24-Hour Blood Pressure Profile in Addison’s Disease

Fallo, Francesco; Fanelli, Gianluca; Cipolla, Antonio; Betterle, Corrado; Boscaro, Marco; Sonino, Nicoletta

doi:10.1093/ajh/7.12.1105

Cited by 32 publications

(17 citation statements)

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“…The CTS of AI is highly abnormal, with alteration of the Φ and absence of many circadian rhythms, for example, serum glucose and insulin sensitivity (Björnsdottir et al, 2015;Meyer et al, 2012), BP (Fallo et al, 1994), H 2 O diuresis (Azerad et al, 1957), muscle strength (Reinberg et al, 1971(Reinberg et al, , 1974, sleep staging and fatigue (García-Borreguero et al, 2000;Kong et al, 1999;Langenheim et al, 2013) and certain hormones -cortisol, renin, angiotensin, aldosterone and thyroid stimulating hormone in serum and 17-hydroxycorticosteroid (17-OHCS) and 17-ketosteroid (17-KS) metabolites in urine, plus urinary K + and Na + (Azerad et al, 1957;Björnsdottir et al, 2015;Chan & Debono, 2010;Cugini et al, 1993;Reinberg et al, 1971Reinberg et al, , 1974Samuels, 2000).…”

Section: Adrenocortical Insufficiencymentioning

confidence: 99%

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Smolensky

Hermida

Reinberg

et al. 2016

Chronobiology International

156

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Biological processes are organized in time as innate rhythms defined by the period (τ), phase (peak [Φ] and trough time), amplitude (A, peak-trough difference) and mean level. The human time structure in its entirety is comprised of ultradian (τ < 20 h), circadian (20 h > τ < 28 h) and infradian (τ > 28 h) bioperiodicities. The circadian time structure (CTS) of human beings, which is more complicated than in lower animals, is orchestrated and staged by a brain central multioscillator system that includes a prominent pacemaker - the suprachiasmatic nuclei of the hypothalamus. Additional pacemaker activities are provided by the pineal hormone melatonin, which circulates during the nighttime, and the left and right cerebral cortices. Under ordinary circumstances this system coordinates the τ and Φ of rhythms driven by subservient peripheral cell, tissue and organ clock networks. Cyclic environmental, feeding and social time cues synchronize the endogenous 24 h clocks and rhythms. Accordingly, processes and functions of the internal environment are integrated in time for maximum biological efficiency, and they are also organized and synchronized in time to the external environment to ensure optimal performance and response to challenge. Artificial light at night (ALAN) exposure can alter the CTS as can night work, which, like rapid transmeridian displacement by air travel, necessitates realignment of the Φ of the multitude of 24 h rhythms. In 2001, Stevens and Rea coined the phrase "circadian disruption" (CD) to label the CTS misalignment induced by ALAN and shift work (SW) as a potential pathologic mechanism of the increased risk for cancer and other medical conditions. Current concerns relating to the effects of ALAN exposure on the CTS motivated us to renew our long-standing interest in the possible role of CD in the etiopathology of common human diseases and patient care. A surprisingly large number of medical conditions involve CD: adrenal insufficiency; nocturia; sleep-time non-dipping and rising blood pressure 24 h patterns (nocturnal hypertension); delayed sleep phase syndrome, non-24 h sleep/wake disorder; recurrent hypersomnia; SW intolerance; delirium; peptic ulcer disease; kidney failure; depression; mania; bipolar disorder; Parkinson's disease; Smith-Magenis syndrome; fatal familial insomnia syndrome; autism spectrum disorder; asthma; byssinosis; cancers; hand, foot and mouth disease; post-operative state; and ICU outcome. Poorly conceived medical interventions, for example nighttime dosing of synthetic corticosteroids and certain β-antagonists and cyclic nocturnal enteral or parenteral nutrition, plus lifestyle habits, including atypical eating times and chronic alcohol consumption, also can be causal of CD. Just as surprisingly are the many proven chronotherapeutic strategies available today to manage the CD of several of these medical conditions. In clinical medicine, CD seems to be a common, yet mostly unrecognized, pathologic mechanism of human disease as are the many effective chronotherapeutic int...

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Section: Adrenocortical Insufficiencymentioning

confidence: 99%

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Smolensky

Hermida

Reinberg

et al. 2016

Chronobiology International

156

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“…In addition to low blood pressure, a loss of circadian rhythm of blood pressure has also been recently described (12). To our knowledge, scanty data derived from direct measurements of cardiac function are available in the literature.…”

Section: Discussionmentioning

confidence: 99%

Regression of cardiac abnormalities after replacement therapy in Addison's disease

Fallo

Betterle

Budano

et al. 1999

European Journal of Endocrinology

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Objective: To evaluate by echocardiography the cardiac structure and function in patients with primary adrenocortical insufficiency. Design and Methods: Two-dimensionally guided M-mode echocardiograms and spectral Doppler studies were performed in seven consecutive patients with newly diagnosed autoimmune primary adrenal failure before and 4-8 months after an adequate regimen of steroid substitution. Echocardiographic parameters were also studied in ten healthy controls. Results: In the cases with untreated Addison's disease, both left ventricular end-systolic and enddiastolic dimensions were significantly reduced in comparison with those in controls (P < 0.01). Four patients had echocardiographic signs of mitral valve prolapse (MVP) at the anterior leaflet, with no evidence of mitral regurgitation by Doppler echocardiography. Systolic clicks characteristic of MVP were present on auscultation in two of these cases. Left ventricular chamber size normalized, i.e. significantly increased (P < 0.01), and both echocardiographic and physical signs of MVP resolved after steroid substitution in all patients. All other echocardiographic indices were normal before and after treatment. Conclusions: Patients with untreated Addison's disease have cardiac abnormalities which regress after steroid substitution. A valvular-ventricular disproportion due to the hypovolemic state could explain these findings.

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“…There is evidence to confirm the presence of the glucocorticoid receptor in vascular smooth muscle cells [48,49] and in the vascular endothelium [49][50][51], but little is known about its role at these sites. In vitro experiments with endothelial cell culture models have suggested that glucocorticoids regulate vascular reactivity via suppression of the production of vasodilators, such as prostacyclin and nitric oxide, but conflicting evidence exists in this regard.…”

Section: Vascular Glucocorticoid Effects and Nitric Oxidementioning

confidence: 99%

Glucocorticoid-induced hypertension

2011

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Glucocorticoid-induced hypertension is a common clinical problem that is poorly understood, thus rendering treatment strategies sub-optimal. This form of hypertension has been commonly thought to be mediated by excess sodium and water reabsorption by the renal mineralocorticoid receptor. However, experimental and clinical data in both humans and animal models suggest important roles for the glucocorticoid receptor as well, in both the pathogenesis and maintenance of this hypertension. The glucocorticoid receptor is widely expressed in a number of organ systems relevant to blood pressure regulation, including the kidney, the brain and the vasculature. In vitro studies in isolated kidney tissues as well as in vascular smooth muscle and vascular endothelial cells have attempted to elucidate the molecular physiology of glucocorticoid-induced hypertension, but have generally been limited by the inability to study signaling pathways in an intact organism. More recently, the power of mouse genetics has been employed to examine the tissue-specific contributions of vascular and extra-vascular tissues to this form of hypertension. Here we review recent developments in our understanding of the pathogenesis of glucocorticoid-induced hypertension.

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24-Hour Blood Pressure Profile in Addison’s Disease

Cited by 32 publications

References 0 publications

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Regression of cardiac abnormalities after replacement therapy in Addison's disease

Glucocorticoid-induced hypertension

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