On the Mechanism of Alcohol-Induced Pseudo-Cushing's Syndrome

Veldman, R. Groote; Meinders, A. E.

doi:10.1210/edrv-17-3-262

Cited by 50 publications

(19 citation statements)

References 70 publications

(89 reference statements)

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“…29 In the present study, the lack of compensatory suppression of cortisol secretion in the face of enhanced peripheral sensitivity to cortisol could be explained by factors that increase central drive to corticotropin-releasing hormone and ACTH secretion and thereby overcome any tendency for increased negative feedback. These include psychological stress, 30 depression, alcohol excess, 31 and obesity, 32,33 all of which increase cortisol secretion and have been proposed as independent risk factors for cardiovascular disease. 34,35 In our data, indices of obesity and alcohol intake did not correlate with peripheral glucocorticoid sensitivity, but they were associated with enhanced cortisol secretion and had an additive effect with dermal glucocorticoid sensitivity on insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Increased Glucocorticoid Activity in Men With Cardiovascular Risk Factors

et al. 1998

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Abstract-The association between hypertension and insulin resistance might be explained by increased activity of the principal glucocorticoid, cortisol. Recent data show that the intensity of dermal vasoconstriction after topical application of glucocorticoids is increased in patients with essential hypertension. In this report, we examine whether increased glucocorticoid sensitivity or secretion is associated with insulin resistance and is a cause or consequence of hypertension. We studied 32 men (aged 47 to 56 years) from a cross-sectional study and 105 men (aged 23 to 33 years) in whom predisposition to high blood pressure has been defined by their own blood pressure and the blood pressures of their parents. In both populations, increased dermal glucocorticoid sensitivity was associated with relative hypertension, insulin resistance, and hyperglycemia. In young men with higher blood pressure whose parents also had high blood pressure, enhanced glucocorticoid sensitivity was accompanied by enhanced secretion of cortisol, enhanced ligand-binding affinities for dexamethasone in leukocytes, and impaired conversion of cortisol to inactive metabolites (cortisone and 5␤-dihydrocortisol). Increased tissue sensitivity to cortisol, amplified by enhanced secretion of cortisol, is a feature of the familial predisposition to high blood pressure rather than a secondary effect of high blood pressure. It may be mediated by an abnormal glucocorticoid receptor, and it may contribute to the association between hypertension and insulin resistance. (Hypertension. 1998;31:891-895.)Key Words: receptors, corticosteroid Ⅲ adrenal cortex hormones Ⅲ blood pressure Ⅲ insulin Ⅲ blood vessels M any patients with atheromatous disease have identifiable risk factors, including hypertension, insulin resistance, glucose intolerance, and central obesity. These risk factors often occur together, 1 but the reason for their association is not clear. The same list of abnormalities can be reproduced in Cushing's syndrome, caused by excessive activity of glucocorticoid hormones such as cortisol. In health, the activity of cortisol is determined by a combination of factors, including secretion rate from the adrenal, metabolic clearance rate, and tissue sensitivity. Recent studies suggest that these factors may be abnormal in patients with essential hypertension, in whom impaired metabolism of cortisol 2,3 is accompanied by increased sensitivity to glucocorticoids in the skin. 4 Similarly, in inbred rats with hypertension, glucocorticoid metabolism is impaired 5 and sensitivity of mesenteric vessels to dexamethasone is enhanced. 6 In addition, in rats and humans, polymorphisms of the glucocorticoid receptor gene have been linked with high blood pressure 7,8 and insulin resistance. The aims of the present studies were to establish whether abnormalities of glucocorticoid secretion, metabolism, or tissue sensitivity are (1) associated with hypertension, insulin resistance, glucose intolerance, and obesity and (2) likely to be a cause or consequence of hyp...

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Section: Discussionmentioning

confidence: 99%

Increased Glucocorticoid Activity in Men With Cardiovascular Risk Factors

et al. 1998

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“…In addition, nutritional stress is often associated with a metabolic disorder termed fatty liver syndrome. Red deer stags during the rut in the wild have a high incidence (80%) of fatty liver syndrome (Kapp et al 1989) which may impair liver function reducing the synthesis of CBG (Veldman & Meinders 1996) and can directly inhibit steroidogenesis by limiting the availability of cholesteryl esters used in the synthesis of steroid hormones (Morrow et al 1979, Nakagawa et al 1997.…”

Section: Discussionmentioning

confidence: 99%

Ultradian, circadian and seasonal rhythms in cortisol secretion and adrenal responsiveness to ACTH and yarding in unrestrained red deer (Cervus elaphus) stags

Ingram

Crockford²,

Matthews³

1999

Journal of Endocrinology

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Seasonal changes in the activity and responsiveness of the adrenal gland in red deer (Cervus elaphus) stags were quantified by measuring 24 h endogenous cortisol secretory profiles and plasma cortisol responses to either administration of exogenous ACTH or a standardised stressor during November (period of velvet growth), February (pre-rut), April (mid-rut) and July (post-rut) (southern hemisphere) using a remote blood sampling device (DracPac).Ultradian rhythms in the concentration of plasma cortisol were observed resulting from the episodic secretion of cortisol from the adrenal cortex at a mean rate of 0·8 pulses/h. Circadian rhythms in plasma cortisol concentrations were also found in 11 out of the 20 complete 24 h profiles (mean amplitude, 3·8 1·4 ng/ml).Seasonal rhythms in mean 24 h plasma cortisol concentrations and cortisol pulse parameters were also observed. Mean 24 h plasma cortisol concentrations were higher in November (12·5 1·0 ng/ml) than in February (6·3 1·0 ng/ml), April (4·0 1·0 ng/ml) or July (4·2 1·0 ng/ml). Cortisol pulse height, nadir and amplitude were all significantly higher in November than at other times of the year (P<0·01).Peak cortisol concentrations following infusion of ACTH 1-24 (0·04 IU kg -1 ) were higher (P<0·05) in November (55·8 2·7 ng/ml) and lower (P<0·001) in April (33·7 1·8 ng/ml) than those in February and July (48·7 2·0 ng/ml and 45·4 2·0 ng/ml respectively). The area under the cortisol response curve was significantly smaller (P<0·05) in April (266·6 15·3 ng/ml/ 190 min) than at other times of the year (February, 366·1 15·3 ng/ml/190 min; July, 340·7 15·3 ng/ml/ 190 min and November, 387·8 21·2 ng/ml/190 min).These data demonstrate that the adrenal gland of the red deer stag exhibits ultradian, circadian and seasonal rhythms in activity, and that its responsiveness to ACTH varies with season. November, a period of reproductive quiescence in the southern hemisphere, with new antler growth and rapid weight gain, is associated with higher mean plasma cortisol concentrations and a greater responsiveness to exogenous ACTH. In contrast, the breeding season is associated with lower adrenal activity and responsiveness.

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“…A duração do alcoolismo e o período de abstinência podem alterar a atividade do eixo HHA. A parada abrupta na ingestão de álcool estimula o eixo HHA (talvez secundário ao estresse) e este efeito tende a diminuir com o progredir do período de abstinência (21)(22)(23). Estudos mostram que muitas vezes é necessário um período em torno de 2 a 4 meses de abstinência para que o eixo HHA volte ao estado normal (24)(25)(26).…”

Section: Alcoolismounclassified

“…O fato de apenas alguns etilistas desenvolverem o estado de PC, seja clínico e/ou bioquímico, demonstra que a predisposição genética ou a sensibilidade tanto ao álcool quanto ao cortisol também influenciam na etiopatologia dessa doença (21).…”

Section: Estados De Pseudo-cushingunclassified

Estados de pseudo-Cushing

Romanholi

Salgado

2007

Arq Bras Endocrinol Metab

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Síndromes de pseudo-Cushing são um grupo heterogêneo de doenças, incluindo alcoolismo, anorexia nervosa, obesidade visceral e depressão, que compartilham muitas das características clínicas e bioquímicas da síndrome de Cushing. Os mecanismos responsáveis para a gênese da síndrome de pseudo-Cushing são fracamente compreendidos. Tem sido sugerido que o hipercortisolismo da síndrome de pseudo-Cushing pode ser resultante do aumento da secreção do hormônio liberador de corticotrofina (CRH) hipotalâmico no contexto de um eixo hipotálamo-hipofisário-adrenal que, de outra maneira, está normalmente constituído. A sobreposição substancial entre as características clínicas e laboratoriais entre muitos pacientes com síndrome de Cushing e aqueles com síndrome de pseudo-Cushing pode tornar o diagnóstico diferencial difícil. Distinguir entre síndrome de pseudo-Cushing e síndrome de Cushing verdadeira é crítico para se prevenir o tratamento desnecessário e potencialmente prejudicial de tais pacientes. Esta breve revisão sumariza os principais eventos patofisiológicos das síndromes de pseudo-Cushing e fornece uma estratégia útil para o seu diagnóstico diferencial.

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On the Mechanism of Alcohol-Induced Pseudo-Cushing's Syndrome

Cited by 50 publications

References 70 publications

Increased Glucocorticoid Activity in Men With Cardiovascular Risk Factors

Increased Glucocorticoid Activity in Men With Cardiovascular Risk Factors

Ultradian, circadian and seasonal rhythms in cortisol secretion and adrenal responsiveness to ACTH and yarding in unrestrained red deer (Cervus elaphus) stags

Estados de pseudo-Cushing

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