Effects of Different Treatments for Hyperthyroidism on the Hypothalamic–pituitary–adrenal Axis

Lizcano, Fernando; Salvador, Javier

doi:10.1111/j.1440-1681.2008.04966.x

Cited by 13 publications

(19 citation statements)

References 30 publications

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“…These series of treatment (complete thyroid ablation with high dose of thyroid hormone) are sometimes performed to reduce the recurrence of cancer [11,12]. However, such high dose of thyroid hormone may affect HPA axis, since we have previously reported that hyperthyroid patients show hyperactivity of HPA axis with augmented ACTH responses to exogenous hCRH, but with a practically normal response of cortisol [6]. In the present study, patients with supinduced a hypersensitivity of ACTH to hCRH.…”

Section: Discussionmentioning

confidence: 53%

“…Total (T) T4, TT3, Free T4 and Free T3 levels were measured by radioimmunoassay (RIA) using commercially available kits (CIS Bio-International, Gif-sur-Ivette, France), as reported previously (6). TSH concentrations were measured by IRMA (CIS Bio-International).…”

Section: Hormone Assaysmentioning

confidence: 99%

“…ACTH and cortisol levels were measured by immunoradiometric assay (IRMA) and radioimmunoassay (RIA), respectively, as reported previously (6). Total (T) T4, TT3, Free T4 and Free T3 levels were measured by radioimmunoassay (RIA) using commercially available kits (CIS Bio-International, Gif-sur-Ivette, France), as reported previously (6).…”

Section: Hormone Assaysmentioning

confidence: 99%

“…We have previously demonstrated that hyperthyroid patients have an adrenocorticotropin (ACTH) hypersensitivity to human corticotropin-releasing hormone (hCRH) [6]. On the other hand, another study showed a decreased response of cortisol to ACTH administration, which may be due to diminished adrenocortical reserve [7].…”

mentioning

confidence: 99%

“…Subclinical hyperthyroidism, characterized by low thyroid stimulating hormone (TSH) and normal free thyroid hormone concentrations in serum, has been associated with an independent risk factor for Alzheimer's disease, cognitive dysfunction and cardiovascular diseases [3][4][5].We have previously demonstrated that hyperthyroid patients have an adrenocorticotropin (ACTH) hypersensitivity to human corticotropin-releasing hormone (hCRH) [6]. On the other hand, another study showed a decreased response of cortisol to ACTH administration, which may be due to diminished adrenocortical reserve [7].…”

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confidence: 99%

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Thyroid hormone therapy modulates hypothalamo-pituitary-adrenal axis

Lizcano

Rodríguez

2011

Endocr J

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Thyroid hormones (thyroxine, T4; triiodothyronine, T3) have intricate effects in different organs [1,2]. Subclinical hyperthyroidism, characterized by low thyroid stimulating hormone (TSH) and normal free thyroid hormone concentrations in serum, has been associated with an independent risk factor for Alzheimer's disease, cognitive dysfunction and cardiovascular diseases [3][4][5].We have previously demonstrated that hyperthyroid patients have an adrenocorticotropin (ACTH) hypersensitivity to human corticotropin-releasing hormone (hCRH) [6]. On the other hand, another study showed a decreased response of cortisol to ACTH administration, which may be due to diminished adrenocortical reserve [7]. These findings indicate that hyperthyroidism modulates hypothalamo-pituitary-adrenal (HPA) axis. Patients on thyroid suppression therapy due to differentiated thyroid cancer usually have subclinical hyperthyroidism, which may increase the risks of a mild irreg- Abstract. To observe the influence of thyroid hormone therapy on hypothalamo-pituitary-adrenal (HPA) axis, a group of 14 athyreotic women due to thyroid cancer treatment were studied before and after thyroid suppression therapy with thyroxine (T4). Changes in plasma adrenocorticotropin (ACTH) and cortisol levels in response to human corticotropinreleasing hormone (hCRH; 100μg, i.v.) were estimated under hypothyroid conditions and after T4 suppression therapy with 2.5µg/kg/day for two months (n=14). A group of seven healthy women was evaluated as a control group. A greater increase in ACTH levels by hCRH was observed in patient group both before and after suppression therapy compared than that of control group. Plasma cortisol levels after hCRH stimulation were also greater in patient group both before and after suppression therapy than that of control group. In conclusion, both hypothyroidism and subclinical hyperthyroidism with suppressive doses of thyroid hormone induced a hypersensitivity of ACTH to hCRH. Considering the role of thyroid hormone on HPA axis, the mechanisms of ACTH hypersensitivity may be different between these two conditions.Key words: Adrenocorticotropin, hCRH, Cortisol, Thyroid hormone, Hypothalamo-pituitary-adrenal axis ular heart rhythms and decrease in bone density [8].However, a small number of studies have examined the consequences of thyroid suppression therapy on HPA axis [9]. In order to investigate the changes in HPA axis following thyroid hormone therapy, a group of hypothyroid patients was studied before and after administration of L-T4 (levothyroxine) suppressive doses (2.5µg/ kg/day) for two months. Methods PatientsFourteen hypothyroid women aged between 30 and 57 years (mean age 42.9±3.2 years) were studied. All patients had an ablative therapy for a thyroid cancer with total surgical thyroidectomy and I 131 therapy. During the study, a total body I 131 scan was negative for thyroid remnants, and plasma thyroglobulin levels were below detectable concentration. One month after the ablative therapy, patients reached to hypothyroid s...

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Section: Discussionmentioning

confidence: 53%

Section: Hormone Assaysmentioning

confidence: 99%

Section: Hormone Assaysmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Thyroid hormone therapy modulates hypothalamo-pituitary-adrenal axis

Lizcano

Rodríguez

2011

Endocr J

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Ghrelin and GHRP-6-induced ACTH and cortisol release in thyrotoxicosis

et al. 2009

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Thyrotoxicosis might alter the hypothalamic-pituitary-adrenal (HPA) axis. We evaluated the effects of ghrelin and GHRP-6 on the HPA axis in 20 hyperthyroid patients and in 9 controls. Mean basal cortisol (microg/dl) and ACTH (pg/ml) levels were higher in hyperthyroidism (cortisol: 10.7 +/- 0.7; ACTH: 21.5 +/- 2.9) compared to controls (cortisol: 8.1 +/- 0.7; ACTH: 13.5 +/- 1.8). In thyrotoxicosis Delta AUC cortisol values (microg/dl.90 min) after ghrelin (484 +/- 80) and GHRP-6 (115 +/- 63) were similar to controls (ghrelin: 524 +/- 107; GHRP-6: 192 +/- 73). A significant increase in Delta AUC ACTH (pg/ml x 90 min) after ghrelin was observed in thyrotoxicosis (4,189 +/- 1,202) compared to controls (1,499 +/- 338). Delta AUC ACTH values after GHRP-6 were also higher, although not significantly (patients: 927 +/- 330; controls: 539 +/- 237). In summary, our results suggest that ghrelin-mediated pathways of ACTH release might be activated by thyroid hormone excess, but adrenocortical reserve is maintained.

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Effects of ghrelin, GH-releasing peptide-6 (GHRP-6) and GHRH on GH, ACTH and cortisol release in hyperthyroidism before and after treatment

et al. 2010

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In thyrotoxicosis GH responses to stimuli are diminished and the hypothalamic-pituitary-adrenal axis is hyperactive. There are no data on ghrelin or GHRP-6-induced GH, ACTH and cortisol release in treated hyperthyroidism. We, therefore, evaluated these responses in 10 thyrotoxic patients before treatment and in 7 of them after treatment. GHRH-induced GH release was also studied. Peak GH (μg/L; mean ± SE) values after ghrelin (22.6 ± 3.9), GHRP-6 (13.8 ± 2.3) and GHRH (4.9 ± 0.9) were lower in hyperthyroidism before treatment compared to controls (ghrelin: 67.6 ± 19.3; GHRP-6: 25.4 ± 2.7; GHRH: 12.2 ± 2.8) and did not change after 6 months of euthyroidism (ghrelin: 32.7 ± 4.7; GHRP-6: 15.6 ± 3.6; GHRH: 7.4 ± 2.3), although GH responses to all peptides increased in ~50% of the patients. In thyrotoxicosis before treatment ACTH response to ghrelin was two fold higher (107.4 ± 26.3) than those of controls (54.9 ± 10.3), although not significantly. ACTH response to GHRP-6 was similar in both groups (hyperthyroid: 44.7 ± 9.0; controls: 31.3 ± 7.9). There was a trend to a decreased ACTH response to ghrelin after 3 months of euthyroidism (35.6 ± 5.3; P = 0.052), but after 6 months this decrease was non-significant (50.7 ± 14.0). After 3 months ACTH response to GHRP-6 decreased significantly (20.4 ± 4.2), with no further changes. In hyperthyroidism before treatment, peak cortisol (μg/dL) responses to ghrelin (18.2 ± 1.2) and GHRP-6 (15.9 ± 1.4) were comparable to controls (ghrelin: 16.4 ± 1.6; GHRP-6: 13.5 ± 0.9) and no changes were seen after treatment. Our results suggest that the pathways of GH release after ghrelin/GHRP-6 and GHRH are similarly affected by thyroid hormone excess and hypothalamic mechanisms of ACTH release modulated by ghrelin/GHSs may be activated in this situation.

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Effects of Different Treatments for Hyperthyroidism on the Hypothalamic–pituitary–adrenal Axis

Cited by 13 publications

References 30 publications

Thyroid hormone therapy modulates hypothalamo-pituitary-adrenal axis

Thyroid hormone therapy modulates hypothalamo-pituitary-adrenal axis

Ghrelin and GHRP-6-induced ACTH and cortisol release in thyrotoxicosis

Effects of ghrelin, GH-releasing peptide-6 (GHRP-6) and GHRH on GH, ACTH and cortisol release in hyperthyroidism before and after treatment

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