scholarly journals Effects of Variations in Physiological Cortisol Levels on Thyrotropin Secretion in Subjects with Adrenal Insufficiency: A Clinical Research Center Study1

2000 ◽  
Vol 85 (4) ◽  
pp. 1388-1393
Author(s):  
M. H. Samuels
Keyword(s):  
Total Dose ◽  
Adrenal Insufficiency ◽  
Circadian Variation ◽  
Serum Cortisol ◽  
Physiological Study ◽  
Diurnal Pattern ◽  
Baseline Study ◽  
Tsh Secretion ◽  
Cortisol Levels ◽  
Tsh Levels

Although pharmacological doses of glucocorticoids suppress TSH secretion, less is known regarding the effects of physiological variations in cortisol levels on TSH. To study this issue, seven subjects with primary adrenal insufficiency each underwent four studies. In the first study subjects received infusions of saline for 48 h (baseline study). In the second study subjects received infusions of hydrocortisone for 48 h in a pulsatile and diurnal pattern that replicated serum cortisol levels in healthy subjects (physiological study). In most cases, the dose of hydrocortisone was 19 mg/24 h, but this was adjusted as necessary until the resulting serum cortisol levels reproduced those seen in healthy, nonstressed control subjects. In the third study subjects received the same total dose of hydrocortisone as in the physiological study, but with pulses of equal magnitude spaced evenly throughout the time period (constant study). In the fourth study subjects received the same total dose of hydrocortisone, but with the diurnal pattern shifted 12 h from the physiological infusion (reversed study). TSH levels were measured every 15 min during the final 24 h of each study. During the baseline study, the 24-h mean TSH level was 2.87 ± 0.56 mU/L and did not exhibit any diurnal variation. During the physiological study, daytime TSH levels decreased 39% compared to those during the baseline study due to decreased TSH pulse amplitude, and the normal TSH diurnal rhythm was reestablished. The constant and reversed studies did not lead to significant changes in serum TSH levels compared to baseline. These results suggest that the normal circadian variation in endogenous cortisol levels may control TSH secretion, with maximal TSH suppression seen during the time when cortisol levels are highest. However, changing the diurnal pattern of hydrocortisone infusion did not lead to reciprocal changes in TSH levels, and the specific nature of the interactions between cortisol and TSH within the physiological range remains to be fully elucidated.

scholarly journals Effects of Metyrapone Administration on Thyrotropin Secretion in Healthy Subjects–A Clinical Research Center Study*

2000 ◽  
Vol 85 (9) ◽  
pp. 3049-3052
Author(s):  
M. H. Samuels
Keyword(s):  
Healthy Subjects ◽  
Circadian Variation ◽  
Random Order ◽  
Pulse Amplitude ◽  
Serum Cortisol ◽  
Early Morning ◽  
Free T4 ◽  
Tsh Secretion ◽  
Cortisol Levels ◽  
Tsh Levels

Abstract Although pharmacological doses of glucocorticoids suppress TSH secretion, less is known regarding the effects of physiological variations in cortisol levels on TSH. To study this issue, 12 healthy subjects each underwent 2 studies, in random order: 1) each subject received an infusion of saline for 48 h; and 2) each subject received an infusion of saline and oral administration of metyrapone (500 mg every 4 h) for 48 h. Cortisol and TSH levels were measured every 15 min during the final 24 h of each study, and resulting mean hormone levels during the 24-h periods were compared between the two studies. Metyrapone administration reduced serum cortisol levels by 39% between 0800 and 1345 h and by 47% between 0200 and 0745 h, with no significant changes during other time periods. Metyrapone increased daytime (0800–1945 h) mean TSH levels by 35%, with no change in nocturnal (2000–0745 h) TSH levels. This led to equalization of daytime and nocturnal TSH levels and abolition of the usual circadian variation in TSH. TSH pulse frequency was no different between the two studies, whereas daytime TSH pulse amplitude increased 33% during metyrapone administration. There were no changes in TSH responses to TRH, or in serum T3 or free T4 levels, at the end of the studies. These results suggest that the early morning increase in endogenous cortisol levels in healthy subjects causes the daytime decrease in TSH levels. In addition, these results show that very mild changes in cortisol levels within the physiological range are sufficient to affect TSH secretion.

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.

scholarly journals Assessment of Adrenal Function in Women Heterozygous for Adrenoleukodystrophy1

1997 ◽  
Vol 82 (3) ◽  
pp. 856-860
Author(s):  
Samer S. El-Deiry ◽  
Sakkubai Naidu ◽  
Lewis S. Blevins ◽  
Paul W. Ladenson
Keyword(s):  
Fatty Acid ◽  
Adrenal Insufficiency ◽  
Serum Cortisol ◽  
Chain Fatty Acid ◽  
Acth Stimulation ◽  
Long Chain Fatty Acid ◽  
Increased Risk ◽  
The Mean ◽  
Cortisol Levels ◽  
Long Chain

Abstract Adrenoleukodystrophy (ALD) is an X-linked recessive disorder that destroys the white matter of the brain and is associated with adrenal insufficiency. The prevalence of adrenal dysfunction in 71 women carriers of the X-linked ALD gene was studied. These subjects were identified initially on the basis of being obligate carriers of the X-linked trait by pedigree analysis and were confirmed by plasma very long chain fatty acid levels consistent with a heterozygote status. One subject had well documented overt adrenal insufficiency, diagnosed and treated since age 9 yr. Among the remaining women, the mean serum 0800 h and 1 h post-ACTH cortisol concentrations [16 ± 7 (±sd) and 34 ± 8 μg/dL, respectively] were normal. All subjects had normal ACTH-stimulated serum cortisol levels, i.e. more than 20 μg/dL. However, 4 subjects (6%) had subnormal ACTH-stimulated aldosterone concentrations (mean, 9 ± 6 vs. 42 ± 16 ng/dL for other subjects; P = 0.001, by Mann Whitney rank sum test). Three of these women (75%) were taking nonsteroidal antiinflammatory agents (NSAIDs), whereas only 4 of 67 (6%) subjects with normal aldosterone responsiveness were NSAIDs users (P < 0.01, by Fisher’s exact test). Thus, NSAIDs use was associated with increased risk of hypoaldosteronism (odds ratio, 50.2; 95% confidence interval, 3.3–266; P < 0.002). Three of these four women had symptoms consistent with mineralocorticoid deficiency. Serum sodium and potassium concentrations were normal in all subjects. Basal and metyrapone-stimulated plasma ACTH concentrations were also normal in adequately tested subjects with and without mineralocorticoid insufficiency. Five of eight subjects (63%) who underwent testing with synthetic ovine CRH (oCRH) had abnormalities. Three did not meet the criteria for adequate cortisol stimulation (i.e. >20 μg/dL) and had peak ACTH levels greater than 30 pg/mL. Two other subjects had exaggerated ACTH responses with normal cortisol levels. There were no significant differences in the mean or median levels of very long chain fatty acid, C26:0, C24/22 ratios, or C26/22 ratios among the entire subject group, the subgroup with blunted aldosterone responses to ACTH, and the subgroup with blunted responses to oCRH (P > 0.05, by ANOVA and Kruskall-Wallis test for C26, C24/22 ratio, and C26/22 ratio). We conclude that 1) adrenal cortical insufficiency rarely develops in ALD heterozygotes; 2) isolated mineralocorticoid insufficiency can occur in ALD heterozygotes, as has been previously reported to occur with autoimmune and acquired immunodeficiency syndrome-related adrenal dysfunction; 3) ALD heterozygosity may predispose these individuals to NSAID-related hypoaldosteronism; and 4) a subclinical decrease in glucocorticoid reserve, as measured by oCRH testing, may be present in a majority of these women. Aldosterone levels should be included in the ACTH stimulation testing when seeking evidence of adrenal insufficiency in affected women. NSAIDs should be considered a risk factor for the development of hypoaldosteronism in women heterozygous for ALD.

Rapid adaptations of serum thyrotrophin, triiodothyronine and reverse triiodothyronine levels to short-term starvation and refeeding

1984 ◽  
Vol 105 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Jean-Noel Hugues ◽  
Albert G. Burger ◽  
A. Eugene Pekary ◽  
Jerome M. Hershman
Keyword(s):  
Serum Cortisol ◽  
Starvation Period ◽  
Short Term ◽  
Mean Values ◽  
Fed State ◽  
Tsh Secretion ◽  
The Mean ◽  
Serum Tsh ◽  
Tsh Levels

Abstract. Nutrition influences thyroid function at the level of TSH secretion, at the level of monodeiodination, and possibly elsewhere. In order to study the effect of starvation on TSH secretion, 8 healthy male volunteers fasted for 30 h and were then refed with 800 kcal. Refeeding was performed at 19.00 h and blood was sampled at 20 min intervals until midnight. Control experiments were performed in the same subjects both when they were normally fed and when the starvation period was prolonged a further 5 h until midnight. Starvation decreased serum TSH levels to below 1 mU/l, and without refeeding the nocturnal peak of the TSH nycthemeral rhythm was abolished. With refeeding serum TSH tended to increase towards midnight and was significantly higher than during starvation. However, the serum TSH levels remained significantly below those at the same time of the day in the absence of a preceding starvation period. Serum T3 levels were significantly lower than in the fed state. The mean values were 1.84 ± 0.03 vs 2.30 ± 0.06 nmol/l (120 ±2 vs 150 ± 4 ng/100 ml, mean ± sem P < 0.01). Refeeding did not result in a measurable change in serum T3 concentration (1.80 ± 0.05 nmol/l; 120 ± 3 ng/100 ml, mean ± sem, n.s.). The contrary was true for rT3 levels which increased in starvation and tended to fall with refeeding, but this decrease was not significant. As glucocorticoids have been implicated in the control of monodeiodination and TSH secretion, serum cortisol levels were also measured. They did not differ during the 3 experimental periods. The results show that short-term starvation and refeeding may be a valuable tool for studying in vivo control of TSH secretion. The results show that short-term starvation and refeeding may be a valuable tool for studying in vivo control of TSH secretion.

Is the Correlation between Salivary Cortisol and Serum Cortisol Reliable Enough to Enable Use of Salivary Cortisol Levels in Preterm Infants?

2017 ◽  
Vol 34 (13) ◽  
pp. 1302-1305
Author(s):  
Katherine Wynne-Edwards ◽  
Parthiv Amin ◽  
Ruokun Zhou ◽  
Arun Sundaram ◽  
Tania Martinez-Soto ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Preterm Infants ◽  
Salivary Cortisol ◽  
Saliva Sample ◽  
Serum Cortisol ◽  
Relative Adrenal Insufficiency ◽  
Free Cortisol ◽  
Cortisol Levels ◽  
Paired Serum ◽  
Gestational Age At Birth

Background Newborn premature infants are susceptible to development of relative adrenal insufficiency following transition from fetal to extrauterine life. However, the best diagnostic test for adrenal insufficiency in neonates has yet to be developed. Objectives and Methods The aim of this study was (1) to assess the feasibility of obtaining sufficient saliva sample to allow measurement of cortisol by liquid chromatography coupled to tandem mass spectrometry and (2) to assess the correlation, if any, between salivary and serum cortisol in preterm infants of ≤32 weeks' gestational age at birth. Results Samples for 230 paired serum and saliva cortisol levels from 90 preterm infants were analyzed. 87.5% of samples collected had sufficient salivary volumes for measurement. Despite being statistically significant (p < 0.0001), the correlation (Spearman r = 0.674) between serum and salivary cortisol was not strong. Conclusion Salivary free cortisol measurement is feasible but cannot be used to accurately reflect serum total cortisol. Further studies comparing salivary free cortisol to serum free cortisol and establishing normative data are needed before salivary cortisol can be used for diagnostic purposes.

scholarly journals The Association of Low Blood Glucose and Low Serum Cortisol Levels in Severely Ill Children Admitted to Tertiary Referral Hospitals in Malawi: A Case-Control Study

2021 ◽  
Author(s):  
Fatsani Ngwalangwa ◽  
Clifford Katumbi ◽  
Queen Dube ◽  
Josephine Langton ◽  
Tim Baker ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Adrenal Insufficiency ◽  
Case Control Study ◽  
Serum Cortisol ◽  
Case Control ◽  
Cortisol Levels ◽  
Low Cortisol ◽  
Blood Glucose Concentrations ◽  
Control Study ◽  
Low Serum

Low blood glucose concentrations (< 5 mmol/L) in severely ill children presenting to hospitals in low-income countries are associated with mortality. Adrenal insufficiency with low cortisol levels may contribute to low blood glucose concentrations. Understanding the association between low cortisol and low blood glucose may assist in improving guidelines for management of severely ill children. The study aimed to determine the association between low serum cortisol and low blood glucose in severely ill children. A matched case-control study of children aged 1 month to 15 years was conducted at two tertiary hospitals in Malawi. Cases were children with blood glucose <5 mmol/L. Two age-matched controls with blood glucose of ≥5–15 mmol/L were enrolled per case. Low cortisol was defined as serum cortisol of <25 µg/dL (690 nmol/L) and adrenal insufficiency as serum cortisol of <10 µg/dL (276 nmol/L). A total of 54 cases and 108 controls were enrolled with, median age of 2.8 years (interquartile range [IQR]: 1.7–4.4). The median cortisol level was 58.7 µg/dL (IQR: 42.3–61.8) in cases and 40.9 µg/dL (IQR: 33.7–51.2) in controls (P = 0.911). The proportion of low cortisol was 4/54 (7.4%) in cases and 9/108 (8.3%) in controls. Logistic regression shows no association between low cortisol and low blood glucose (adjusted odds ratio: 0.33; 95% confidence interval, 0.04–3.02). Results suggest that there is no association between low cortisol and low blood glucose among severely ill children presenting to hospitals in Malawi. The reason for low blood glucose needs further investigation.

Effect of metoclopramide-A dopaminergic blocker and endogenous cortisol on TSH secretion in critically ill men

1985 ◽  
Vol 109 (1) ◽  
pp. 70-75 ◽  
Author(s):  
S. Ben Haim ◽  
L. Kahana ◽  
Y. Bentur ◽  
M. Sheinfeld ◽  
L. Levy ◽  
...  
Keyword(s):  
Thyroid Hormones ◽  
Critically Ill ◽  
Control Group ◽  
Basal Cortisol ◽  
Endogenous Cortisol ◽  
Tsh Secretion ◽  
Low Levels ◽  
Cortisol Levels ◽  
Peripheral Metabolism ◽  
Tsh Levels

Abstract. In 17 critically ill men, low levels of FT4, TT4, TT3 and elevated levels of rT3 and cortisol were found. In spite of the low levels of circulating thyroid hormones, TSH levels of the critically ill men were significantly lower than those of the control group, with no correlations to the high cortisol levels. After iv injection of metoclopramide (MCP), a dopamine (DA) receptor blocker, the TSH and prolactin (Prl) increments in the critically ill patients were significantly lower than in the controls. No correlation was observed between basal cortisol levels and integrated TSH response to MCP. It is suggested that increased DA tone or high cortisol levels are not responsible for the lower basal TSH levels and for the blunted TSH or Prl responses to MCP in the critically ill. High levels of cortisol may be responsible for the altered TT4 peripheral metabolism to TT3 and rT3 in these patients.

scholarly journals A Predictive Risk Score to Diagnose Adrenal Insufficiency in Outpatients: A 7 Year Retrospective Cohort Study

Medicines ◽  
2021 ◽  
Vol 8 (3) ◽  
pp. 13
Author(s):  
Worapaka Manosroi ◽  
Tanyong Pipanmekaporn ◽  
Jiraporn Khorana ◽  
Pichitchai Atthakomol ◽  
Mattabhorn Phimphilai
Keyword(s):  
Adrenal Insufficiency ◽  
Risk Score ◽  
Predictive Factors ◽  
Multivariable Analysis ◽  
Positive Likelihood Ratio ◽  
Serum Cortisol ◽  
Risk Level ◽  
Dynamic Tests ◽  
Cortisol Levels ◽  
Predictive Risk

Background: The diagnosis of adrenal insufficiency (AI) requires dynamic tests which may not be available in some institutions. This study aimed to develop a predictive risk score to help diagnose AI in outpatients with indeterminate serum cortisol levels. Methods: Five hundred and seven patients with intermediate serum cortisol levels (3–17.9 µg/dL) who had undergone ACTH (adrenocorticotropin) stimulation tests were included in the study. A predictive risk score was created using significant predictive factors identified by multivariable analysis using Poisson regression clustered by ACTH dose. Results: The seven predictive factors used in the development of a predictive model with their assigned scores are as follows: chronic kidney disease (9.0), Cushingoid appearance in exogenous steroid use (12.0), nausea and/or vomiting (6.0), fatigue (2.0), basal cortisol <9 µg/dL (12.5), cholesterol <150 mg/dL (2.5) and sodium <135 mEq/L (1.0). Predictive risk scores range from 0–50.0. A high risk level (scores of 19.5–50.0) indicates a higher possibility of having AI (positive likelihood ratio (LR+) = 11.75), while a low risk level (scores of <19.0) indicates a lower chance of having AI (LR+ = 0.09). The predictive performance of the scoring system was 0.82 based on the area under the curve. Conclusions: This predictive risk score can help to determine the probability of AI and can be used as a guide to determine which patients need treatment for AI and which require dynamic tests to confirm AI.

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