Dissociated 24-Hour Patterns of Somatotropin and Prolactin in Fatal Familial Insomnia

Portaluppi, Francesco; Cortelli, Pietro; Avoni, Patrizia; Vergnani, L; Maltoni, Paolo; Pavani, A; Sforza, Émilia; Manfredini, Roberto; Montagna, Pasquale; Roiter, Ignazio; Gambetti, Pierluigi; Fersini, C; Lugaresi, E

doi:10.1159/000126901

Cited by 33 publications

(8 citation statements)

References 32 publications

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“…It should be noted that our results obtained in healthy subjects do not fit with the current view that insomnia lowers GH secretion (Lieb et al. , 1999; Portaluppi et al. , 1995; Vgontzas et al.…”

Section: Discussioncontrasting

confidence: 99%

The 24‐h growth hormone rhythm in men: sleep and circadian influences questioned

Brandenberger¹,

Weibel²

2004

Journal of Sleep Research

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SUMMAR Y The 24-h rhythm of growth hormone (GH) is thought to be controlled primarily by sleep processes with a weak circadian component. This concept has been recently questioned in sleep-deprived persons. To test the notion of a high sleep-dependency of GH release, we established simultaneous 24-h rhythms of GH and melatonin, a circadian marker, in night workers who form a model for challenging sleep and circadian processes. Ten day-active subjects and 11 night workers were studied during their usual sleep-wake schedule, with sleep from 23:00 to 07:00 hours and 07:00 to 15:00 hours, respectively. Experiments were conducted in sleep rooms under continuous nutrition, bed rest, and dim light. Melatonin and GH were measured every 10 min over 24 h. In day-active subjects, melatonin and GH showed the well-known 24-h profiles, with a major sleep-related GH pulse accounting for 52.8 ± 3.5% of the 24-h GH production and the onset of the melatonin surge occurring at 21:53 hours ± 18 min. In night workers, melatonin showed variable circadian adaptation, with the onset of secretion varying between 21:45 and 05:05 hours. The sleeprelated GH pulse was lowered, but the reduction was compensated for by the emergence of large individual pulses occurring unpredictably during waking periods, so that the total amount of GH secreted during the 24 h was constant. One cannot predict the degree of GH adaptation from the highly variable melatonin shift. These results argue against the concept that sleep processes exert a predominant influence on GH release whatever the conditions. When sleep and circadian processes are misaligned, the blunting of the sleep-related GH pulse is counteracted, as in sleep-deprived persons, by a compensatory mechanism promoting GH pulses during wakefulness.k e y w o r d s circadian rhythm, growth hormone, melatonin, night work, sleep

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Section: Discussioncontrasting

confidence: 99%

The 24‐h growth hormone rhythm in men: sleep and circadian influences questioned

Brandenberger¹,

Weibel²

2004

Journal of Sleep Research

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“…Hormonal studies in our patient demonstrated a flattening of circadian rhythmicity, which has also been described in cases of FFI (Portaluppi et al . 1995).…”

Section: Discussionsupporting

confidence: 87%

Transient total sleep loss in cerebral Whipple's disease: a longitudinal study

Voderholzer

Riemann

Gann

et al. 2002

Journal of Sleep Research

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SUMMAR Y A case with transient, almost complete sleep loss caused by cerebral manifestation of Whipple's disease (WD) is presented. Cerebral WD is rare and in most cases occurs after gastrointestinal infection. In our case, a progressive and finally almost complete sleep loss was the initial and predominant symptom. Polysomnographic studies in several consecutive nights and over 24 h showed a total abolition of the sleep-wake cycle with nocturnal sleep duration of less than 15 min. Endocrine tests revealed hypothalamic dysfunction with flattening of circadian rhythmicity of cortisol, TSH, growth hormone and melatonin. Cerebrospinal fluid (CSF) hypocretin was reduced.[ 18 F]Deoxyglucose positron emission tomography (FDG-PET) revealed hypermetabolic areas in cortical and subcortical areas including the brainstem, which might explain sleep pathology and vertical gaze palsy. In the course of treatment with antibiotics and additional carbamazepine for 1 year, insomnia slowly and gradually improved. Endocrine investigations at 1-year follow-up showed persistent flattening of circadian rhythmicity. The FDG-PET indicated normalized metabolism in distinct regions of the brain stem which paralleled restoration of sleep length. The extent of sleep disruption in this case of organic insomnia was similar to cases of familial fatal insomnia, but was at least partially reversible with treatment.k e y w o r d s cerebral Whipple's disease, functional brain imaging, hypocretin, infectious disease, insomnia, orexin, sleep loss

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“…-Sleep disorders [delayed sleep phase syndrome (Skene et al, 1999), non-24 h sleep/ wake disorder and sleep/wake schedule disorder (Dagan & Abadi, 2001;Uchiyama & Lockley, 2015), recurrent hypersomnia (Billiard et al, 2011), SW sleep disorder (Schwartz & Roth, 2006)] -SW intolerance (Andlauer & Reinberg, 1979;Reinberg et al, 1983Reinberg et al, , 1988) -Delirium (Fitzgerald et al, 2013) -Peptic ulcer disease (Moore & Merki, 1997;Moore & Smolensky, 1991) -Affective disorders [depression (BicakovaRocher et al, 1996;Rosenwasser & WirtzJustice, 1997;Salgado-Delgado et al, 2011), mania (Klemfuss & Kripke, 1989), bipolar disorder (Abreu & Bragança, 2015)] -Parkinson's disease (Bordet et al, 2003;Fertl et al, 1991;Willison et al, 2013) -Autism spectrum disorder (Botbol et al, 2013;Tordjman et al, 2015) -Smith-Magenis syndrome (Chen et al, 2015) -Fatal familial insomnia [autosomal dominant prion brain disease (Montagna et al, 1995;Portaluppi et al, 1994aPortaluppi et al, , 1994bPortaluppi et al, , 1995] -Kidney failure, especially end-stage disease (Biasioli et al, 1988;Farfel et al, 1978;Hillier et al, 1980;Koch et al, 2009;Mojón et al, 2013;Portaluppi et al, 1990;Raff & Trivedi, 2012;Russcher et al, 2015;Wheatley et al, 1989) -Pulm...…”

Section: Discussionmentioning

confidence: 99%

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

Smolensky

Hermida

Reinberg

et al. 2016

Chronobiology International

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151

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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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Dissociated 24-Hour Patterns of Somatotropin and Prolactin in Fatal Familial Insomnia

Cited by 33 publications

References 32 publications

The 24‐h growth hormone rhythm in men: sleep and circadian influences questioned

The 24‐h growth hormone rhythm in men: sleep and circadian influences questioned

Transient total sleep loss in cerebral Whipple's disease: a longitudinal study

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

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