scholarly journals Cushing’s Syndrome Effects on the Thyroid

2021 ◽  
Vol 22 (6) ◽  
pp. 3131
Author(s):  
Rosa Maria Paragliola ◽  
Andrea Corsello ◽  
Giampaolo Papi ◽  
Alfredo Pontecorvi ◽  
Salvatore Maria Corsello
Keyword(s):  
Thyroid Function ◽  
Cushing’S Syndrome ◽  
Immunological Tolerance ◽  
Cushing's Syndrome ◽  
Autoimmune Thyroid Diseases ◽  
Central Hypothyroidism ◽  
Immunological Mechanism ◽  
Autoimmune Thyroid ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

The most known effects of endogenous Cushing’s syndrome are the phenotypic changes and metabolic consequences. However, hypercortisolism can exert important effects on other endocrine axes. The hypothalamus–pituitary–thyroid axis activity can be impaired by the inappropriate cortisol secretion, which determinates the clinical and biochemical features of the “central hypothyroidism”. These findings have been confirmed by several clinical studies, which also showed that the cure of hypercortisolism can determine the recovery of normal hypothalamus–pituitary–thyroid axis activity. During active Cushing’s syndrome, the “immunological tolerance” guaranteed by the hypercortisolism can mask, in predisposed patients, the development of autoimmune thyroid diseases, which increases in prevalence after the resolution of hypercortisolism. However, the immunological mechanism is not the only factor that contributes to this phenomenon, which probably includes also deiodinase-impaired activity. Cushing’s syndrome can also have an indirect impact on thyroid function, considering that some drugs used for the medical control of hypercortisolism are associated with alterations in the thyroid function test. These considerations suggest the utility to check the thyroid function in Cushing’s syndrome patients, both during the active disease and after its remission.

scholarly journals The Hypothalamic-Pituitary-Thyroid Axis in Cushing Syndrome before and after Curative Surgery

2020 ◽  
Author(s):  
Skand Shekhar ◽  
Raven McGlotten ◽  
Sunyoung Auh ◽  
Kristina I Rother ◽  
Lynnette K Nieman
Keyword(s):  
Thyroid Function ◽  
Cushing’S Syndrome ◽  
Cushing Syndrome ◽  
Cushing's Syndrome ◽  
Curative Surgery ◽  
Central Hypothyroidism ◽  
Duration Of Symptoms ◽  
Before And After ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

Abstract Background We do not fully understand how hypercortisolism causes central hypothyroidism or what factors influence recovery of the hypothalamic-pituitary-thyroid axis. We evaluated thyroid function during and after cure of Cushing’s syndrome (CS). Methods We performed a retrospective cohort study of adult patients with CS seen from 2005 – 2018 (cohort 1, c1, n=68) or 1985 – 1994 (cohort 2, c2, n=55) at a clinical research center. Urine (UFC) and diurnal serum cortisol (F: ~8AM and ~midnight (PM)), morning triiodothyronine (T3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) (c1) or hourly TSH from 1500-1900h (day) and 2400-04000h (night) (c2), were measured before and after curative surgery. Results While hypercortisolemic, 53% of c1 had central hypothyroidism (low/low normal fT4 + unelevated TSH). Of those followed long-term, 31% and 44% had initially subnormal FT4 and T3, respectively, which normalized 6—12 months after cure. Hypogonadism was more frequent in hypothyroid (69%) compared to euthyroid (13%) patients. Duration of symptoms, AM and PM F, ACTH, and UFC were inversely related to TSH, FT4 and/or T3 levels (r -0.24 to -0.52, P <0.0001 to 0.02). In c2, the nocturnal surge of TSH (mIU/L) was subnormal before (day 1.00±0.04 vs night 1.08±0.05, p=0.3) and normal at a mean of 8 months after cure (day 1.30±0.14 vs night 2.17±0.27, p=0.01). UFC >1000 μg /day was an independent adverse prognostic marker of time to thyroid hormone recovery. Conclusions Abnormal thyroid function, likely mediated by subnormal nocturnal TSH, is prevalent in Cushing’s syndrome and is reversible after cure.

scholarly journals Diminished and irregular TSH secretion with delayed acrophase in patients with Cushing's syndrome

2009 ◽  
Vol 161 (5) ◽  
pp. 695-703 ◽  
Author(s):  
Ferdinand Roelfsema ◽  
Alberto M Pereira ◽  
Nienke R Biermasz ◽  
Marijke Frolich ◽  
Daniel M Keenan ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Approximate Entropy ◽  
Pituitary Surgery ◽  
Pulse Frequency ◽  
Cushing's Syndrome ◽  
Pituitary Thyroid Axis ◽  
Tsh Secretion ◽  
Thyroid Axis ◽  
Serum Tsh ◽  
Active Disease

ContextThe hypothalamus–pituitary–thyroid axis in Cushing's syndrome may be altered. Previous reports have shown diminished serum TSH concentration and decreased response to TRH.ObjectiveWe analyzed serum TSH profiles in relation to cortisol profiles in patients with hypercortisolism of pituitary (n=16) or primary-adrenal origin (n=11) and after remission by pituitary surgery (n=7) in order to delineate aberrations in the hypothalamus–pituitary–thyroid system.InterventionPatients and controls (n=27) underwent a 24-h blood sampling study. Serum TSH and cortisol were measured with precise methods, and data were analyzed with a deconvolution program, approximate entropy (ApEn), and cosinor regression.ResultsPulsatile TSH secretion and mean TSH pulse mass were diminished during hypercortisolism, independently of etiology (P<0.001). TSH secretion was increased in patients in remission only during daytime due to increased basal secretion (P<0.01). Pulse frequency and half life of TSH were similar in patients and controls. TSH ApEn (irregularity) was increased in patients with hypercortisolism (P<0.01), but was normal in cured patients. Cross-ApEn between TSH and cortisol, a measure of pattern synchrony loss, was increased in active disease, indicating (partial) loss of secretory synchrony. The TSH rhythm was phase delayed in hypercortisolemic patients, but normal in cured patients (P<0.01). Free thyroxine levels were decreased only in pituitary-dependent hypercortisolism compared with controls (P=0.003). Total 24-h TSH correlated negatively and linearly with log-transformed cortisol secretion (R=0.43, P=0.001).ConclusionCortisol excess decreases TSH secretion by diminishing pulsatile release, whereas surgically cured patients have elevated nonpulsatile TSH release. Diminished TSH secretory regularity in active disease suggests glucocorticoid-induced dysregulation of TRH or somatostatinergic/annexin-1 control.

scholarly journals Chronothyroidology: Chronobiological Aspects in Thyroid Function and Diseases

Life ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 426
Author(s):  
Giuseppe Bellastella ◽  
Maria Ida Maiorino ◽  
Lorenzo Scappaticcio ◽  
Annamaria De Bellis ◽  
Silvia Mercadante ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Biological Rhythms ◽  
Cellular Level ◽  
Scientific Discipline ◽  
Biological Phenomena ◽  
Pituitary Thyroid Axis ◽  
Circadian Organization ◽  
Thyroid Axis ◽  
Central Clock ◽  
Thyroid Dysfunctions

Chronobiology is the scientific discipline which considers biological phenomena in relation to time, which assumes itself biological identity. Many physiological processes are cyclically regulated by intrinsic clocks and many pathological events show a circadian time-related occurrence. Even the pituitary–thyroid axis is under the control of a central clock, and the hormones of the pituitary–thyroid axis exhibit circadian, ultradian and circannual rhythmicity. This review, after describing briefly the essential principles of chronobiology, will be focused on the results of personal experiences and of other studies on this issue, paying particular attention to those regarding the thyroid implications, appearing in the literature as reviews, metanalyses, original and observational studies until 28 February 2021 and acquired from two databases (Scopus and PubMed). The first input to biological rhythms is given by a central clock located in the suprachiasmatic nucleus (SCN), which dictates the timing from its hypothalamic site to satellite clocks that contribute in a hierarchical way to regulate the physiological rhythmicity. Disruption of the rhythmic organization can favor the onset of important disorders, including thyroid diseases. Several studies on the interrelationship between thyroid function and circadian rhythmicity demonstrated that thyroid dysfunctions may affect negatively circadian organization, disrupting TSH rhythm. Conversely, alterations of clock machinery may cause important perturbations at the cellular level, which may favor thyroid dysfunctions and also cancer.

scholarly journals Dopamine agonist-responsive Cushing’s disease

2019 ◽  
Vol 12 (2) ◽  
pp. bcr-2018-228045
Author(s):  
Gurpreet Anand ◽  
Andrea Bink ◽  
Felix Beuschlein ◽  
Christoph Schmid
Keyword(s):  
Growth Hormone ◽  
Dopamine Agonist ◽  
Cushing’S Syndrome ◽  
Tumour Size ◽  
Hypogonadotropic Hypogonadism ◽  
Immunohistochemical Analysis ◽  
Cushing's Syndrome ◽  
Central Hypothyroidism ◽  
Mri Scans

A 47-year-old Caucasian man was referred to our clinic with a severe clinical and biochemical phenotype of endogenous hypercortisolism for further evaluation and treatment. In addition to confirming adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome, we found left temporal hemianopsia, massively increased prolactin, increased growth hormone/insulin-like growth factor 1 values, hypogonadotropic hypogonadism and central hypothyroidism. As the cause of these abnormalities we revealed an invasive macroadenoma of the pituitary secreting ACTH, prolactin and growth hormone, resulting not only in a clinically predominant picture of Cushing’s syndrome but also causing hypogonadotropic hypogonadism and central hypothyroidism. The patient responded surprisingly well to dopamine agonist treatment leading not only to normalisation of prolactin levels but also to clinical and biochemical remission of Cushing’s syndrome. Tumour size decreased successively in follow-up MRI scans. Despite lacking immunohistochemical analysis of tumour tissue, we assume plurihormonal secretion of ACTH, prolactin and growth hormone from pituitary macroadenoma, which fortunately responded well to dopamine agonist treatment.

Plasma neurotensin levels in humans: relation to hormone levels in diseases involving the hypothalamo-pituitary-thyroid axis

1995 ◽  
Vol 133 (5) ◽  
pp. 534-538 ◽  
Author(s):  
Rose-Marie Schimpff ◽  
Micheline Gourmelen ◽  
Valérie Scarcériaux ◽  
Anne-Marie Lhiaubet ◽  
William Rostène
Keyword(s):  
Healthy Adults ◽  
Thyroid Status ◽  
Central Hypothyroidism ◽  
Mean Values ◽  
Hormone Levels ◽  
Percentage Decrease ◽  
Pituitary Thyroid Axis ◽  
Endocrine Status ◽  
Thyroid Axis ◽  
Adult Volunteers

Schimpff R-M, Gourmelen M, Scarcériaux V, Lhiaubet A-M, Rostène W. Plasma neurotensin levels in humans: relation to hormone levels in diseases involving the hypothalamo-pituitary-thyroid axis. Eur J Endocrinol 1995;133:534–8. ISSN 0804–4643 This study was aimed to investigate, in humans, the possible relationship between plasma neurotensin (NT) levels and the activity of the hypothalamo-pituitary-thyroid axis. Neurotensin was measured by radioimmunoassay in 14 healthy adult volunteers and in 41 patients among whom 10 were considered as controls and 31 had thyroid dysfunction according to free thyroxine and thyrotropin plasma values. Basal NT levels were not significantly different in healthy adults and in control patients: 9.7 ± 1.1 fmol/ml (mean±sem) vs 13.3 ± 2.9fmol/ml, respectively. In patients with central hypothyroidism the NT level was significantly lower (5.7 ± 1.2 vs healthy volunteers and controls; p < 0.05) and in patients with peripheral hypothyroidism and hyperthyroidism the NT level was significantly higher (35.9 ± 12.8 and 29.9 ± 9.5 fmol/ml, respectively, vs healthy adults (p < 0.01) and vs controls (p < 0.05)). After thyrotropin-releasing hormone (TRH) injection (250 μg iv) in nine subjects (two control patients, five patients with hypothyroidism and two patients with hyperthyroidism), NT levels decreased independently of the endocrine status from mean values of 13.4 ± 8.4 at basal level to 7.3 ± 0.8 fmol/ml 30 min after injection (p < 0.01 on paired percentage decrease values). These data suggest that plasma NT levels in humans depend upon the pituitary-thyroid status and indicate that TRH could exert a negative regulation on circulating NT levels. R-M Schimpff, INSERM U 339. Hôpital St Antoine, 184 rue du Faubourg, St Antoine, Paris 75012, France

THE EFFECT OF STREPTOZOTOCIN-INDUCED DIABETES ON THE PITUITARY-THYROID AXIS IN GOITROGEN-TREATED RATS

1977 ◽  
Vol 86 (1) ◽  
pp. 128-139 ◽  
Author(s):  
Isabel Pericás ◽  
Trinidad Jolín
Keyword(s):  
Body Weight ◽  
Thyroid Function ◽  
Growth Response ◽  
Thyroid Tissue ◽  
Diabetic Rats ◽  
Poor Growth ◽  
Pituitary Thyroid Axis ◽  
Tsh Secretion ◽  
Thyroid Axis ◽  
Intact Rats

ABSTRACT Studies of pituitary and thyroid function have been carried out in normal (intact) and diabetic Wistar rats. Diabetes was induced by a single streptozotocin injection (7 mg/100 g body weight). The animals were fed a low iodine diet (LID), and received a daily sc injection of either KClO4 (20 mg/100 g body weight) or propylthiouracil (PTU) (1.5 mg/100 g body weight) to induce hypothyroidism. Control groups received the same LID but supplemented with 0.8 μg I/g dry weight. In intact rats goitrogen-treatment induces an increase in thyroid weight and in plasma TSH concentration. However, the plasma TSH response to goitrogen-treatment in diabetics indicates that pituitary TSH secretion increases following a reduction in plasma PBI, but the response is less marked than in controls. The difference in plasma TSH between control and diabetic rats provides an explanation for the findings that diabetes diminishes the thyroid growth response to goitrogen-treatment. Moreover, in intact rats the low pituitary TSH content is a consequence of the increase in pituitary TSH secretion, while in the diabetics the low pituitary TSH content cannot be explained by an increase in TSH secretion. The effect of diabetes on the pituitary-thyroid axis cannot be attributed specifically to poor growth, because the changes in pituitary-thyroid function which are observed in the diabetic groups are not seen in intact rats with a growth rate similar to that of insulin deficient rats. Insulin administration to goitrogen-treated diabetic rats results in 1) an increase in the ability of the thyroid tissue to respond to its trophic hormone, 2) an increase in pituitary TSH secretion in response to the lowering of plasma PBI and, 3) an increase in thyroid growth response to goitrogen-treatment. Results are discussed in relation to the assumption that the lack of adequate insulin levels, or its metabolic defects, diminishes the full response of the thyroid to TSH, and affects the pituitary TSH secretion probably as a consequence of altered hypothalamic control of the pituitary function.

scholarly journals Clinical Significance of Autoantibodies to Parietal Cells in Patients with Autoimmune Thyroid Diseases

Folia Medica ◽  
2013 ◽  
Vol 55 (2) ◽  
pp. 26-32 ◽  
Author(s):  
Julieta B. Gerenova ◽  
Irena M. Manolova ◽  
Vania I. Tzoneva
Keyword(s):  
Atrophic Gastritis ◽  
Clinical Significance ◽  
Thyroid Function ◽  
Hashimoto’S Thyroiditis ◽  
Thyroid Diseases ◽  
Parietal Cells ◽  
Hashimoto's Thyroiditis ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Function Group

ABSTRACT Clinical significance of autoantibodies to parietal cells (PCA) in patients with autoimmune thyroid diseases (ATD) remains contradictory. AIM: To characterize the frequency of PCA in patients with ATD; to clarify the role of gender and age in PCA positivity; to analyze the association of PCA with gastric or haematologic symptoms and with the levothyroxine dose required to achieve a serum TSH level within the normal range in treated Hashimoto’s thyroiditis (HT) patients. PATIENTS AND METHODS: PCA were measured using ELISA in 137 HT patients, divided into tree subgroups according to the thyroid function: group I included subjects with normal thyroid function; group II included patients with hypothyroidism, in group III were enrolled subjects treated with levothyroxine (LT4). We also studied the PCA positivity in 14 patients with active Graves’ disease and in 23 healthy controls. RESULTS: PCA positivity was found in 51 patients with autoimmune thyroid diseases, with an overall prevalence of 33.8%. No significant differences in PCA were observed between the groups of HT patients. The frequency of PCA in both genders was similar and there were no difference depending on age. In 7.3% of HT patients in different stages of disease we found clinically relevant gastric and/or haematologic symptoms; in 70% of them PCA were positive (OR = 5.5; 95% CI: 1.2 - 28.4; p = 0.009). PCA positive hypothyroid HT patients required higher LT4 doses than PCA negative (1.46 μg/kg vs 1.24 μg/kg, p = 0.04). CONCLUSIONS: PCA may be present in different stages in HT patients; this does not depend on the severity of disease. PCA concentrations may predict symptoms of atrophic gastritis in patients with Hashimoto’s thyroiditis. PCA positive HT patients require higher replacement doses of LT4. Presence of anemia, particularly microcytic anemia, was suggestive of undiagnosed atrophic gastritis.

scholarly journals Primary thyroid disorders in endogenous Cushing's syndrome

2002 ◽  
pp. 305-311 ◽  
Author(s):  
H Niepomniszcze ◽  
F Pitoia ◽  
SB Katz ◽  
R Chervin ◽  
OD Bruno
Keyword(s):  
Cushing’S Syndrome ◽  
Dynamic Testing ◽  
Imaging Techniques ◽  
Serum Cortisol ◽  
Cushing's Syndrome ◽  
Control Group ◽  
Thyroid Disorders ◽  
Thyroid Antibodies ◽  
Autoimmune Thyroid ◽  
Free Cortisol

OBJECTIVE: To study the prevalence of primary thyroid disorders in patients who underwent endogenous hypercortisolism. DESIGN: Retrospective evaluation of 59 patients with Cushing's syndrome (CS) who had, at least, a record of thyroid palpation by expert endocrinologists and basal measurements of TSH by second generation assays. When available, tri-iodothyronine and thyroxine serum levels, TRH-TSH tests and anti-thyroid antibodies were also analyzed. There were two age- and gender-matched control groups. The 'goiter control group' comprised 118 healthy subjects who underwent thyroid palpation. The 'antibody control group' was composed of 40 individuals who attended the blood bank of our hospital. Antibodies against thyroperoxidase and measurements of TSH were analyzed in their blood samples. METHODS: Available files of 83 CS patients admitted to our endocrine unit from 1985 to 1998 were examined. Fifty-nine patients (52 women and 7 men) with a mean age of 36.2 years (range 14-61 years) met the above requirements. Diagnosis of hypercortisolism had been established by a standard 1-mg overnight dexamethasone suppression test and urinary free cortisol (UFC). Etiological diagnosis involved dynamic testing, measurements of ACTH levels and imaging techniques. After treatment, all but one of the patients were cured or controlled of their hypercortisolism. This was established by the finding of subnormal serum cortisol concentrations and/or subnormal 24-h UFC levels. Primary thyroid disorders were defined by the presence of one or more of the following diagnostic criteria: (i) goiter, (ii) positive anti-thyroid antibodies and/or (iii) primary thyroid function abnormalities. RESULTS: Eighteen (30.5%) patients had goiter (diffuse in 78% and nodular in 22%), 14 (23.7%) had primary subclinical hypothyroidism and 5 (8.4%) had hyperthyroidism. In 41 patients evaluated for antithyroid antibodies, it was found that 23 (56.1%) had positive titers. In a group of patients in which thyroid autoantibodies were measured both before and after resolution of hypercortisolism, prevalences of positive titers were 26.7% and 86.7% respectively (P=0.001). The overall frequency of primary thyroid abnormalities in our patients with Cushing's syndrome was 55.9%. CONCLUSIONS: Patients with endogenous Cushing's syndrome exhibit a remarkably high prevalence of primary thyroid disease. Resolution of hypercortisolism seems to trigger the development of autoimmune thyroid disorders in presumably predisposed subjects.

Somatostatin immunoneutralization stimulates thyroid function in fowl

1986 ◽  
Vol 110 (1) ◽  
pp. 127-132 ◽  
Author(s):  
S.-K. Lam ◽  
S. Harvey ◽  
T. R. Hall ◽  
G. S. G. Spencer
Keyword(s):  
Thyroid Gland ◽  
Thyroid Function ◽  
Inhibitory Control ◽  
Domestic Fowl ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

ABSTRACT The influence of somatostatin on thyroid function has been examined in immature domestic fowl passively immunized with somatostatin antiserum. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations were markedly increased within 10 min of antisomatostatin administration and remained raised for at least 5 h. The increases in the T3 and T4 concentrations following somatostatin immunoneutralization were directly related to the volume of antisera administered. The increase in the T3 concentration exceeded the increase in the T4 concentration, resulting in a T3: T4 ratio greater than unity. While the raised T4 concentration began to decline 30 min after antisomatostatin administration, raised T3 concentrations were sustained for at least 2 h, and further increased the plasma T3: T4 ratio. These results demonstrate that somatostatin immunoneutralization stimulates thyroid function in fowl. The magnitude and rapidity of the thyroidal responses to somatostatin immunoneutralization suggests that they occur independently of the hypothalamic-pituitary-thyroid axis. Somatostatin appears to exert a tonic inhibitory control on avian thyroid function, possibly by effects mediated at the thyroid gland to inhibit T4 release and by peripheral effects to suppress the conversion of T4 and T3. J. Endocr. (1986) 110, 127–132

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