tsh Levels

Custro N, Scafidi V, Gallo S, Notarbartolo A. Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness. Eur J Endocrinol 1994;130:132–6. ISSN 0804–4643. Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l, The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay from midnight (0 degrees) of the highest level in the rhythm) was −9.9 degrees. In contrast, severely ill patients showed only slight and anticipated elevations of serum TSH levels (mesor 0.93 mU/l, amplitude 0.22 mU/l, acrophase +82.4 degrees). Moreover, whereas the episodic TSH secretion in healthy individuals consisted of 5–8 pulses/24 h, mainly clustered around midnight, only one pulse of reduced amplitude was detected in two of the eight severely ill patients and no pulses in the other six. Since earlier studies have indicated that the loss of TSH pulsatility is associated with the relative insensitivity of the thyrotrophs to low thyroid hormone levels and our analytical procedures have demonstrated that 24 h pulsatile pattern of TSH closely overlapped with baseline TSH secretion, it seems reasonable to assume that low-thyroid-hormone state, deficient pulsatile TSH secretion and altered nyctohemeral TSH periodicity do not coincide by chance, but that there is a causal relationship between such abnormalities in severely ill patients. Nicola Custro, Cattedra di Patologia Medica, Via del Vespro, n.141, 90127 Palermo, Italy

Bombesin inhibits thyrotrophin secretion in rats

1985 ◽  
Vol 108 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
Masahiro Chaya
Keyword(s):  
Thyroid Hormone ◽  
Plasma Concentrations ◽  
Treated Group ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Tsh Secretion ◽  
The Central Nervous System ◽  
Thyroid Hormone Levels ◽  
Tsh Levels

Abstract. The effects of peripheral administration of bombesin on thyrotrophin-releasing hormone (TRH) and thvrotrophin (TSH) secretion in rats were studied. Bombesin (200 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after bombesin injection, whereas plasma concentrations tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by bombesin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine pre-treated group, the inhibitory effect of bombesin on TSH levels was prevented, but not in the l-Dopa- or 5-hydroxytryptophan pre-treated group. These drugs alone had no effect on plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity in plasma or hypothalamus in vitro after bombesin injection did not differ from that of the controls. These findings suggest that bombesin acts on the hypothalamus to inhibit TRH release, and that its effects are at least partially modified by amines of the central nervous system.

scholarly journals Thyrotropin Levels during Hydrocortisone Infusions That Mimic Fasting-Induced Cortisol Elevations: A Clinical Research Center Study1

1997 ◽  
Vol 82 (11) ◽  
pp. 3700-3704 ◽  
Author(s):  
M. H. Samuels ◽  
P. A. McDaniel
Keyword(s):  
Healthy Subjects ◽  
Serum Cortisol ◽  
Similar Degree ◽  
Trh Stimulation ◽  
Clinical Research Center ◽  
Tsh Secretion ◽  
Cortisol Levels ◽  
High Doses ◽  
Serum Tsh ◽  
Tsh Levels

Both short term fasting and administration of high doses of glucocorticoids lead to marked suppression of serum TSH levels in healthy subjects. However, it is not known whether the more mild serum cortisol elevations seen during fasting can account for fasting-induced TSH suppression. To study this question, eight healthy subjects each underwent three 2-day studies: 1) baseline (ad libitum diet), 2) fasting (56 h of total caloric deprivation), 3) hydrocortisone (HC) infusions at a dose and pulsatile pattern that reproduced cortisol levels measured during each subject’s fasting study. Subjects required 34–46 mg HC/24 h to achieve these cortisol levels. During each study, blood samples were drawn every 15 min during the final 24 h for serum cortisol and TSH levels. A TRH stimulation test was performed at the end of each study. By design, fasting and HC infusions induced similar mild increases in 24-h serum cortisol levels (32% over baseline), with the most significant increases seen between 1400–0200 h. Fasting decreased 24-h mean and pulsatile TSH levels 65% from baseline, whereas HC infusions decreased mean and pulsatile TSH levels 51% from baseline. Daytime (0800–0200 h) TSH levels were identical in the two studies, whereas nocturnal (0200–0800 h) TSH levels during HC infusions fell midway between baseline and fasting studies. Serum total T3 and TSH responses to TRH were decreased to a similar degree by fasting or HC infusions. These results suggest that mild elevations in endogenous cortisol levels may mediate at least in part fasting-induced changes in TSH secretion and thyroid hormone levels. In addition, these data show that near-physiological doses of HC and resulting changes in serum cortisol levels within the normal range can cause significant decreases in serum TSH levels.

Effects of eledoisin on thyrotrophin secretion in rats

1985 ◽  
Vol 110 (1) ◽  
pp. 90-94
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
De Heng Sun ◽  
Masahiro Chaya
Keyword(s):  
Central Nervous System ◽  
Thyroid Hormone ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
The Central Nervous System ◽  
Thyroid Hormone Levels ◽  
Tsh Levels

Abstract. The effect of peripheral administration of eledoisin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Eledoisin (500 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after eledoisin injection, whereas its plasma concentration tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by eledoisin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine-pretreated group, the inhibitory effect of eledoisin on TSH levels was prevented, but not in the l-dopa- or 5-hydroxytryptophan-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. The inactivation of TRH immunoreactivity by plasma or hypothalamus in vitro after eledoisin injection did not differ from that of controls. These findings suggest that eledoisin acts on the hypothalamus to inhibit TRH release, and its effects are modified by amines of the central nervous system.

Linear modulation of serum thyrotrophin by thyroid hormone treatment in hypothyroidism

1980 ◽  
Vol 95 (4) ◽  
pp. 472-478 ◽  
Author(s):  
A. Eugene Pekary ◽  
Jerome M. Hershman ◽  
Clark T. Sawin
Keyword(s):  
Thyroid Hormone ◽  
Hormone Replacement ◽  
Hormone Treatment ◽  
Significant Negative Correlation ◽  
Thyroid Hormone Replacement ◽  
Basal Serum ◽  
Thyroid Hormone Levels ◽  
Peak Versus ◽  
Hypothyroid Patients ◽  
Serum Tsh

Abstract. Basal serum TSH and the peak TSH response to a 500 μg TRH bolus were measured in 57 euthyroid and in 29 hypothyroid subjects either receiving graded thyroid hormone replacement or acutely removed from full replacement therapy. Serum TSH, total T4 and T3 were determined by sensitive radioimmunoassay methods. The peak versus basal TSH data for hypothyroid patients were linear within individuals. The regression slope of the peak versus basal TSH data for all hypothyroid subjects did not differ significantly from the corresponding slope for all euthyroid subjects. Basal and peak TSH versus T3 and T4 data for hypothyroid patients were also linear within each individual. Moreover, the regression of the basal TSH values averaged over the non-replacement to full replacement state against the TSH versus T3 slope had a significant negative correlation. This trend leads to an array of regression lines which average to the familiar hyperbolic relationship between thyrotrophin and thyroid hormone levels in man.

scholarly journals Inhibition of pituitary type 2 deiodinase by reverse triiodothyronine does not alter thyroxine-induced inhibition of thyrotropin secretion in hypothyroid rats

2005 ◽  
Vol 153 (3) ◽  
pp. 429-434 ◽  
Author(s):  
P Cettour-Rose ◽  
T J Visser ◽  
A G Burger ◽  
F Rohner-Jeanrenaud
Keyword(s):  
Specific Inhibitor ◽  
Adult Rats ◽  
Reverse T3 ◽  
Brown Adipose ◽  
Tsh Secretion ◽  
Serum T3 ◽  
Serum T4 ◽  
Serum Tsh ◽  
Tsh Levels

Objectives: Intrapituitary triiodothyronine (T3) production plays a pivotal role in the control of TSH secretion. Its production is increased in the presence of decreased serum thyroxine (T4) concentrations and the enzyme responsible, deiodinase type 2 (D2), is highest in hypothyroidism. In order to document the role of this enzyme in adult rats we developed an experimental model that inhibited this enzyme using the specific inhibitor, reverse T3 (rT3). Methods: Hypothyroidism was induced with propylthiouracil (PTU; 0.025 g/l in drinking water) which in addition blocked deiodinase type 1 (D1) activity, responsible for the rapid clearance of rT3 in vivo. During the last 7 days of the experiment, the hypothyroid rats were injected (s.c.) for 4 days with 0.4 or 0.8 nmol T4 per 100 g body weight (bw) per day. For the last 3 days, the same amount of T4 was infused via s.c. minipumps. In additional groups, 25 nmol rT3/100 g bw per day were added to the 3-day infusion of T4. Results: Infusion of 0.4 nmol T4/100 g bw per day did not affect the high serum TSH levels, 0.8 nmol T4/100 g bw per day decreased them to 57% of the hypothyroid values. The infusions of rT3 inhibited D2 activity in all organs where it was measured: the pituitary, brain cortex and brown adipose tissue (BAT). In the pituitary, the activity was 27%, to less than 15% of the activity in hypothyroidism. Despite that, serum TSH levels did not increase, serum T4 concentrations did not change and the changes in serum T3 were minimal. Conclusions: We conclude that in partly hypothyroid rats, a 3-day inhibition of D2 activity, without concomitant change in serum T4 and minimal changes in serum T3 levels, is not able to upregulate TSH secretion and we postulate that this may be a reflection of absent or only minimal changes in circulating T3 concentrations.

The interaction of GHRH with TRH in acromegaly: a controlled study

1991 ◽  
Vol 125 (4) ◽  
pp. 337-341 ◽  
Author(s):  
Bert-Jan Looij ◽  
Ferdinand Roelfsema ◽  
Marijke Frölich ◽  
Arie C. Nieuwenhuijzen Kruseman
Keyword(s):  
Healthy Subjects ◽  
Bolus Injection ◽  
Controlled Study ◽  
Healthy Individuals ◽  
Tsh Secretion ◽  
Single Blind ◽  
Modest Effect

Abstract. In a single-blind placebo-controlled study, the effect of an iv bolus injection of 100 μg GHRH(1–29)NH2 on the response to 200 μg TRH was assessed in 10 untreated patients with acromegaly to determine whether GHRH interacts with TRH in acromegaly, as previously described in healthy subjects. The combination of GHRH(1–29)NH2 with TRH resulted in a larger increment of peak and of integrated plasma TSH and PRL levels than after TRH alone. GHRH alone had no effect on TSH secretion and only a modest effect on PRL secretion. These findings suggest that in acromegaly, like in healthy individuals, GHRH potentiates the TSH response to TRH and that the effects of GHRH and TRH on PRL secretion are additive.

scholarly journals Analysis of Hypothalamic TRH Neurons in Regulating Thyroid Hormone Levels

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A849-A849
Author(s):  
Ricardo H Costa e Sousa ◽  
Rodrigo Rorato ◽  
Anthony Neil Hollenberg ◽  
Kristen R Vella
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Designer Drugs ◽  
Mrna Levels ◽  
Hormone Levels ◽  
Males And Females ◽  
Thyroid Hormone Levels ◽  
Hpt Axis ◽  
Tsh Levels

Abstract Thyroid hormone (TH) is a major regulator of development and metabolism. An important mechanism controlling TH production is the negative feedback at the hypothalamic and pituitary level and it has been suggested that thyroid hormone receptor β (TRβ) is the main mediator of TH actions in the hypothalamic paraventricular nucleus (PVN). Nevertheless, the direct actions of TH and TRβ in the negative regulation of TRH have yet to be demonstrated in vivo. Here we used two approaches to investigate the TRH neuron. First, we used a chemogenetic tool to directly investigate the role of TRH neurons on the regulation of thyroid hormone levels. Mice expressing Cre-recombinase in TRH neurons received bilateral injections of the activating designer receptors exclusively activated by designer drugs (DREADD) directly into the PVN. Activation of TRH neurons produced a rapid and sustained increase in circulating TSH levels in both males and females. TSH levels increased approximately 10-fold from baseline within 15 minutes of injection of CNO, returning to baseline within 2.5 hours. TH levels were increased approximately 2-fold in males and females. Therefore, using a chemogenetic approach, we were able to directly evaluated the role of PVN TRH neurons on the control of thyroid activity, for the first time. Next, we generated mice deficient in TRβ specifically in neurons expressing melanocortin 4 receptor (MC4R), which overlaps with TRH expression in the PVN. Knockout mice (KO) developed normally and showed no change in TH and TSH levels. TRH mRNA levels in the PVN of KO mice were similar to control mice. To investigate if the deletion of TRβ in the PVN changes the sensitivity of the HPT axis to T3, mice were rendered hypothyroid and given increasing doses of T3 for 2 weeks. Results show no difference in TRH mRNA or serum TSH between controls and KO. Surprisingly, despite the presence of detectable genomic recombination on the TRβ gene in the PVN, there was no difference in TRβ mRNA expression between control and KO mice, suggesting that either MC4R-positive neurons do not express TRβ or they represent a very small population of TRβ-positive cells in the PVN. Present data show that TRH neuron activation rapidly stimulates TSH release and increases TH levels, demonstrating a major role of these neurons in the regulation of the hypothalamic-pituitary-thyroid (HPT) axis. Nevertheless, deletion of TRβ from MC4R neurons had no major effect on either TRH or TH levels in in mice. Additionally, TRβ in MC4R-positive TRH neurons in the PVN is not necessary for TH-induced suppression of TRH mRNA. Although further studies are necessary, these data suggest that there are distinct populations of hypophysiotropic TRH neurons in the PVN, some of which are not regulated by thyroid hormone and TRβ.

scholarly journals A rare mutation of thyroid hormone receptor beta gene in thyroid hormone resistance syndrome

2021 ◽  
Vol 2021 ◽  
Author(s):  
Michela Del Prete ◽  
Fabrizio Muratori ◽  
Irene Campi ◽  
Gianleone Di Sacco ◽  
Federico Vignati ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Genetic Test ◽  
List Type ◽  
Thyroid Function Tests ◽  
Resistance To Thyroid Hormone ◽  
Hereditary Syndrome ◽  
Serum Tsh ◽  
Receptor Beta ◽  
Tsh Levels

Summary Resistance to thyroid hormone (RTH) is a rare hereditary syndrome with impaired sensitivity to thyroid hormones (TH) and reduced intracellular action of triiodothyronine (T3) caused by genetic variants of TH receptor beta (TRB) or alpha (TRA). RTH type beta (RTHβ) due to dominant negative variants in the TRB gene usually occurs with persistent elevation of circulating free TH, non-suppressed serum TSH levels responding to a thyrotropin-releasing hormone (TRH) test, an absence of typical symptoms of hyperthyroidism and goiter. Here, we present a rare variant in the TRB gene reported for the first time in an Italian patient with generalized RTHβ syndrome. The patient showed elevated TH, with non-suppressed TSH levels and underwent thyroid surgery two different times for multinodular goiter. The genetic test showed a heterozygous mutation in exon 9 of the TRB gene resulting in the replacement of threonine (ACG) with methionine (ATG) at codon 310 (p.M310T). RTHβ syndrome should be considered in patients with elevated TH, non-suppressed TSH levels and goiter. Learning points Resistance to thyroid hormone (RTH) is a rare autosomal dominant hereditary syndrome with impaired tissue responsiveness to thyroid hormones (TH). Diagnosis of RTH is usually based on the clinical finding of discrepant thyroid function tests and confirmed by a genetic test. RTH is a rare condition that must be considered for the management of patients with goiter, elevation of TH and non-suppressed serum TSH levels in order to avoid unnecessary treatments.

scholarly journals Association between Thyroid Stimulating Hormone and Respiratory Distress Syndrome of Newborn in the Preterm Infants

2020 ◽  
Author(s):  
Young Jin Kim ◽  
Byoung Kook Kim ◽  
Yong Hyuk Kim
Keyword(s):  
Thyroid Hormone ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Gestational Age ◽  
Distress Syndrome ◽  
Control Group ◽  
Lower Serum ◽  
Significant Difference ◽  
Serum Tsh ◽  
Tsh Levels

Abstract Background: Various hormones are known to influence the production and secretion of pulmonary surfactant. But the relationship between respiratory distress syndrome (RDS) and thyroid hormone has yet to be clarified. Methods: 126 infants with gestational age between 24 and 34 weeks who were hospitalized at the neonatal ICU of the Wonju Severance Christian Hospital from April 2017 to February 2019 were included in the study. Infants were divided into 3 groups by gestational age – 24 weeks 0 days to 28 weeks 0 days, 28 weeks 0 days to 31 weeks 0 days, and 31 weeks 0 days to 33 weeks 0 days, each with 18, 34, and 74 subjects, respectively. Among the subjects, there were 56 infants with RDS and 70 infants without RDS.Results: The group with lowest gestational age showed T3 and fT4 level that was lower than those of other groups (p<0.05) on the day of birth but there was no difference in the TSH level (p=0.129). T3 and TSH level were lower in the RDS group compared with the control group on the day of birth (p<0.05). Free thyroxine (fT4) level was higher in the control group on the day of birth but without any significant difference. Multiple logistic regression analysis showed that lower serum TSH levels on the day of birth was associated with a higher incidence of RDS (p<0.05).Conclusion: The incidence of RDS was significantly higher in infants with lower serum TSH levels at birth, but there was no significant difference in RDS incidence according to serum thyroid hormone levels.

INFLUENCE OF TESTOSTERONE ON THE SECRETION OF THYROTROPHIN IN THE RAT

1965 ◽  
Vol 50 (1) ◽  
pp. 155-160 ◽  
Author(s):  
G. P. van Rees ◽  
E. L. Noach ◽  
J. A. M. J. van Dieten
Keyword(s):  
Thyroid Hormone ◽  
Testosterone Propionate ◽  
Male Rats ◽  
Thyroxine Treatment ◽  
High Doses ◽  
Serum Tsh ◽  
Tsh Levels

ABSTRACT Castration of male rats decreases both pituitary and serum TSH-levels. Administration of testosterone propionate increases serum TSH-levels in castrated males, but its effect on pituitary TSH-content appears to be complex: whereas treatment with physiological amounts of testosterone prevents the decrease induced by castration, administration of high doses of testosterone results in low pituitary TSH-contents not unlike those seen in untreated castrated rats. Testosterone administered to thyroxine-maintained thyroidectomized rats had the same effects as mentioned above, but if thyroxine treatment was omitted, no effect of testosterone on pituitary and serum TSH-levels could be observed. It is thought that testosterone interferes with the effect of thyroid hormone on the secretion of TSH.

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