Thyroid Axis in Patients With Cushing's Syndrome

Duick, Daniel S.

doi:10.1001/archinte.1979.03630440033013

Cited by 55 publications

(15 citation statements)

References 42 publications

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“…However, as mentioned above, the thyroid gland displays evident signs of activation that are in agreement with the enhanced plasmatic levels of T3 and T4 reported after adrenalectomy (MITSUMA and NOGIMORI, 1982). Similarly serum concentration of thyroxine is elevated in patients receiving prolonged therapy with glucocorticoids or with an endogenous Cushing's syndrome (DUICK and WAHNER, 1979;TAVIANINI et al, 1989).…”

Section: Discussionsupporting

confidence: 82%

Analysis of the Pituitary‐Thyroid Axis in Bilaterally Adrenalectomized or Adrenal Transplanted Rats

Sarrı́a

Losada

Oliver

1994

Anat Histol Embryol

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The percentage, distribution, shape, intensity of staining and morphometrical parameters of the pituitary TSH immunoreactive cells and the histological features of the thyroid glands, were compared between adult rats with intact adrenals, without adrenals and biadrenalectomized animals with neonatal adrenal grafts. After the removal of the adrenal glands, TSH immunoreactive cells increased in percentage and exhibited a higher complexity of the cellular outline, than that of the intact animals. The nuclear, cytoplasmic and cell areas were significantly increased. However the bigger enhancement of the cytoplasmic area relative to the nuclear area, produced a decrease in the nuclear/cell area ratio. The thyroid glands showed some histological evidences of activation. After the transplantation of neonatal adrenal glands to adult rats, several adrenocortical nodules were present in the lumen of the small bowel segment. These adrenal masses induced a great decrease in the TSH cell area, which coupled with a smaller but significant variation of the nuclear area, led to an increase in the nuclear/cell area ratio relative to that observed in adrenalectomized animals. In addition, the distribution, shape and intensity of the immunoreactive material was similar to that observed in intact animals. In this experimental group, thyroid histology was observed to be similar to that of the intact animals.

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Section: Discussionsupporting

confidence: 82%

Analysis of the Pituitary‐Thyroid Axis in Bilaterally Adrenalectomized or Adrenal Transplanted Rats

Sarrı́a

Losada

Oliver

1994

Anat Histol Embryol

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“…Activation of the HPA axis is associated with decreased production of thyroid-stimulating hormone (TSH) and inhibition of the enzymatic conversion (5-deiodinase) of the relatively inactive thyroxine (T4) to the more biologically active triiodothyronine (T3) in peripheral tissues ("euthyroid sick" syndrome). 96,97 Although the exact mechanism(s) for these phenomena is not known, the increased levels of glucocorticoids are considered the primary cause. Inhibition of thyrotropin-releasing hormone (TRH) and TSH secretion by CRH-stimulated increases in SRIF might also participate in the central component of the thyroid axis suppression during stress.…”

Section: Adaptive Stress Response-metabolic Interactions and Complicamentioning

confidence: 99%

Stress, Visceral Obesity, and Metabolic Complications

Kyrou

Chrousos

Tsigos³

2006

Annals of the New York Academy of Sciences

299

267

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Stress is a state of threatened homeostasis or disharmony caused by intrinsic or extrinsic adverse forces and is counteracted by an intricate repertoire of physiologic and behavioral responses that aim to reestablish the challenged body equilibrium. The adaptive stress response depends upon an elaborate neuroendocrine, cellular, and molecular infrastructure, the stress system. Crucial functions of the stress system response are mediated by the hypothalamic-pituitary-adrenal (HPA) axis and the central and peripheral components of the autonomic nervous system (ANS). The integrity of the HPA axis and the ANS and their precise interactions with other CNS components are essential for a successful response to the various stressors. Chronic stress represents a prolonged threat to homeostasis by persistent or frequently repeated stressors and may lead to manifestations that characterize a wide range of diseases and syndromes. Such states progressively lead to a deleterious overload with complications caused by both the persistent stressor and the detrimental prolongation of the adaptive response. The metabolic syndrome can be described as a state of deranged metabolic homeostasis characterized by the combination of central obesity, insulin resistance, dyslipidemia, and hypertension. The incidence of both obesity and the metabolic syndrome in modern Western societies has taken epidemic proportions over the past decades and often correlates with indices of stress in the affected populations. Stress, primarily through hyperactivation of the HPA axis, appears to contribute to the accumulation of fat tissue, and vice versa, obesity itself seems to constitute a chronic stressful state and may cause HPA axis dysfunction. In addition, the description of obesity as a systemic low grade inflammatory condition that contributes to the derangement of the metabolic equilibrium implies that the proinflammatory cytokines which are secreted by the adipocytes hold a potentially important pathogenetic role. In this article we describe the physiology of the stress system response, with emphasis on metabolism, and review the recent data that implicate several neuroendocrine and inflammatory mechanisms mobilized during chronic stress in the development of the metabolic complications that characterize central obesity and the metabolic syndrome.

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“…A parallel phenomenon is the suppression of thyroid axis function. Glucocorticoid‐induced suppressed secretion of TSH and decreased conversion of the relatively inactive thyroxine (T4) to the potent triiodothyronine (T3) in peripheral tissues occur during stress 25,26 . In addition, endogenous TRH and TSH secretion may be suppressed by CRH‐induced somatostatin.…”

Section: Interactions Of the Hpa Axis With The Reproductive Growth mentioning

confidence: 99%

The Hypothalamic‐Pituitary‐Adrenal Axis and the Female Reproductive System

Magiakou

Mastorakos

Webster

et al. 1997

Annals of the New York Academy of Sciences

221

119

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The hypothalamic-pituitary-adrenal (HPA) axis and the female reproductive system are intertwined and exhibit a complex relationship. Thus, the HPA axis exerts profound, mostly inhibitory effects, on the reproductive axis, with corticotropin-releasing hormone (CRH) and CRH-induced propiomelanocortin peptides inhibiting hypothalamic GnRH secretion, and with glucocorticoids inhibiting pituitary LH and ovarian estrogen and progesterone secretion and rendering estrogen-target tissues, such as the endometrium, resistant to the gonadal steroid. These effects of the HPA axis are responsible for the "hypothalamic" amenorrhea of stress, depression and eating disorders, and the hypogonadism of Cushing's syndrome. Conversely, estrogen directly stimulates the CRH gene, which may explain the slight hypercortisolism of females and the preponderance of depressive, anxiety, and eating disorders, as well as Cushing's disease in women. Interestingly, several components of the HPA axis and their receptors are present in reproductive tissues, as autocoid regulators of their various functions. These include ovarian and endometrial CRH, which may participate in the inflammatory processes of the ovary, that is, ovulation and luteolysis, and of the endometrium, that is, implantation and menstruation. Finally, the hypercortisolism of the latter half of pregnancy can be explained by high levels of placenta CRH in plasma. This hypercortisolism causes a transient adrenal suppression in the postpartum period, which may explain the postpartum blues/depression and autoimmune phenomena of this period.

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Thyroid Axis in Patients With Cushing's Syndrome

Cited by 55 publications

References 42 publications

Analysis of the Pituitary‐Thyroid Axis in Bilaterally Adrenalectomized or Adrenal Transplanted Rats

Analysis of the Pituitary‐Thyroid Axis in Bilaterally Adrenalectomized or Adrenal Transplanted Rats

Stress, Visceral Obesity, and Metabolic Complications

The Hypothalamic‐Pituitary‐Adrenal Axis and the Female Reproductive System

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